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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="species">mouse</item><item key="factors"><item><item key="GSM9025"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM9025"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM9025"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM9025"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM9025"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM9025"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM902517"><item key="GENOTYPE">IL-1R knock-out</item></item></item><item><item key="GSM902517"><item key="GENOTYPE">IL-1R knock-out</item></item></item><item><item key="GSM902517"><item key="GENOTYPE">IL-1R knock-out</item></item></item><item><item key="GSM902517"><item key="GENOTYPE">IL-1R knock-out</item></item></item><item><item key="GSM902517"><item key="GENOTYPE">IL-1R knock-out</item></item></item><item><item key="GSM902517"><item key="GENOTYPE">IL-1R knock-out</item></item></item></item><item key="id">6831</item><item key="pop_total">0</item><item key="platform">6</item><item key="summary_wrapped">Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation...</item><item key="pubmed_id">23209417</item><item key="geo_gse_id">E-GEOD-36826</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">1</item><item key="sample_count">12</item><item key="tags"><item>neutrophil</item><item>skin</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_id_plat">E-GEOD-36826_A-AFFY-45</item><item key="slug">neutrophil-derived-il-1-is-sufficient-for-abscess</item><item key="geo_gds_id"/><item key="name">Neutrophil-derived IL-1&#946; is sufficient for abscess formation in immunity against Staphylococcus aureus in mice</item><item key="created">Nov.12, 2014</item><item key="summary">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.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-36826</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-36826/samples/</item></data></biogps>
