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22.1: Anatomy and Normal Microbiota of the Respiratory Tract - Biology

22.1: Anatomy and Normal Microbiota of the Respiratory Tract - Biology


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Learning Objectives

  • Describe the major anatomical features of the upper and lower respiratory tract
  • Describe the normal microbiota of the upper and lower respiratory tracts
  • Explain how microorganisms overcome defenses of upper and lower respiratory-tract membranes to cause infection
  • Explain how microbes and the respiratory system interact and modify each other in healthy individuals and during an infection

clinical focus - part 1

John, a 65-year-old man with asthma and type 2 diabetes, works as a sales associate at a local home improvement store. Recently, he began to feel quite ill and made an appointment with his family physician. At the clinic, John reported experiencing headache, chest pain, coughing, and shortness of breath. Over the past day, he had also experienced some nausea and diarrhea. A nurse took his temperature and found that he was running a fever of 40 °C (104 °F).

John suggested that he must have a case of influenza (flu), and regretted that he had put off getting his flu vaccine this year. After listening to John’s breathing through a stethoscope, the physician ordered a chest radiography and collected blood, urine, and sputum samples.

Exercise (PageIndex{1})

Based on this information, what factors may have contributed to John’s illness?

The primary function of the respiratory tract is to exchange gases (oxygen and carbon dioxide) for metabolism. However, inhalation and exhalation (particularly when forceful) can also serve as a vehicle of transmission for pathogens between individuals.

Anatomy of the Upper Respiratory System

The respiratory system can be conceptually divided into upper and lower regions at the point of the epiglottis, the structure that seals off the lower respiratory system from the pharynx during swallowing (Figure (PageIndex{1})). The upper respiratory system is in direct contact with the external environment. The nares (or nostrils) are the external openings of the nose that lead back into the nasal cavity, a large air-filled space behind the nares. These anatomical sites constitute the primary opening and first section of the respiratory tract, respectively. The nasal cavity is lined with hairs that trap large particles, like dust and pollen, and prevent their access to deeper tissues. The nasal cavity is also lined with a mucous membrane and Bowman’s glands that produce mucus to help trap particles and microorganisms for removal. The nasal cavity is connected to several other air-filled spaces. The sinuses, a set of four, paired small cavities in the skull, communicate with the nasal cavity through a series of small openings. The nasopharynx is part of the upper throat extending from the posterior nasal cavity. The nasopharynx carries air inhaled through the nose. The middle ear is connected to the nasopharynx through the eustachian tube. The middle ear is separated from the outer ear by the tympanic membrane, or ear drum. And finally, the lacrimal glands drain to the nasal cavity through the nasolacrimal ducts (tear ducts). The open connections between these sites allow microorganisms to move from the nasal cavity to the sinuses, middle ears (and back), and down into the lower respiratory tract from the nasopharynx.

The oral cavity is a secondary opening for the respiratory tract. The oral and nasal cavities connect through the fauces to the pharynx, or throat. The pharynx can be divided into three regions: the nasopharynx, the oropharynx, and the laryngopharynx. Air inhaled through the mouth does not pass through the nasopharynx; it proceeds first through the oropharynx and then through the laryngopharynx. The palatine tonsils, which consist of lymphoid tissue, are located within the oropharynx. The laryngopharynx, the last portion of the pharynx, connects to the larynx, which contains the vocal fold (Figure (PageIndex{1})).

Exercise (PageIndex{2})

  1. Identify the sequence of anatomical structures through which microbes would pass on their way from the nares to the larynx.
  2. What two anatomical points do the eustachian tubes connect?

Anatomy of the Lower Respiratory System

The lower respiratory system begins below the epiglottis in the larynx or voice box (Figure (PageIndex{2})). The trachea, or windpipe, is a cartilaginous tube extending from the larynx that provides an unobstructed path for air to reach the lungs. The trachea bifurcates into the left and right bronchi as it reaches the lungs. These paths branch repeatedly to form smaller and more extensive networks of tubes, the bronchioles. The terminal bronchioles formed in this tree-like network end in cul-de-sacs called the alveoli. These structures are surrounded by capillary networks and are the site of gas exchange in the respiratory system. Human lungs contain on the order of 400,000,000 alveoli. The outer surface of the lungs is protected with a double-layered pleural membrane. This structure protects the lungs and provides lubrication to permit the lungs to move easily during respiration.

