About: Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces

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About: Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces
Creator	Pickl, Winfried Kratzer, Bernhard Smole, Ursula
Source	Medline; PMC
abstract	Maintenance of homeostasis at body barriers that are constantly challenged by microbes, toxins and potentially bioactive (macro)molecules requires complex, highly orchestrated mechanisms of protection. Recent discoveries in respiratory research have shed light on the unprecedented role of airway epithelial cells (AEC), which, besides immune cells homing to the lung, also significantly contribute to host defence by expressing membrane‐bound and soluble pattern recognition receptors (sPRR). Recent evidence suggests that distinct, evolutionary ancient, sPRR secreted by AEC might become activated by usually innocuous proteins, commonly referred to as allergens. We here provide a systematic overview on sPRR detectable in the mucus lining of AEC. Some of them become actively produced and secreted by AECs (like the pentraxins C‐reactive protein and pentraxin 3; the collectins mannose binding protein and surfactant proteins A and D; H‐ficolin; serum amyloid A; and the complement components C3 and C5). Others are elaborated by innate and adaptive immune cells such as monocytes/macrophages and T cells (like the pentraxins C‐reactive protein and pentraxin 3; L‐ficolin; serum amyloid A; and the complement components C3 and C5). Herein we discuss how sPRRs may contribute to homeostasis but sometimes also to overt disease (e.g. airway hyperreactivity and asthma) at the alveolar–air interface.
has issue date	2020-04-27(xsd:dateTime)
bibo:doi	10.1002/eji.201847811
bibo:pmid	32246830
has license	cc-by
sha1sum (hex)	e68fcaea83739d0f9d8e4dc26665c3de518619ad
schema:url	https://doi.org/10.1002/eji.201847811
resource representing a document's title	Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces
has PubMed Central identifier	PMC7216992
has PubMed identifier	32246830
schema:publication	Eur J Immunol
resource representing a document's body	covid:e68fcaea83739d0f9d8e4dc26665c3de518619ad#body_text
is schema:about of	named entity 'alveolar' named entity 'C-reactive protein' named entity 'pentraxins' named entity 'serum' named entity 'pentraxin' named entity 'asthma' named entity 'air interface' named entity 'Soluble' named entity 'mucosal surfaces' named entity 'amyloid' named entity 'airway' named entity 'homeostasis' named entity 'ASTHMA' named entity 'airway hyperreactivity' named entity 'complement' named entity 'ficolin' named entity 'homeostasis' named entity 'pattern recognition' named entity 'AIRWAY' named entity 'MUCOSAL' named entity 'SOLUBLE' named entity 'DISEASE' named entity 'OVERT' named entity 'ALVEOLAR' named entity 'C-reactive protein' named entity 'pentraxins' named entity 'pattern recognition' named entity 'COMPLEMENT COMPONENTS' named entity 'HOW' named entity 'homeostasis' named entity 'disease' named entity 'PENTRAXIN 3' named entity 'SERUM AMYLOID A' named entity 'AIR' named entity 'BUT' named entity 'complement' named entity 'serum amyloid A' named entity 'pentraxin' named entity 'asthma' named entity 'mucosal surfaces' named entity 'DISCUSS' named entity 'HOMEOSTASIS' named entity 'L-FICOLIN' named entity 'AIRWAY HYPERREACTIVITY' named entity 'homeostasis' named entity 'Soluble' named entity 'molecules' named entity 'Guardians' named entity 'regulators' named entity 'C-REACTIVE PROTEIN' named entity 'PROTEIN ' named entity 'MOLECULES' named entity 'REGULATORS' named entity 'HOMEOSTASIS' named entity 'PATTERN RECOGNITION' named entity 'GUARDIANS' named entity 'SURFACES' named entity 'CLINICAL' named entity 'INTERFACE' named entity 'CONTRIBUTE ' named entity 'REVIEW'
is part of of	Maintenance of homeostasis at body barriers that are constantly challenged by microbes, toxins and potentially bioactive (macro)molecules requires complex, highly orchestrated mechanisms of protection. Recent discoveries in respiratory research have shed light on the unprecedented role of airway epithelial cells (AEC), which, besides immune cells homing to the lung, also significantly contribute to host defence by expressing membrane‐bound and soluble pattern recognition receptors (sPRR). Recent evidence suggests that distinct, evolutionary ancient, sPRR secreted by AEC might become activated by usually innocuous proteins, commonly referred to as allergens. We here provide a systematic overview on sPRR detectable in the mucus lining of AEC. Some of them become actively produced and secreted by AECs (like the pentraxins C‐reactive protein and pentraxin 3; the collectins mannose binding protein and surfactant proteins A and D; H‐ficolin; serum amyloid A; and the complement components C3 and C5). Others are elaborated by innate and adaptive immune cells such as monocytes/macrophages and T cells (like the pentraxins C‐reactive protein and pentraxin 3; L‐ficolin; serum amyloid A; and the complement components C3 and C5). Herein we discuss how sPRRs may contribute to homeostasis but sometimes also to overt disease (e.g. airway hyperreactivity and asthma) at the alveolar–air interface. Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces covid:e68fcaea83739d0f9d8e4dc26665c3de518619ad#body_text

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