363:
residents: secretions from airway epithelial cells (especially goblet cells), secretions from submucosal glands and transudate from plasma. Moreover, the pool of available nutrients is increased by the activities of some members of the microbiota. Macromolecular components of respiratory secretions (proteins, glycoproteins, lipids, nucleic acids) are converted to nutrients (e.g. carbohydrates, amino acids). Thus, the metabolic activity of present bacteria allow for the colonization of new species. The commensal bacteria are nonpathogenic and defend our airways against the pathogens. There are several possible mechanisms. Commensals are the native competitors of pathogenic bacteria, because they tend to occupy the same ecological niche inside the human body. Secondly, they are able to produce antibacterial substances called bacteriocins which inhibit the growth of pathogens.
403:
304:) have activated particular pattern recognition receptors on/in epithelial cells, the proinflammatory signaling pathways are activated. This results mainly in IL-1, IL-6 and IL-8 production. These cytokines induce chemotaxis to the site of infection in its target cells (e.g., neutrophils, dendritic cells and macrophages). On the other hand, representatives of standard microbiota induce only weak signals preventing inflammation. The mechanism of distinguishing between harmless and harmful bacteria on the molecular as well as on physiological levels is not completely understood.
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222:. They are aerobes as well as anaerobes and aerotolerant bacteria. The microbial communities are highly variable in particular individuals and compose of about 140 distinct families. The bronchial tree for instance contains a mean of 2000 bacterial genomes per cm surface. The harmful or potentially harmful bacteria are also detected routinely in respiratory specimens. The most significant are
1418:
36:
296:. The airway epithelium has a complex structure consisting of at least seven diverse cell types interacting with each other by means of tight junctions. Epithelial cells can transmit immunostimulatory signals to underlying tissues taking part in the mechanisms of innate and adaptive immune response. The key transmitters of these signals are dendritic cells. Once pathogenic bacteria (e.g.,
342:
attachment of one or more ubiquitin (Ub) monomers. The inhibition of ubiquitination leads to reduction of inflammation, because only polyubiquitinated (IκB-κ is targeted for degradation by the 26 S proteasome, allowing NF-κB translocation to the nucleus and activation the transcription of effector genes (for example IL-8). Probiotic bacteria such as
1430:
351:, attenuates pro-inflammatory cytokine expression by promoting nuclear export of NF-κB subunit RelA, through a peroxisome proliferator activated receptor γ (PPAR-γ)-dependent pathway. PPAR-γ target transcriptionally active Rel A and induce early nuclear clearance limiting the duration of NF-κB action.
285:
The airway epithelium together with alveolar macrophages and dendritic cells play a major role in the initial recognition of bacterial products getting into the lower airways with the air. Since some of these products are potent proinflammatory stimuli it is extremely important for the immune system
434:, along with similar species that can colonize and act symbiotically but can cause disease if they begin to take over the tissues they have colonized or invade other tissues, have been called "pathobionts". MRSA can similarly colonize people without making them sick. The presence of such genera as
346:
are able to modulate the activity of the Ub-proteasome system via inducing reactive oxygen species (ROS) production in epithelial cells. In mammalian cells, ROS have been shown to serve as critical second messengers in multiple signal transduction pathways in response to proinflammatory cytokines.
325:
which translocates from the cytoplasm into the nucleus and activates pro-inflammatory genes in epithelial cells and macrophages. The DNA-binding protein complex recognizes a discrete nucleotide sequence (5’-GGG ACT TTC T-3’) in the upstream region of a variety of response genes. The activation of
341:
are able to prohibit the ubiquitination of NF-κB inhibitor molecule nuclear factor of NF-κB light polypeptide gene enhancer in B-cells inhibitor alpha (IκB-κ). Another explanation of commensal tolerance of the epithelium refers to the post-translational modification of a protein by the covalent
362:
The airways are continually exposed to a multitude of microorganisms, some of which are able to persist and even colonize respiratory tract. This is possible due to the presence of nutrients, oxygen, and optimal growth temperature. There are several host-derived nutrient sources for microbial
321:(RLRs) which recognize a broad variety of microbial structural components. After recognition of pathogenic bacteria proinflammatory pathways are activated and cellular components of the adaptive and innate immunity are recruited to the infection site. One key regulator in this process is
347:
Bacterially induced ROS causes oxidative inactivation of the catalytic cysteine residue of Ub 12 resulting in incomplete but transient loss of cullin-1 neddylation and consequent effects on NF-κB and β-catenin signaling. Another commensal species,
240:. They are known to cause respiratory disorders under particular conditions namely if the human immune system is impaired. The mechanism by which they persist in the lower airways in healthy individuals is unknown.
497:
High-throughput sequencing and the whole genome sequencing approaches will provide the further information about the complexity and physiological implication of commensal bacteria in the lower respiratory tract.
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This process becomes much more intriguing when taking into account that commensals often share their surface molecules with pathogens. Epithelial cells are equipped with very sensitive recognition tools –
537:
Erb-Downward, John R.; Thompson, Deborah L.; Han, Meilan K.; Freeman, Christine M.; McCloskey, Lisa; Schmidt, Lindsay A.; Young, Vincent B.; Toews, Galen B.; et al. (2011). Bereswill, Stefan (ed.).
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are the main producers of bacteriocins in respiratory tract. Moreover, commensals are known to induce Th1 response and anti-inflammatory interleukin (IL)-10, antimicrobial peptides, FOXP3, secretory
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Cox, Michael J.; Allgaier, Martin; Taylor, Byron; Baek, Marshall S.; Huang, Yvonne J.; Daly, Rebecca A.; Karaoz, Ulas; Andersen, Gary L.; et al. (2010). Ratner, Adam J. (ed.).