Defenses of the Respiratory System

The inner lining of the respiratory system consists of mucous membranes (Figure (PageIndex{3})) and is protected by multiple immune defenses. The goblet cells within the respiratory epithelium secrete a layer of sticky mucus. The viscosity and acidity of this secretion inhibits microbial attachment to the underlying cells. In addition, the respiratory tract contains ciliated epithelial cells. The beating cilia dislodge and propel the mucus, and any trapped microbes, upward to the epiglottis, where they will be swallowed. Elimination of microbes in this manner is referred to as the mucociliary escalator effect and is an important mechanism that prevents inhaled microorganisms from migrating further into the lower respiratory tract.

The upper respiratory system is under constant surveillance by mucosa-associated lymphoid tissue (MALT), including the adenoids and tonsils. Other mucosal defenses include secreted antibodies (IgA), lysozyme, surfactant, and antimicrobial peptides called defensins. Meanwhile, the lower respiratory tract is protected by alveolar macrophages. These phagocytes efficiently kill any microbes that manage to evade the other defenses. The combined action of these factors renders the lower respiratory tract nearly devoid of colonized microbes.

Exercise (PageIndex{3})

  1. Identify the sequence of anatomical structures through which microbes would pass on their way from the larynx to the alveoli.
  2. Name some defenses of the respiratory system that protect against microbial infection.

Normal Microbiota of the Respiratory System

The upper respiratory tract contains an abundant and diverse microbiota. The nasal passages and sinuses are primarily colonized by members of the Firmicutes, Actinobacteria, and Proteobacteria. The most common bacteria identified include Staphylococcus epidermidis, viridans group streptococci (VGS), Corynebacterium spp. (diphtheroids), Propionibacterium spp., and Haemophilus spp. The oropharynx includes many of the same isolates as the nose and sinuses, with the addition of variable numbers of bacteria like species of Prevotella, Fusobacterium, Moraxella, and Eikenella, as well as some Candida fungal isolates. In addition, many healthy humans asymptomatically carry potential pathogens in the upper respiratory tract. As much as 20% of the population carry Staphylococcus aureus in their nostrils.1 The pharynx, too, can be colonized with pathogenic strains of Streptococcus, Haemophilus, and Neisseria.

The lower respiratory tract, by contrast, is scantily populated with microbes. Of the organisms identified in the lower respiratory tract, species of Pseudomonas, Streptococcus, Prevotella, Fusobacterium, and Veillonella are the most common. It is not clear at this time if these small populations of bacteria constitute a normal microbiota or if they are transients.

Many members of the respiratory system’s normal microbiota are opportunistic pathogens. To proliferate and cause host damage, they first must overcome the immune defenses of respiratory tissues. Many mucosal pathogens produce virulence factors such as adhesins that mediate attachment to host epithelial cells, or polysaccharide capsules that allow microbes to evade phagocytosis. The endotoxins of gram-negative bacteria can stimulate a strong inflammatory response that damages respiratory cells. Other pathogens produce exotoxins, and still others have the ability to survive within the host cells. Once an infection of the respiratory tract is established, it tends to impair the mucociliary escalator, limiting the body’s ability to expel the invading microbes, thus making it easier for pathogens to multiply and spread.

Vaccines have been developed for many of the most serious bacterial and viral pathogens. Several of the most important respiratory pathogens and their vaccines, if available, are summarized in Table (PageIndex{1}). Components of these vaccines will be explained later in the chapter.

Table (PageIndex{1}): Some Important Respiratory Diseases and Vaccines
DiseasePathogenAvailable Vaccine(s)2
Chickenpox/shinglesVaricella-zoster virusVaricella (chickenpox) vaccine, herpes zoster (shingles) vaccine
Common coldRhinovirusNone
DiphtheriaCorynebacterium diphtheriaeDtaP, Tdap, DT,Td, DTP
Epiglottitis, otitis mediaHaemophilus influenzaeHib
InfluenzaInfluenza virusesInactivated, FluMist
MeaslesMeasles virusMMR
PertussisBordetella pertussisDTaP, Tdap
PneumoniaStreptococcus pneumoniaePneumococcal conjugate vaccine (PCV13), pneumococcal polysaccharide vaccine (PPSV23)
Rubella (German measles)Rubella virusMMR
Severe acute respiratory syndrome (SARS)SARS-associated coronavirus (SARS-CoV)None
TuberculosisMycobacterium tuberculosisBCG

Exercise (PageIndex{4})

  1. What are some pathogenic bacteria that are part of the normal microbiota of the respiratory tract?
  2. What virulence factors are used by pathogens to overcome the immune protection of the respiratory tract?

