About: Alveolar Macrophage Chemokine Secretion Mediates Neutrophilic Lung Injury in Nox2-Deficient Mice

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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	Alveolar Macrophage Chemokine Secretion Mediates Neutrophilic Lung Injury in Nox2-Deficient Mice
Creator	Potera, Renee Cao, Mou Hogg, Richard Hook, Jessica Jordan, Lin Moreland, Jessica
Source	PMC
abstract	Acute lung injury (ALI), developing as a component of the systemic inflammatory response syndrome (SIRS), leads to significant morbidity and mortality. Reactive oxygen species (ROS), produced in part by the neutrophil NADPH oxidase 2 (Nox2), have been implicated in the pathogenesis of ALI. Previous studies in our laboratory demonstrated the development of pulmonary inflammation in Nox2-deficient (gp91(phox-/y)) mice that was absent in WT mice in a murine model of SIRS. Given this finding, we hypothesized that Nox2 in a resident cell in the lung, specifically the alveolar macrophage, has an essential anti-inflammatory role. Using a murine model of SIRS, we examined whole-lung digests and bronchoalveolar lavage fluid (BALf) from WT and gp91(phox-/y) mice. Both genotypes demonstrated neutrophil sequestration in the lung during SIRS, but neutrophil migration into the alveolar space was only present in the gp91(phox-/y) mice. Macrophage inflammatory protein (MIP)-1α gene expression and protein secretion were higher in whole-lung digest from uninjected gp91(phox-/y) mice compared to the WT mice. Gene expression of MIP-1α, MCP-1, and MIP-2 was upregulated in alveolar macrophages obtained from gp91(phox-/y) mice at baseline compared with WT mice. Further, ex vivo analysis of alveolar macrophages, but not bone marrow-derived macrophages or peritoneal macrophages, demonstrated higher gene expression of MIP-1α and MIP-2. Moreover, isolated lung polymorphonuclear neutrophils migrate to BALf obtained from gp91(phox-/y) mice, further providing evidence of a cell-specific anti-inflammatory role for Nox2 in alveolar macrophages. We speculate that Nox2 represses the development of inflammatory lung injury by modulating chemokine expression by the alveolar macrophage.
has issue date	2018-10-04(xsd:dateTime)
bibo:doi	10.1007/s10753-018-0883-7
bibo:pmid	30288635
has license	no-cc
sha1sum (hex)	3d18b563ab98fb5d524247e8832d25188705809f
schema:url	https://doi.org/10.1007/s10753-018-0883-7
resource representing a document's title	Alveolar Macrophage Chemokine Secretion Mediates Neutrophilic Lung Injury in Nox2-Deficient Mice
has PubMed Central identifier	PMC6775637
has PubMed identifier	30288635
schema:publication	Inflammation
resource representing a document's body	covid:3d18b563ab98fb5d524247e8832d25188705809f#body_text
is schema:about of	named entity 'Further' named entity 'macrophages' named entity 'Nox2' named entity 'peritoneal' named entity 'ALVEOLAR SPACE' named entity 'GENE EXPRESSION' named entity 'BUT' named entity 'ALVEOLAR MACROPHAGE' named entity 'PATHOGENESIS' named entity 'GENOTYPES' named entity 'NOX2' named entity 'ALI' named entity 'GP91' named entity 'LABORATORY' named entity 'MCP-1' named entity 'compared' named entity 'lung' named entity 'secretion' named entity 'ALI' named entity 'alveolar macrophage' named entity 'Nox2' named entity 'MIP' named entity 'studies' named entity 'Nox2' named entity 'developing' named entity 'macrophages' named entity 'phox' named entity 'MIP-1α' named entity 'development' named entity 'SIRS' named entity 'alveolar' named entity 'alveolar macrophages' named entity 'chemokine' named entity 'bone marrow' named entity 'morbidity' named entity 'peritoneal' named entity 'BALf' named entity 'alveolar macrophages' named entity 'Nox2' named entity 'macrophages' named entity 'MCP-1' named entity 'upregulated' named entity 'gene expression' named entity 'Alveolar Macrophage' named entity 'Nox2' named entity 'demonstrated' named entity 'Nox2' named entity 'mice' named entity 'LPS' named entity 'vascular bed' named entity 'genotypes' named entity 'E. coli' named entity 'ALI' named entity 'secretion' named entity 'secretion' named entity 'zymosan' named entity 'PBS' named entity 'LPS' named entity 'secretion' named entity 'neutrophil' named entity 'neutrophils' named entity 'mice' named entity 'PMNs' named entity 'inflammatory cell' named entity 'pathogenesis' named entity 'protein' named entity 'hemocytometer' named entity 'inflammation' named entity 'Complementary DNA' named entity 'neutrophils' named entity 'oxidative stress' named entity 'lung injury' named entity 'RPMI' named entity 'JAK' named entity 'chemokines' named entity 'Sidak'

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