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to distinguish between pathogens and non-pathogenic commensals. This prevents the development of constant inflammation and forms tolerance against harmless microbiota.
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Hilty, Markus; Burke, Conor; Pedro, Helder; Cardenas, Paul; Bush, Andy; Bossley, Cara; Davies, Jane; Ervine, Aaron; et al. (2010). Neyrolles, Olivier (ed.).
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In contrast, harmless bacteria do not cause the translocation of NF-κB into the nucleus thus preventing the inflammation although they can express the same
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Kumar, Amrita; Wu, Huixia; Collier-Hyams, Lauren S; Hansen, Jason M; Li, Tengguo; Yamoah, Kosj; Pan, Zhen-Qiang; Jones, Dean P; Neish, Andrew S (2007).
1308:
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Sha, Q.; Truong-Tran, AQ; Plitt, JR; Beck, LA; Schleimer, RP (2004). "Activation of Airway
Epithelial Cells by Toll-Like Receptor Agonists".
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Huang, Yvonne J.; Kim, Eugenia; Cox, Michael J.; Brodie, Eoin L.; Brown, Ron; Wiener-Kronish, Jeanine P.; Lynch, Susan V. (2010).
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The balance between pathogens and commensals is extremely important in the maintenance of homeostasis in the respiratory tract.
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NF-κB by a number of stimuli: bacterial cell walls or inflammatory cytokines results in its translocation to the nucleus.
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972:"A Persistent and Diverse Airway Microbiota Present during Chronic Obstructive Pulmonary Disease Exacerbations"
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Changes in microbial community composition seem to play a role in progression of such pulmonary disorders as
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333:(MAMPs). One possible mechanism explaining this effect was suggested by Neish showing that non-pathogenic
230:
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833:
Kumar, Himanshu; Kawai, Taro; Akira, Shizuo (2011). "Pathogen
Recognition by the Innate Immune System".
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164:. The bacterial part of the microbiota has been more closely studied. It consists of a core of nine
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923:"Commensal bacteria modulate cullin-dependent signaling via generation of reactive oxygen species"
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particularly on the mucous layer and the epithelial surfaces. These microorganisms include
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1083:"Composition and immunological significance of the upper respiratory tract microbiota"
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1021:"Airway Microbiota and Pathogen Abundance in Age-Stratified Cystic Fibrosis Patients"
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present in the upper respiratory tract, and on skin and in the gut mucosa.
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Beck, James M.; Young, Vincent B.; Huffnagle, Gary B. (1 February 2012).
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present mostly in healthy individual cohort. The relative abundance of
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Figure 2: Distribution of fungal genera in different body sites
786:"The human lung and Aspergillus: You are what you breathe in?"
29:
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Uhlemann, AC; Otto, M; Lowy, FD; DeLeo, FR (January 2014).
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The fungal genera that are commonly found make up the lung
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American
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is correlated with stable COPD state. On the other hand,
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Schenck, LP; Surette, MG; Bowdish, DM (November 2016).
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599:"Disordered Microbial Communities in Asthmatic Airways"
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microbial community consisting of a complex variety of
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Richardson, M; Bowyer, P; Sabino, R (1 April 2019).
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313:(TLRs), nucleotide-binding oligomerization domain
60:. Unsourced material may be challenged and removed.
1136:Clinical, Cosmetic and Investigational Dermatology
494:are found most often in cystic fibrosis patients.
406:Ecological modeling of the respiratory microbiome
247:, in the microbiota of the lung, and include
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27:Community of microorganisms from the lung
317:(NLRs) and retinoic acid-inducible gene
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976:OMICS: A Journal of Integrative Biology
705:Cui L, Morris A, Ghedin E (July 2013).
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412:chronic obstructive pulmonary disease
331:microbe-associated molecular patterns
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482:is increased in asthmatic children.
58:adding citations to reliable sources
835:International Reviews of Immunology
294:Mechanisms underlying inflammation
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1187:Infection, Genetics and Evolution
1132:"Microbiome in atopic dermatitis"
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45:needs additional citations for
281:Role of the epithelial barrier
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1199:10.1016/j.meegid.2013.04.030
1046:10.1371/journal.pone.0011044
847:10.3109/08830185.2010.529976
658:"The microbiome of the lung"
624:10.1371/journal.pone.0008578
565:10.1371/journal.pone.0016384
796:(Supplement_2): S145–S154.
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1373:Human Microbiome Project
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900:10.1165/rcmb.2003-0388OC
237:Streptococcus pneumoniae
1345:Disorders and therapies
1099:10.1002/1873-3468.12455
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662:Translational Research
484:Pseudomonas aeruginosa
426:is part of the normal
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319:(RIG)-I-like receptors
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231:Haemophilus influenzae
988:10.1089/omi.2009.0100
488:Staphylococcus aureus
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398:Clinical significance
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225:Moraxella catarrhalis
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492:Burkholderia cepacia
315:(NOD)-like receptors
54:improve this article
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1037:2010PLoSO...511044C
615:2010PLoSO...5.8578H
556:2011PLoSO...616384E
513:List of human flora
394:(sIgA) production.
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335:S. typhimurium
311:toll like receptors
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711:Genome Med
524:References
464:Veillonela
448:Prevotella
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428:microbiota
358:Physiology
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468:Rhizobium
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1316:Placenta
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1168:28260936
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