About: Relevance of granulocyte apoptosis to resolution of inflammation at the respiratory mucosa

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About: Relevance of granulocyte apoptosis to resolution of inflammation at the respiratory mucosa Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Relevance of granulocyte apoptosis to resolution of inflammation at the respiratory mucosa
Creator	Duffin, R Haslett, C Leitch, A Rossi, A
Source	PMC
abstract	The respiratory mucosa is responsible for gas exchange and is therefore, of necessity, exposed to airborne pathogens, allergens, and foreign particles. It has evolved a multi-faceted, physical and immune defense system to ensure that in the majority of instances, potentially injurious invaders are repelled. Inflammation, predominantly mediated by effector cells of the granulocyte lineage including neutrophils and eosinophils, is a form of immune defense. Where inflammation proves unable to remove an inciting stimulus, chronic inflammatory disease may supervene because of the potential for tissue damage conferred by the presence of large numbers of frustrated, activated granulocytes. Successful recovery from inflammatory disease and resolution of inflammation rely on the clearance of these cells. Ideally, they should undergo apoptosis prior to phagocytosis by macrophage, dendritic, or epithelial cells. The outcome of inflammation can have serious sequelae for the integrity of the respiratory mucosa leading to disease. Therapeutic strategies to drive resolution of inflammation may be directed at the induction of granulocyte apoptosis and the enhancement of granulocyte clearance. SUPPLEMENTARY INFORMATION: The online version of this article (doi:10.1038/mi.2008.31) contains supplementary material, which is available to authorized users.
has issue date	2008-07-02(xsd:dateTime)
bibo:doi	10.1038/mi.2008.31
bibo:pmid	19079199
has license	no-cc
sha1sum (hex)	1a78508db82bf2b5fd113b29f81563dc9153ead3
schema:url	https://doi.org/10.1038/mi.2008.31
resource representing a document's title	Relevance of granulocyte apoptosis to resolution of inflammation at the respiratory mucosa
has PubMed Central identifier	PMC7102379
has PubMed identifier	19079199
schema:publication	Mucosal Immunol
resource representing a document's body	covid:1a78508db82bf2b5fd113b29f81563dc9153ead3#body_text
is schema:about of	named entity 'MEDIATED' named entity 'OUTCOME' named entity 'GRANULOCYTES' named entity 'RESPIRATORY MUCOSA' named entity 'AIRBORNE' named entity 'ENHANCEMENT' named entity 'DENDRITIC' named entity 'DEFENSE' covid:arg/1a78508db82bf2b5fd113b29f81563dc9153ead3 named entity 'Therapeutic strategies' named entity 'granulocytes' named entity 'sequelae' named entity 'eosinophils' named entity 'granulocyte' named entity 'granulocyte' named entity 'phagocytosis' named entity 'inflammation' named entity 'apoptosis' named entity 'phosphatidylserine' named entity 'lungs' named entity 'permeabilization' named entity 'apoptotic cells' named entity 'alveolar macrophages' named entity 'antibiotics' named entity 'gene' named entity 'ARDS' named entity 'inflammatory disease' named entity 'IgE' named entity 'neutrophils' named entity 'transcription' named entity 'enzyme' named entity 'neutrophils' named entity 'Neutrophils' named entity 'IPF' named entity 'lipoxin' named entity 'inflammation' named entity 'neutrophil' named entity 'allergy' named entity 'loss of function' named entity 'receptor' named entity 'eosinophil' named entity 'macrophages' named entity 'caspase-3' named entity 'neutrophil' named entity 'apoptosis' named entity 'apoptosis' named entity 'Neutrophil' named entity 'P. aeruginosa' named entity 'Neutrophils' named entity 'TH17 cells' named entity 'ultraviolet irradiation' named entity 'chronic granulomatous disease' named entity 'theophylline' named entity 'caspase-3' named entity 'formylated' named entity 'apoptotic' named entity 'inflammation' named entity 'upper airways' named entity 'ARDS' named entity 'eczema' named entity 'pathogenesis' named entity 'apoptotic cells' named entity 'granulocyte' named entity 'mucosa' named entity 'blood samples' named entity 'macrophage phagocytosis' named entity 'IL-8' named entity 'infertility' named entity 'inflammatory cytokines' named entity 'Stenotrophomonas maltophilia' named entity 'knockout mouse' named entity 'neutrophils' named entity 'IL-5' named entity 'neutrophil' named entity 'fibrotic' named entity 'aspergillosis' named entity 'respiratory mucosa' named entity 'extracellular matrix proteins'

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