Signs and Symptoms of Respiratory Infection

Microbial diseases of the respiratory system typically result in an acute inflammatory response. These infections can be grouped by the location affected and have names ending in “itis”, which literally means inflammation of. For instance, rhinitis is an inflammation of the nasal cavities, often characteristic of the common cold. Rhinitis may also be associated with hay fever allergies or other irritants. Inflammation of the sinuses is called sinusitis inflammation of the ear is called otitis. Otitis media is an inflammation of the middle ear. A variety of microbes can cause pharyngitis, commonly known as a sore throat. An inflammation of the larynx is called laryngitis. The resulting inflammation may interfere with vocal cord function, causing voice loss. When tonsils are inflamed, it is called tonsillitis. Chronic cases of tonsillitis may be treated surgically with tonsillectomy. More rarely, the epiglottis can be infected, a condition called epiglottitis. In the lower respiratory system, the inflammation of the bronchial tubes results in bronchitis. Most serious of all is pneumonia, in which the alveoli in the lungs are infected and become inflamed. Pus and edema accumulate and fill the alveoli with fluids (called consolidations). This reduces the lungs’ ability to exchange gases and often results in a productive cough expelling phlegm and mucus. Cases of pneumonia can range from mild to life-threatening, and remain an important cause of mortality in the very young and very old.

Exercise (PageIndex{5})

Describe the typical symptoms of rhinitis, sinusitis, pharyngitis, and laryngitis.

SMOKING-ASSOCIATED PNEUMONIA

Camila is a 22-year-old student who has been a chronic smoker for 5 years. Recently, she developed a persistent cough that has not responded to over-the-counter treatments. Her doctor ordered a chest radiograph to investigate. The radiological results were consistent with pneumonia. In addition, Streptococcus pneumoniae was isolated from Camila’s sputum.

Smokers are at a greater risk of developing pneumonia than the general population. Several components of tobacco smoke have been demonstrated to impair the lungs’ immune defenses. These effects include disrupting the function of the ciliated epithelial cells, inhibiting phagocytosis, and blocking the action of antimicrobial peptides. Together, these lead to a dysfunction of the mucociliary escalator effect. The organisms trapped in the mucus are therefore able to colonize the lungs and cause infections rather than being expelled or swallowed.

Key Concepts and Summary

  • The respiratory tract is divided into upper and lower regions at the epiglottis.
  • Air enters the upper respiratory tract through the nasal cavity and mouth, which both lead to the pharynx. The lower respiratory tract extends from the larynx into the trachea before branching into the bronchi, which divide further to form the bronchioles, which terminate in alveoli, where gas exchange occurs.
  • The upper respiratory tract is colonized by an extensive and diverse normal microbiota, many of which are potential pathogens. Few microbial inhabitants have been found in the lower respiratory tract, and these may be transients.
  • Members of the normal microbiota may cause opportunistic infections, using a variety of strategies to overcome the innate nonspecific defenses (including the mucociliary escalator) and adaptive specific defenses of the respiratory system.
  • Effective vaccines are available for many common respiratory pathogens, both bacterial and viral.
  • Most respiratory infections result in inflammation of the infected tissues; these conditions are given names ending in -itis, such as rhinitis, sinusitis, otitis, pharyngitis, and bronchitis.

Multiple Choice

Which of the following is not directly connected to the nasopharynx?

A. middle ear
B. oropharynx
C. lacrimal glands
D. nasal cavity

C

What type of cells produce the mucus for the mucous membranes?

A. goblet cells
B. macrophages
C. phagocytes
D. ciliated epithelial cells

A

Which of these correctly orders the structures through which air passes during inhalation?

A. pharynx → trachea → larynx → bronchi
B. pharynx → larynx → trachea → bronchi
C. larynx → pharynx → bronchi → trachea
D. larynx → pharynx → trachea → bronchi

B

The ___________ separates the upper and lower respiratory tract.

A. bronchi
B. larynx
C. epiglottis
D. palatine tonsil

C

Which microbial virulence factor is most important for attachment to host respiratory tissues?

A. adhesins
B. lipopolysaccharide
C. hyaluronidase
D. capsules

A

Fill in the Blank

Unattached microbes are moved from the lungs to the epiglottis by the _______ effect.

mucociliary escalator

Many bacterial pathogens produce _______ to evade phagocytosis.

capsules

The main type of antibody in the mucous membrane defenses is _______.

