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Splenic B cells from Hymenolepis diminuta-infected mice ameliorate colitis independent of T cells and via cooperation with macrophages

ABSTRACT: Mouse infection with the tapeworm Hymenolepis diminuta leads to a less severe DNBS-colitis. Increased Th2 and regulatory cytokine production in the spleen is a hallmark of Hymenolepis diminuta infection, therefore we hypothesized that given this microenvironment, splenic adaptive cells acquire an anti-inflammatory phenotype. We tested the ability of putative splenic regulatory B cells generated by Hymenolepis diminuta infection to down-regulate intestinal inflammation. We found that unlike splenic B cells from uninfected mice, splenic B cells from Hymenolepis diminuta -infected animals ameliorated chemically-induced colitis.

ORGANISM(S): Mus musculus

PROVIDER: GSE61460 | GEO | 2015/02/20

SECONDARY ACCESSION(S): PRJNA261161

REPOSITORIES: GEO

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Project description:Abstract Introduction Several environmental stimuli may influence lupus, especially viral infection. We utilize an imiquimod-induced lupus mouse model focusing on TLR7 pathway and use proteomics analysis to figure out the specific pathway related to viral infection and its related protein expressions in splenic B cells, hoping to get an insight on B cell responses to viral infection in lupus model. Material and methods. FVB/N wild type mouse was used treated with imiquimod for 8 weeks to induce lupus symptoms and signs, and splenocytes were retrieved, and B cells were selected and conducted proteomic analysis. The B cells were co-cultured with CD40L+ feeder cells for another one week before Western blot analysis. Panther pathway analysis was used to disclose the pathways activated and protein-protein interactome analyzed by STRING database in this lupus murine model. Results. The lupus model is well established and well demonstrated with serology evidence and pathology proof of lupus-mimic organ damage. Proteomics data of splenic B cells revealed the most important pathways activated (fold enrichment >100) were positive regulation of MDA-5 signaling pathway, negative regulation of IP-10 production, negative regulation of chemokine (C-X-C motif) ligand 2 production and positive regulation of RIG-I signaling pathway. A unique protein-protein interactome containing 10 genes was discovered, within which ISG15, IFIH1, IFIT1, DDX60, and DHX58 have been demonstrated to be downstream effectors of MDA5 signaling. Finally, B cells intracellular cytosolic proteins were determined with Western blot experiment and the MDA5-related pathway activation is still evident. Conclusion. In this experiment, we confirmed that the B cells in lupus murine model focusing on TLR7 pathway were activated through MDA5 signaling pathway, an important RNA sensor implicated in the detection of viral infections and autoimmune. The MDA5 agonists/antagonist RNAs and detailed molecular interactions inside B cells are worthy further investigation for lupus therapy.

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Splenic B cells from Hymenolepis diminuta-infected mice ameliorate colitis independent of T cells and via cooperation with macrophages

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