About: Sex-specific regulation of chemokine Cxcl5/6 controls neutrophil recruitment and tissue injury in acute inflammatory states

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About: Sex-specific regulation of chemokine Cxcl5/6 controls neutrophil recruitment and tissue injury in acute inflammatory states 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	Sex-specific regulation of chemokine Cxcl5/6 controls neutrophil recruitment and tissue injury in acute inflammatory states
Creator	Thiemermann, Christoph Gilroy, Derek Beyrau, Martina Duchene, Johan Madalli, Shimona Motwani, Madhur Nourshargh, Sussan Patel, Nimesh Scotland, Ramona Whiteford, James Nandhra, Inderpal
Source	PMC
abstract	BACKGROUND: Tissue infiltration by neutrophils during acute inflammatory states causes substantial tissue injury. While the magnitude of tissue neutrophil accumulation in innate immune responses is profoundly greater in males than females, fundamental aspects of the molecular mechanisms underlying these sex differences remain largely unknown. METHODS: We investigated sex differences in neutrophil stimulation and recruitment in ischemia/reperfusion (I/R; mesenteric or renal) or carrageenan pleurisy in rats or mice, as well as skin injury in human volunteers. The induction of potent chemoattractive mediators (chemokines) and neutrophil adhesion molecules were measured by real-time PCR, flow cytometry, and protein assays. RESULTS: Mesenteric I/R in age-matched Wistar rats resulted in substantially more neutrophil accumulation and tissue injury at 2 h reperfusion in males than females. Using intravital microscopy, we show that the immediate (<30 min) neutrophil response to I/R is similar in males and females but that prolonged neutrophil recruitment occurs in males at sites local and distal to inflammatory insult partly due to an increase in circulating neutrophil populations with elevated surface expression of adhesion molecules. Sex differences in neutrophil kinetics were correlated with sustained induction of chemokine Cxcl5 in the tissue, circulation, and bone marrow of males but not females. Furthermore, blockade of Cxcl5 in males prior to ischemia resulted in neutrophil responses that were similar in magnitude to those in females. Conversely, administration of Cxcl5 to males in the absence of I/R was sufficient to increase levels of systemic neutrophils. Cxcl5 treatment of bone marrow neutrophils in vitro caused substantial induction of neutrophil-mobilizing cytokine granulocyte colony-stimulating factor (GCSF) and expression of β2 integrin that accounts for sexual dimorphism in circulating neutrophil populations in I/R. Moreover, male Cxcl5-stimulated bone marrow neutrophils had an increased capacity to adhere to β2 integrin ligand ICAM-1, implicating a greater sensitivity of male leukocytes to Cxcl5-mediated activation. Differential induction of Cxcl5 (human CXCL6) between the sexes was also evident in murine renal I/R, rat pleurisy, and human skin blisters and correlated with the magnitude of neutrophil accumulation in tissues. CONCLUSIONS: Our study reveals that sex-specific induction of chemokine Cxcl5/CXCL6 contributes to sexual dimorphism in neutrophil recruitment in diverse acute inflammatory responses partly due to increased stimulation and trafficking of bone marrow neutrophils in males. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13293-015-0047-5) contains supplementary material, which is available to authorized users.
has issue date	2015-11-26(xsd:dateTime)
bibo:doi	10.1186/s13293-015-0047-5
bibo:pmid	26617980
has license	cc-by
sha1sum (hex)	c3d0cb6f9abb81adb9d8c4b601902c4d03c880bc
schema:url	https://doi.org/10.1186/s13293-015-0047-5
resource representing a document's title	Sex-specific regulation of chemokine Cxcl5/6 controls neutrophil recruitment and tissue injury in acute inflammatory states
has PubMed Central identifier	PMC4661984
has PubMed identifier	26617980
schema:publication	Biol Sex Differ
resource representing a document's body	covid:c3d0cb6f9abb81adb9d8c4b601902c4d03c880bc#body_text
is schema:about of	named entity 'infiltration' named entity 'INFLAMMATORY' named entity 'molecular mechanisms' named entity 'neutrophil' named entity 'neutrophils' named entity 'neutrophil' named entity 'chemokine' named entity 'acute inflammatory' named entity 'reperfusion' named entity '2.0' named entity 'necrosis' named entity 'neutrophil' named entity 'reperfusion' named entity 'Cxcl5' named entity 'mRNA' named entity 'mesentery' named entity 'reperfusion' named entity 'erythrocytes' named entity 'adhesion molecules' named entity 'reperfusion' named entity 'bone marrow' named entity 'leukocytes' named entity 'asthma' named entity 'neutrophil' named entity 'ischemia' named entity 'intravital microscopy' named entity 'preclinical' named entity 'reperfusion' named entity 'red blood cell' named entity 'absolute magnitude' named entity 'correlation' named entity 'protein' named entity 'Topical application' named entity 'mice' named entity 'anti-inflammatory' named entity 'bone marrow' named entity 'male mammals' named entity 'neutrophils' named entity 'Cxcl5' named entity 'reperfusion' named entity 'neutrophils' named entity 'Cxcl5' named entity 'neutrophil' named entity 'chemokine' named entity 'neutrophil' named entity 'superior mesenteric artery' named entity 'mRNA' named entity 'RNA' named entity 'vasculature' named entity 'inflammatory response' named entity 'Cxcl5' named entity 'protein' named entity 'Ccl3' named entity 'neutrophils' named entity 'secondary injury' named entity 'leukocyte' named entity 'pro-inflammatory' named entity 'Cxcl5' named entity 'kinetics' named entity 'Cxcl5' named entity 'Cxcl1' named entity 'Leukocyte' named entity 'polymorphisms' named entity 'neutrophils' named entity 'Sustained release' named entity 'Bone marrow' named entity 'leukocyte' named entity 'tissue injury' named entity 'EDTA' named entity 'GCSF' named entity 'RPMI'

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