IgA

_______ results from an inflammation of the “voice box.”

Laryngitis

_______ phagocytize potential pathogens in the lower lung.

Alveolar macrophages

Short Answer

Explain why the lower respiratory tract is essentially sterile.

Explain why pneumonia is often a life-threatening disease.

Critical Thinking

Name each of the structures of the respiratory tract shown, and state whether each has a relatively large or small normal microbiota.

(credit: modification of work by National Cancer Institute)

Cystic fibrosis causes, among other things, excess mucus to be formed in the lungs. The mucus is very dry and caked, unlike the moist, more-fluid mucus of normal lungs. What effect do you think that has on the lung’s defenses?

Why do you think smokers are more likely to suffer from respiratory tract infections?

Footnotes

  1. 1 J. Kluytmans et al. “Nasal Carriage of Staphylococcus aureus: Epidemiology, Underlying Mechanisms, and Associated Risks.” Clinical Microbiology Reviews 10 no. 3 (1997):505–520.
  2. 2 Full names of vaccines listed in table: Haemophilus influenzae type B (Hib); Diphtheria, tetanus, and acellular pertussis (DtaP); tetanus, diphtheria, and acellular pertussis (Tdap); diphtheria and tetanus (DT); tetanus and diphtheria (Td); diphtheria, pertussis, and tetanus (DTP); Bacillus Calmette-Guérin; Measles, mumps, rubella (MMR)

The respiratory microbiota during health and disease: a paediatric perspective

Recent studies investigating the relationship between the microbiota and disease are demonstrating novel concepts that could significantly alter the way we treat disease and promote health in the future. It is suggested that the microbiota acquired during childhood may shape the microbial community and affect immunological responses for later life, and could therefore be important in the susceptibility towards disease. Several diseases, including asthma, pneumonia, and otitis media, are associated with changes in composition and diversity of the respiratory microbiota. This review summarises current literature, focusing on the composition and development of the respiratory microbiota in children and its relationship with respiratory diseases.


Introduction

The human microbiome is a complex community of microorganisms, living in a symbiotic relationship in human microhabitats. Due to microbial niche specificity, microbial composition and function vary according to the different human body sites, such as the gastrointestinal tract, skin, and airways [1, 2].

Since a healthy adult breathes more than 7000 l of air a day, the upper respiratory tract (URT) is constantly bathed in airflow from the external environment. Along with the air, 10 4 –10 6 bacterial cells per cubic meter of air are inhaled per day. Besides these biological particulates, the URT is exposed to atmospheric physical and chemical parameters, including varying humidity, oxygen, immunological factors, or nutrients. Along with the anatomy, these factors shape specific microenvironments in the URT such as the nasal cavity, sinuses, nasopharynx, and oropharynx [3,4,5]. As a consequence, specific microenvironments in the URT harbor different microbial communities composed of variable proportions of resident and transient microorganisms [6].

Like other human body sites, the upper respiratory tract is colonized by a variety of different microbial species directly after birth. It has been shown that the initial colonization depends on delivery mode (vaginal delivery or caesarean section), and the most drastic changes occur during the first year of life, probably driven by the maturation of the immune system [7]. Later on, this first microbial community transforms into the adult URT microbiome, becoming less dense and more diverse. In the elderly, the distinct microbiomes of specific microenvironments become more similar [8, 9].

Many studies report that the nasal microbiome of healthy humans is primarily composed of the phyla Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria with representatives of genera Bifidobacterium, Corynebacterium, Staphylococcus, Streptococcus, Dolosigranulum, and Moraxella predominating [9,10,11,12]. However, most research focuses on the bacteria in the human nasal cavity, while other components of the microbiome, such as viruses, archaea, and fungi, are seldom specifically addressed and thus likely overlooked [13].

Human health has been described as the outcome of the complex interaction between the microbiome and its human host [14]. Functional or compositional perturbations of the microbiome can occur at different body sites and this dysbiosis has been linked with various diseases for example, inflammatory bowel disease and metabolic disorders have been linked to dysbiosis in the microbiome of the gastrointestinal tract and URT infections (URTI, such as chronic rhinosinusitis [CRS]) with dysbiosis in the URT [15,16,17,18]. These dysbioses are often characterized by a loss of beneficial, commensal bacteria, which protect against overgrowth of opportunistic pathogenic bacteria [6, 19, 20].

