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E-GEOD-36826

ABSTRACT: Neutrophil-derived IL-1Î² is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

OTHER RELATED OMICS DATASETS IN: PRJNA156821

DISEASE(S): Staphylococcus Aureus Cutaneous Infection,Normal

PROVIDER: E-GEOD-36826 | ExpressionAtlas | 2015-07-08

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-36826-analysis-methods.tsv	Tabular
	E-GEOD-36826-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-36826-configuration.xml	Xml
	E-GEOD-36826-percentile-ranks.tsv	Tabular
	E-GEOD-36826.condensed-sdrf.tsv	Tabular

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Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils. Lesional skin biopsies obtained from C57BL/6J WT mice or IL-1R-deficient mice at 4 hours post-infection with Staphylococcus aureus. Uninfected skin biopsies were also collected from WT and IL-1R-deficient mice.

2012-12-05 | E-GEOD-36826 | biostudies-arrayexpress

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

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Phenotype and expression profile analysis of Staphylococcus aureus biofilms and planktonic cells in response to Licochalcone A

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