Project description:To elucidate IL-17A-dependent immune mechanims involved in regulating host defense, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating protective immunity that failed to be upregulated in the absence of IL-17RA signaling. Whole small intestine tissue collected from IL-17RA-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Giardia muris infection and from uninfected controls. Expression levels of several genes that may have anti-parasitic potential (Defb1, Retnlb, Saa1, Saa2) and may be involved in parasite clearance were, on average, lower or unchanged in IL-17RA deficient compared to wild-type mice after infection. Two weeks after Giardia muris challenge, total RNA was extracted and analyzed from tissue of the small intestines of infected IL-17RA-deficient and wild-type mice, and compared to uninfected controls. Each sample contained equal amounts of total RNA from 6 female mice which were pooled and used in the experiment.
Project description:To elucidate IL-17A-dependent immune mechanims involved in regulating host defense, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating protective immunity that failed to be upregulated in the absence of IL-17RA signaling. Whole small intestine tissue collected from IL-17RA-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Giardia muris infection and from uninfected controls. Expression levels of several genes that may have anti-parasitic potential (Defb1, Retnlb, Saa1, Saa2) and may be involved in parasite clearance were, on average, lower or unchanged in IL-17RA deficient compared to wild-type mice after infection.
Project description:Comparative analysis of renal gene expression between wild type and mice deficient in IL-17 receptor signaling following disseminated candidiasis. The hypothesis to be tested in the present study was that there should be a differential renal gene expresion in the absence of IL-17 receptor signaling following disseminated candidiasis. Wild type and IL-17RA-/- mice were systemically infected with Candida albicans and 48 hour post infection renal gene expression was analyzed.
Project description:Mice deficient for IL-17RA are more likely to develop lymphoid follicles and gastric cancer and express higher levels of many genes associated with inflammation and cancer in response to H. pylori infection
Project description:IL-17RA knockout mice presented increased tissue parasitism during T. cruzi infection that correlated with a reduced frequency of parasite-specific CD8+ T cells. Parasite-specific CD8+ T cells from KO mice showed similar proliferation rate but increased mortality and an exhausted phenotype when compared to WT counterparts. We hypothesize that during T. cruzi infection, IL-17RA signaling in CD8+ T cells is required for the regulation of a transcriptional program that prevents accelerated mortality and exhaustion and sustain the development of robust cytotoxic response required for efficient parasite control.
Project description:Nasopharyngeal colonization by Streptococcus pneumoniae (Spn) is common and often asymptomatic, yet prolonged colonization increases the risk of transmission and invasive pneumococcal disease, particularly early in life. Host immune pathways that prevent persistent colonization remain poorly understood. Here, we examined how IL-1R and IL-17RA signaling shape host transcriptional responses during pneumococcal colonization of the upper respiratory tract. Using a mouse model of Spn colonization, we performed bulk RNA-sequencing on nasal lavages from mock-treated and Spn-colonized wild-type, Il1r1-/- and Il17ra-/- mice. In wild-type mice, colonization induced robust upregulation of inflammatory and innate immune gene programs, whereas many of these responses were attenuated in Il1r1-/- and Il17ra-/- mice. Taken together, this analysis demonstrates that IL-1R and IL-17RA signaling are required for full activation of host transcriptional responses that limit persistent Spn colonization.
Project description:Trichuris muris (T. muris) induces chronic colitis in susceptible mouse strains with clinical, histological, and immunological homology to human Crohn's disease. Gene expression profiling was performed on colon tissue of resistant (BALB/c) and susceptible (AKR) mice following T. muris infection.
Project description:We used microarrays to compare gene expression profile of spleen CD8 T cells from IL-17RA KO and WT mice at different time-point after T. cruzi infection.