Currently, several different therapies are suggested for the treatment of inflammatory URTIs [21,22,23,24]. Antibiotics as well as intranasal corticosteroids are used, combining antimicrobial and anti-inflammatory properties [21, 24]. These treatments cause a loss of microbial diversity, potentially leading to an increase of Gram-negative bacteria in the nose [25,26,27].

In the case of chronic rhinosinusitis, sinus surgery (aiming at improving drainage of the mucus), combined with different antibiotics is the most common treatment [22]. Although this type of therapy is highly invasive, its outcomes are usually satisfactory [28]. However, airway diseases might also be prevented and treated with less aggressive therapies such as saline rinses, cleaning the nasal mucosa from inflammatory mediators and other pollutants [23].

Comparative URT microbiome research faces various methodological problems, including choice of sampling techniques (e.g., swabs, nasal rinses, and dry filter papers) and sampling sites. In most cases anterior nares, middle meatus, and nasopharynx are the preferred sites for sampling [9, 11, 12, 29,30,31], as other areas are not easily accessible. This often results in a discrepancy of research question and study protocol, as, e.g., the middle meatus is sampled instead of the sinuses when chronic rhinosinusitis is studied [29]. However, microbiome dysbiosis often extends to locations beyond the sites of the studied disease, so that significant alterations in the microbial community structure in adjacent locations can be observed as well [6, 32]. Nevertheless, in order to prove or reject a research hypothesis, the sampling sites for microbiome analyses need to be chosen wisely [6].

The aim of this review is to summarize the current information about the microbiome in the upper respiratory tract discuss methodological issues such as sampling methods and sites present the link between URT microbiome composition, immune system, and certain diseases have a look at the influence of common therapies on the URT microbiome and identify the current gaps in our knowledge.

Details of cited studies, including sampling, sample processing protocol, studied population and sites, and results are summarized in Additional file 1.


Anatomical development and the microbiota

Anatomical development and physiology. The development of the structures of the human respiratory tract is a complex multistage process that begins in the fourth week of gestation with the development of the nasal placodes, the oropharyngeal membrane and the lung buds 8,9 . The anatomy of the URT at birth is substantially different from the configuration in adults owing to the higher position of the larynx, which results in a large nasopharynx relative to the oropharynx 10 . In addition, the lack of alveoli in the newborn lungs underlines the immaturity of the LRT at birth. Indeed, the formation of alveoli begins in a late fetal stage and their development continues throughout the first three years of life 11 . By adulthood, many distinct subcompartments have developed in the respiratory tract, each of which has specific microbial, cellular and physiological features, such as oxygen and carbon dioxide tension, pH, humidity and temperature (Fig. 1).

Microbiota and the morphogenesis of the respiratory tract. Similar to the anatomical development of the respiratory tract, the initial acquisition of microorganisms marks the establishment of the respiratory microbiota in early life. The establishment of the respiratory microbiota is thought to have an effect on the morphogenesis of the respiratory tract. Indeed, germ-free rodents tend to have smaller lungs 12 and a decreased number of mature alveoli 5 . The latter finding was supported by experiments in which the nasal cavities of germ-free mouse pups were colonized with Lactobacillus spp., after which the number of mature alveoli normalized 5 . Intriguingly, the nasopharyngeal-associated lymphoid tissue (NALT) also develops mostly after birth, which suggests that its development requires environmental cues — for example, from the local microbiota 13 .

Development of healthy microbiota. In contrast to the long-standing hypothesis that we are born sterile, it was recently suggested that babies acquire microorganisms in utero 14,15 , although this suggestion is controversial 16 . Irrespectively, the transfer of maternal antibodies and microbial molecules in utero markedly influences postnatal immune development 17,18 . This, in turn, primes the newborn for the substantial exposure to microorganisms that occurs after birth. During the first hours of life, a wide range of microorganisms can be detected in the URT of healthy term neonates 19,20 . At first, these microorganisms are nonspecific and are of presumed maternal origin. During the first week of life, niche differentiation in the URT leads to a high abundance of Staphylococcus spp., followed by the enrichment of Corynebacterium spp. and Dolosigranulum spp., and the subsequent predominance of Moraxella spp. 20 . Microbiota profiles that are characterized by Corynebacterium spp. and Dolosigranulum spp. early in life, and Moraxella spp. at 4–6 months of age, have been shown to correlate to a stable bacterial community composition and respiratory health 21,22 .

