About: Defensins and Sepsis

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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	Defensins and Sepsis
Creator	Chen, Qi-Xing Cheng, Bao-Li Fang, Xiang-Ming Xie, Guo-Hao
Source	Medline; PMC
abstract	Sepsis is a leading cause of mortality and morbidity in the critical illness. Multiple immune inflammatory processes take part in the pathogenesis of sepsis. Defensins are endogenous antimicrobial peptides with three disulphide bonds created by six cysteine residues. Besides the intrinsic microbicidal properties, defensins are active players which modulate both innate and adaptive immunity against various infections. Defensins can recruit neutrophils, enhance phagocytosis, chemoattract T cells and dendritic cells, promote complement activation, and induce IL-1β production and pyrotosis. Previous publications have documented that defensins play important roles in a series of immune inflammatory diseases including sepsis. This review aims to briefly summarize in vitro, in vivo, and genetic studies on defensins' effects as well as corresponding mechanisms within sepsis and highlights their promising findings which may be potential targets in future therapies of sepsis.
has issue date	2014-08-19(xsd:dateTime)
bibo:doi	10.1155/2014/180109
bibo:pmid	25210703
has license	cc-by
sha1sum (hex)	6d08d5d8add16122735dcfa90a4c36f8d2a348ea
schema:url	https://doi.org/10.1155/2014/180109
resource representing a document's title	Defensins and Sepsis
has PubMed Central identifier	PMC4151856
has PubMed identifier	25210703
schema:publication	Biomed Res Int
resource representing a document's body	covid:6d08d5d8add16122735dcfa90a4c36f8d2a348ea#body_text
is schema:about of	named entity 'genetic studies' named entity 'production' named entity 'Multiple' named entity 'This' named entity 'infections' named entity 'EFFECTS' named entity 'DENDRITIC CELLS' named entity 'ROLES' named entity 'INFECTIONS' named entity 'STUDIES' named entity 'REVIEW' named entity 'PREVIOUS' named entity 'NEUTROPHILS' named entity 'BONDS' named entity 'SEPSIS' named entity 'PROMOTE' named entity 'THERAPIES' named entity 'DISULPHIDE' named entity 'PEPTIDES' named entity 'LEADING' named entity 'IN VIVO' named entity 'SERIES' named entity 'PROPERTIES' named entity 'CAUSE' named entity 'PLAY' named entity 'DEFENSINS' named entity 'IMPORTANT' named entity 'ADAPTIVE IMMUNITY' named entity 'CREATED BY' named entity 'T CELLS' named entity 'IN VITRO' named entity 'PROCESSES' named entity 'PATHOGENESIS' named entity 'VARIOUS' named entity 'HAVE' named entity 'MODULATE' named entity 'DOCUMENTED' named entity 'THEIR' named entity 'ANTIMICROBIAL' named entity 'IL-1 PRODUCTION' named entity 'INTRINSIC' named entity 'FINDINGS' named entity 'FUTURE' named entity 'INFLAMMATORY' named entity 'PUBLICATIONS' named entity 'MORTALITY' named entity 'ACTIVE' named entity 'SEPSIS' named entity 'INFLAMMATORY DISEASES' named entity 'MECHANISMS' named entity 'POTENTIAL' named entity 'ENHANCE' named entity 'TARGETS' named entity 'IS A' named entity 'MAY BE' named entity 'AIMS' named entity 'CYSTEINE' named entity 'GENETIC' named entity 'ENDOGENOUS' named entity 'INDUCE' named entity 'MORBIDITY' named entity 'PHAGOCYTOSIS' named entity 'PLAYERS' named entity 'COMPLEMENT ACTIVATION' named entity 'DEFENSINS' named entity 'INCLUDING' named entity 'MULTIPLE' named entity 'CRITICAL ILLNESS' named entity 'IMMUNE' named entity 'inflammatory processes' named entity 'sepsis' named entity 'mechanisms' named entity 'immune' named entity 'highlights' named entity 'phagocytosis' named entity 'mortality' named entity 'therapies' named entity 'inflammatory processes'

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