About: The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation

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About: The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation 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	The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation
Creator	Hussell, Tracy Grabiec, Aleksander
Source	Medline; PMC
abstract	Acute and chronic inflammatory responses in the lung are associated with the accumulation of large quantities of immune and structural cells undergoing apoptosis, which need to be engulfed by phagocytes in a process called ‘efferocytosis’. Apoptotic cell recognition and removal from the lung is mediated predominantly by airway macrophages, though immature dendritic cells and non-professional phagocytes, such as epithelial cells and mesenchymal cells, can also display this function. Efficient clearance of apoptotic cells from the airways is essential for successful resolution of inflammation and the return to lung homeostasis. Disruption of this process leads to secondary necrosis of accumulating apoptotic cells, release of necrotic cell debris and subsequent uncontrolled inflammatory activation of the innate immune system by the released ‘damage associated molecular patterns’ (DAMPS). To control the duration of the immune response and prevent autoimmune reactions, anti-inflammatory signalling cascades are initiated in the phagocyte upon apoptotic cell uptake, mediated by a range of receptors that recognise specific phospholipids or proteins externalised on, or secreted by, the apoptotic cell. However, prolonged activation of apoptotic cell recognition receptors, such as the family of receptor tyrosine kinases Tyro3, Axl and MerTK (TAM), may delay or prevent inflammatory responses to subsequent infections. In this review, we will discuss recent advances in our understanding of the mechanism controlling apoptotic cell recognition and removal from the lung in homeostasis and during inflammation, the contribution of defective efferocytosis to chronic inflammatory lung diseases, such as chronic obstructive pulmonary disease, asthma and cystic fibrosis, and implications of the signals triggered by apoptotic cells in the susceptibility to pulmonary microbial infections.
has issue date	2016-03-08(xsd:dateTime)
bibo:doi	10.1007/s00281-016-0555-3
bibo:pmid	26957481
has license	cc-by
sha1sum (hex)	d78837afeedbb3c9dfa91a675aa03d34ef5a4387
schema:url	https://doi.org/10.1007/s00281-016-0555-3
resource representing a document's title	The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation
has PubMed Central identifier	PMC4896990
has PubMed identifier	26957481
schema:publication	Semin Immunopathol
resource representing a document's body	covid:d78837afeedbb3c9dfa91a675aa03d34ef5a4387#body_text
is schema:about of	named entity 'subsequent' named entity 'duration' named entity 'structural' named entity 'leads' named entity 'mediated' named entity 'Apoptotic' named entity 'DRS' named entity 'PROTEINS' named entity 'REMOVAL' named entity 'CELL UPTAKE' named entity 'DURATION' named entity 'LUNG' named entity 'PROFESSIONAL' named entity 'MOLECULAR' named entity 'DISRUPTION' named entity 'RELEASED' named entity 'SUBMISSION' named entity 'INNATE IMMUNE SYSTEM' named entity 'NON-' named entity 'SUCCESSFUL' named entity 'CLEARANCE' named entity 'MESENCHYMAL CELLS' named entity 'AXL' named entity 'PHAGOCYTES' named entity 'NEED' named entity 'INFLAMMATORY' named entity 'PHOSPHOLIPIDS' named entity 'DENDRITIC CELLS' named entity 'UNCONTROLLED' named entity 'CELL DEBRIS' named entity 'ACCUMULATING' named entity 'PATTERNS' named entity 'INFLAMMATORY RESPONSES' named entity 'NECROTIC' named entity 'AIRWAYS' named entity 'RECENT' named entity 'STRUCTURAL' named entity 'DISPLAY' named entity 'FUNCTION' named entity 'FAMILY' named entity 'ANTI-INFLAMMATORY' named entity 'APOPTOTIC' named entity 'ACUTE' named entity 'MACROPHAGES' named entity 'TO CONTROL' named entity 'CHRONIC' named entity 'AIRWAY' named entity 'PROLONGED' named entity 'MEDIATED' named entity 'PROCESS' named entity 'QUANTITIES' named entity 'SECRETED' named entity 'IMMUNOPATHOLOGY' named entity 'LUNG INFLAMMATION' named entity 'SIGNALLING' named entity 'CELLS' named entity 'RETURN TO' named entity 'APOPTOTIC CELL CLEARANCE' named entity 'ESSENTIAL' named entity 'ROLE' named entity 'MACROPHAGES' named entity 'FOLLOWING' named entity 'ACUTE' named entity 'HOMEOSTASIS' named entity 'OUR' named entity 'TYROSINE KINASES' named entity 'DISCUSS' named entity 'ASSOCIATED WITH' named entity 'REVIEW' named entity 'ACTIVATION' named entity 'LEADS' named entity 'RESOLUTION' named entity 'INFLAMMATION' named entity 'EFFICIENT' named entity 'SUBSEQUENT' named entity 'INFECTIONS' named entity 'RELATED' named entity 'SECONDARY' named entity 'IMMUNE' named entity 'AUTOIMMUNE REACTIONS'

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