Birth mode and feeding type are important drivers of the early maturation of the microbiota, with children who are born vaginally and/or are breastfed transitioning towards a presumed health-promoting microbiota profile more often and more swiftly 20,23 . These findings were corroborated by epidemiological findings that showed breastfeeding-mediated protection against infections 24 , which is presumably a consequence of the transfer of maternal antibodies 18 and beneficial microorganisms in breast milk, such as Bifidobacterium spp. and Lactobacillus spp. 25,26 . Conversely, the development of the respiratory microbiota can be disturbed, for example, through the use of antibiotics, which are commonly used in young children to treat infections 27 . Antibiotic perturbations were characterized by a decreased abundance of presumed beneficial commensal bacteria, such as Dolosigranulum spp. and Corynebacterium spp. in the URT of healthy children 22,28,29 . This, in turn, might increase the risk of respiratory tract infections following antibiotic treatment 30 . In addition, season, vaccination, presence of siblings, day-care attendance, exposure to smoke and prior infections can also affect the infant microbiota 22,31,32,33,34,35 , which indicates that the microbiota during early life is dynamic and affected by numerous host and environmental factors (Fig. 2). Host genetics seems to have a minor effect on the URT microbiota in healthy individuals, only influencing nasal bacterial density and not the composition of the microbiota 36 . By contrast, the composition of the sputum microbiota seems to be influenced equally by host genetics and environmental factors 37 .

During early life, microbial communities in the respiratory tract are highly dynamic and are driven by multiple factors, including mode of birth, feeding type, crowding conditions and antibiotic treatment. Together, these host and environmental factors can change the composition of the microbiota towards a stable community at equilibrium that is resistant to pathogen overgrowth, or, conversely, an unstable community develops that is predisposed to infection and inflammation.

Although the gut microbiota matures into an adult-like community during the first 3 years of life 38 , the time that is required to establish a stable respiratory microbiota remains to be determined. Although niche differentiation occurs as early as 1 week after birth 20 , the respiratory microbiota evolves throughout the first few years of life 21,33,39 . After the respiratory microbiota is established, antibiotic treatment remains an important perturbing factor of the microbial equilibrium throughout life 40 . Active smoking also affects the microbial communities in the URT 37,41 however, in the LRT, smoking has no clear influence on the composition of the microbiota 42 . Interestingly, it has been suggested that the niche-specific differences disappear again in the elderly 43 .

Remarkably, not only exposure to beneficial bacteria seems to be important but also the timing of these exposures seems to play a crucial part in the maintenance of respiratory health, as especially aberrant respiratory colonization patterns in infancy seem to be a major determinant of respiratory disease later in life 21,22,44 . This could be due to the effect of host–microbial interactions in immune education during early life 6 . It has been proposed that the dynamic nature of the developing microbiota early in life might provide a window of opportunity for the modulation of the microbiota towards a beneficial composition 45 however, the extent of this period of time is currently unknown.


General Signs and Symptoms of Oral and GI Disease

Despite numerous defense mechanisms that protect against infection, all parts of the digestive tract can become sites of infection or intoxication. The term food poisoning is sometimes used as a catch-all for GI infections and intoxications, but not all forms of GI disease originate with foodborne pathogens or toxins.

In the mouth, fermentation by anaerobic microbes produces acids that damage the teeth and gums. This can lead to tooth decay, cavities, and periodontal disease, a condition characterized by chronic inflammation and erosion of the gums. Additionally, some pathogens can cause infections of the mucosa, glands, and other structures in the mouth, resulting in inflammation, sores, cankers, and other lesions. An open sore in the mouth or GI tract is typically called an ulcer.

Infections and intoxications of the lower GI tract often produce symptoms such as nausea, vomiting, diarrhea, aches, and fever. In some cases, vomiting and diarrhea may cause severe dehydration and other complications that can become serious or fatal. Various clinical terms are used to describe gastrointestinal symptoms. For example, gastritis is an inflammation of the stomach lining that results in swelling and enteritis refers to inflammation of the intestinal mucosa. When the inflammation involves both the stomach lining and the intestinal lining, the condition is called gastroenteritis. Inflammation of the liver is called hepatitis. Inflammation of the colon, called colitis, commonly occurs in cases of food intoxication. Because an inflamed colon does not reabsorb water as effectively as it normally does, stools become watery, causing diarrhea. Damage to the epithelial cells of the colon can also cause bleeding and excess mucus to appear in watery stools, a condition called dysentery.

