Airway Epithelial Innate Immunity

Besides providing an essential protective barrier, airway epithelial cells directly sense pathogens and respond defensively. This is a frontline component of the innate immune system with specificity for different pathogen classes. It occurs in the context of numerous interactions with leukocytes, b...

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Autores principales: Sebastian L. Johnston, David L. Goldblatt, Scott E. Evans, Michael J. Tuvim, Burton F. Dickey
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Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/c1b95d1322db4000acdcfad1d0d43dc5
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spelling oai:doaj.org-article:c1b95d1322db4000acdcfad1d0d43dc52021-12-01T07:50:05ZAirway Epithelial Innate Immunity1664-042X10.3389/fphys.2021.749077https://doaj.org/article/c1b95d1322db4000acdcfad1d0d43dc52021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.749077/fullhttps://doaj.org/toc/1664-042XBesides providing an essential protective barrier, airway epithelial cells directly sense pathogens and respond defensively. This is a frontline component of the innate immune system with specificity for different pathogen classes. It occurs in the context of numerous interactions with leukocytes, but here we focus on intrinsic epithelial mechanisms. Type 1 immune responses are directed primarily at intracellular pathogens, particularly viruses. Prominent stimuli include microbial nucleic acids and interferons released from neighboring epithelial cells. Epithelial responses revolve around changes in the expression of interferon-sensitive genes (ISGs) that interfere with viral replication, as well as the further induction of interferons that signal in autocrine and paracrine manners. Type 2 immune responses are directed primarily at helminths and fungi. Prominent pathogen stimuli include proteases and chitin, and important responses include mucin hypersecretion and chitinase release. Type 3 immune responses are directed primarily at extracellular microbial pathogens, including bacteria and fungi, as well as viruses during their extracellular phase of infection. Prominent microbial stimuli include bacterial wall components, such as lipopeptides and endotoxin, as well as microbial nucleic acids. Key responses are the release of reactive oxygen species (ROS) and antimicrobial peptides (AMPs). For all three types of response, paracrine signaling to neighboring epithelial cells induces resistance to infection over a wide field. Often, the epithelial effector molecules themselves also have signaling properties, in addition to the release of inflammatory cytokines that boost local innate immunity. Together, these epithelial mechanisms provide a powerful first line of pathogen defense, recruit leukocytes, and instruct adaptive immune responses.Sebastian L. JohnstonDavid L. GoldblattDavid L. GoldblattDavid L. GoldblattScott E. EvansMichael J. TuvimBurton F. DickeyFrontiers Media S.A.articleairwayepitheliuminnate immunityimmunitymucusPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic airway
epithelium
innate immunity
immunity
mucus
Physiology
QP1-981
spellingShingle airway
epithelium
innate immunity
immunity
mucus
Physiology
QP1-981
Sebastian L. Johnston
David L. Goldblatt
David L. Goldblatt
David L. Goldblatt
Scott E. Evans
Michael J. Tuvim
Burton F. Dickey
Airway Epithelial Innate Immunity
description Besides providing an essential protective barrier, airway epithelial cells directly sense pathogens and respond defensively. This is a frontline component of the innate immune system with specificity for different pathogen classes. It occurs in the context of numerous interactions with leukocytes, but here we focus on intrinsic epithelial mechanisms. Type 1 immune responses are directed primarily at intracellular pathogens, particularly viruses. Prominent stimuli include microbial nucleic acids and interferons released from neighboring epithelial cells. Epithelial responses revolve around changes in the expression of interferon-sensitive genes (ISGs) that interfere with viral replication, as well as the further induction of interferons that signal in autocrine and paracrine manners. Type 2 immune responses are directed primarily at helminths and fungi. Prominent pathogen stimuli include proteases and chitin, and important responses include mucin hypersecretion and chitinase release. Type 3 immune responses are directed primarily at extracellular microbial pathogens, including bacteria and fungi, as well as viruses during their extracellular phase of infection. Prominent microbial stimuli include bacterial wall components, such as lipopeptides and endotoxin, as well as microbial nucleic acids. Key responses are the release of reactive oxygen species (ROS) and antimicrobial peptides (AMPs). For all three types of response, paracrine signaling to neighboring epithelial cells induces resistance to infection over a wide field. Often, the epithelial effector molecules themselves also have signaling properties, in addition to the release of inflammatory cytokines that boost local innate immunity. Together, these epithelial mechanisms provide a powerful first line of pathogen defense, recruit leukocytes, and instruct adaptive immune responses.
format article
author Sebastian L. Johnston
David L. Goldblatt
David L. Goldblatt
David L. Goldblatt
Scott E. Evans
Michael J. Tuvim
Burton F. Dickey
author_facet Sebastian L. Johnston
David L. Goldblatt
David L. Goldblatt
David L. Goldblatt
Scott E. Evans
Michael J. Tuvim
Burton F. Dickey
author_sort Sebastian L. Johnston
title Airway Epithelial Innate Immunity
title_short Airway Epithelial Innate Immunity
title_full Airway Epithelial Innate Immunity
title_fullStr Airway Epithelial Innate Immunity
title_full_unstemmed Airway Epithelial Innate Immunity
title_sort airway epithelial innate immunity
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/c1b95d1322db4000acdcfad1d0d43dc5
work_keys_str_mv AT sebastianljohnston airwayepithelialinnateimmunity
AT davidlgoldblatt airwayepithelialinnateimmunity
AT davidlgoldblatt airwayepithelialinnateimmunity
AT davidlgoldblatt airwayepithelialinnateimmunity
AT scotteevans airwayepithelialinnateimmunity
AT michaeljtuvim airwayepithelialinnateimmunity
AT burtonfdickey airwayepithelialinnateimmunity
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