Think About It

Key Concepts and Summary

  • The digestive tract, consisting of the oral cavity, pharynx, esophagus, stomach, small intestine, and large intestine, has a normal microbiota that is important for health.
  • The constant movement of materials through the gastrointestinal canal, the protective layer of mucus, the normal microbiota, and the harsh chemical environment in the stomach and small intestine help to prevent colonization by pathogens.
  • Infections or microbial toxins in the oral cavity can cause tooth decay, periodontal disease, and various types of ulcers.
  • Infections and intoxications of the gastrointestinal tract can cause general symptoms such as nausea, vomiting, diarrhea, and fever. Localized inflammation of the GI tract can result in gastritis, enteritis, gastroenteritis, hepatitis, or colitis, and damage to epithelial cells of the colon can lead to dysentery.
  • Foodborne illness refers to infections or intoxications that originate with pathogens or toxins ingested in contaminated food or water.

Multiple Choice

Which of the following is NOT a way the normal microbiota of the intestine helps to prevent infection?

  1. It produces acids that lower the pH of the stomach.
  2. It speeds up the process by which microbes are flushed from the digestive tract.
  3. It consumes food and occupies space, outcompeting potential pathogens.
  4. It generates large quantities of oxygen that kill anaerobic pathogens.

What types of microbes live in the intestines?

  1. Diverse species of bacteria, archaea, and fungi, especially Bacteroides and Firmicutes bacteria
  2. A narrow range of bacteria, especially Firmicutes
  3. A narrow range of bacteria and fungi, especially Bacteroides
  4. Archaea and fungi only

Fill in the Blank

The part of the gastrointestinal tract with the largest natural microbiota is the _________.


Respiratory System In Human Anatomy

In the process of exchange of gases human body gains oxygen and gets rid of carbon dioxide. The organs of the respiratory system include the nose pharynx larynx trachea bronchi and their smaller branches and the lungs which contain the alveoli.

Human Respiratory System Anatomy Art Print Poster

Retain more of what youre.

Respiratory system in human anatomy. Most of the organs of the respiratory system help to distribute air but only the tiny. Anatomy of the respiratory system. Respiratory system is the system of respiratory passages lungs and respiratory muscles of human body.

The nose is a structure of the face made of cartilage bone muscle and skin that supports and protects the anterior portion of the nasal cavity. The nose and nasal cavity form the main external opening for the respiratory system and are the first section of the bodys airwaythe respiratory tract through which air moves. The respiratory zone includes all the organs and structures that are directly involved in gas exchange including the respiratory bronchioles alveolar ducts and alveoli.

Study better with osmosis prime. The respiratory system which includes air passages pulmonary vessels the lungs and breathing muscles aids the body in the exchange of gases between the air and blood and between the blood and the bodys billions of cells. Anatomy of the respiratory system nose and nasal cavity.

Anatomy of the respiratory system the respiratory system also referred to as the ventilator system is a complex biological system comprised of several organs that facilitate the inhalation and exhalation of oxygen and carbon dioxide in living organisms or in other words breathing. Respiratory system is responsible for exchange of gases between the human body and the surroundings. Find more videos at httposmsitmore.

Such structures include the nasal cavity pharynx larynx trachea and most of the bronchial tree. The respiratory system refers to the series of organs responsible for gas exchange in the body.

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Conclusions and perspectives

There is clear evidence that bacteria, either endogenous microbiota or exogenous probiotics, can influence pulmonary barrier and immune functions as well as susceptibility to and the course of several respiratory diseases including infections. Modern style of living such as smoking, comorbidities such as diabetes as well as excessive medical treatment and elevated concentrations of antibiotics in food can influence compositions of human microbiota. Alterations in microbiota can therefore be associated with differential risk for and severity of disease including pulmonary ones. The mutual interactions of the gut microbiota with development of immunity and immune reactions associated with health and disease are well documented and of high translational relevance, but nevertheless, still an emerging field. Notably, several studies indicate that the gut microbiota composition can also distally influence pulmonary barrier and immune functions. In contrast, our knowledge of other body sites’ microbiota functions as well their putative systemic interactions with distal epithelia-specific microbiota are yet to be explored in more detail. Similarly, the knowledge on proximal effects of microbiota on local epithelial and immune cells outside of the gut is pretty limited. In this respect, the recently described lower RT microbiota requires to be studied in detail to delineate its function in lung morphogenesis, barrier function, pulmonary immunity, and host defense. Most importantly, effects of the bacterial communities of the lung need to be differentiated from those implemented by the gut and other distal microbiota such as those from upper respiratory tract, oral-nasal cavity or skin, or PAMPs and metabolites thereof. This is a pretty difficult task as differential colonization specifically targeting either gut or lung is almost impossible.

In contrast to the gut microbiota, there is a magnitude lower bacterial number in the lung, which may or may not correspond to its potential for lower RT barrier function. Neither the physiological niches of the lung microbiota nor its metabolic traits have been studied yet. Therefore, it is unclear whether and how much these community members are either relevant space holders or whether they produce sufficient amounts of metabolites/PAMPs to affect host barrier function. However, interspecies communication may still contribute to community stability and flexibility, and those pulmonary microcolonies as observed by FISH [4] may spatially influence lung tissue thereby generating distinct environments within the lung landscape. These communities shed PAMPs in close proximity to the alveolar and bronchiolar epithelia and likely interact with resident alveolar macrophages and DCs thereby influencing innate defense functions and downstream acquired immunity in the lung. Therefore, compositions of these communities need to be characterized in detail and mapped to the lung landscape both, in the murine model but more importantly in humans. Such studies require novel bronchoscopy methods for humans to assure sterile probing in order to better distinct upper from lower RT microbiota or adequately designed postsurgery or posthumous sampling approaches. Furthermore, analysis of the lung commensal's physiology calls for improved culture techniques to study the metabolism of individual members or whole communities in vitro. Finally the question arises whether RT colonizers, which are otherwise opportunistic pathogens such as S. aureus or C. pneumoniae among others, are relevant members of the microbiota. Certain RT microbiota compositions may keep these species at bay and from colonizing deeper pulmonary airways. Similarly, pathogens adapted to humans may cause little pathology but may lead to severe disease when host microbiota is altered, be it by comorbidities or antibiotic treatment, a hypothesis, which needs to be explored in TB (Box 1).

Box 1. Urgent research questions

  1. Are alterations in pulmonary microbiota cause or consequence of lung disease (the Hen-Egg problem)?
  2. Are pulmonary barrier and immune functions determined specifically by lower respiratory tract microbiota or by those from distal epithelia, or both?
  3. What is the metabolic state of RT microbiota, and where are niches for commensal bacteria in the lower RT?
  4. Do changes in microbiota compositions by comorbidities directly affect pulmonary disease outcome and long-term pathology?
  5. How does the RT microbiota – immune system interaction influence invasiveness of RT opportunistic pathogens?
  6. Can opportunistic pathogens such as S. aureus, S. pneumoniae, M. pneumoniae, C. pneumoniae, or T. whipplei, which are otherwise normal respiratory tract colonizers in healthy individuals, be considered part of the microbiota?
  7. How does respiratory tract microbiota dysbiosis by antibiotics, coinfection, comorbidities contribute to reactivation of latent infections such as TB?
  8. Where does the lower respiratory tract microbiota originate from, that is, maternal amniotic, vaginal, oral, enviromental?
  9. Do (RT) microbiota compositions influence effectiveness of vaccines?
  10. Can therapeutic RT microbiota recolonization or metabolites thereof be employed to treat chronic pulmonary diseases such as COPD, asthma, or even TB?

Interspecies communication between pure colonizers and opportunists or production of antimicrobials may affect susceptibility or protection against infection as it has been shown for lactobacillus products, which can, for example, inhibit P. aeruginosa virulence factors [146] . Furthermore, lung epithelial and resident myeloid cells in the lung may sense microbiota-derived products and promote cell autonomous antimicrobials defense mechanisms such as mucus production [4] , AMP secretion or MX protein expression, as known from the gut [147] . The human microbiome shares T cell epitopes not only with pathogens but also with host proteins providing a good reason to believe that commensal bacteria can also shape T cell responses [148] . Commensals may thereby also influence vaccine efficacy by either priming or tolerizing the immune system against vaccine proteins. In this context, the observation that BCG vaccination has an even lower efficacy against tuberculosis in areas close to the equator was linked to differential abundance of environmental mycobacteria, primarily the opportunistic M. avium [149-151] .

Thus, mutual microbe-host interactions can have as far reached consequences as influencing vaccine efficacy. The lower RT microbiota therefore represent an intriguing target for prophylaxis and therapeutic intervention, and future studies need to reveal whether reconstitution therapy can be as effective for pulmonary diseases as it was recently shown for fecal microbiota transplantation in inflammatory bowel disease or C. difficile infection [152, 153] .


Watch the video: ΚΑΝΩ ΜΠΑΝΙΟ (May 2022).


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