The lower detection limit of these was 16 pg/mL for all assays. Samples

below the detection levels were assigned a theoretical value of one-half the detection limit. WT and knockout mice were infected i.v., via the lateral tail vein, with 1 × 104 CFU C. albicans ATCC strain 90028 as previously described [22]. Mice were observed twice daily for signs of disease and lethality. The kidney fungal burden was determined exactly as previously described [22]. Cytokine levels and log CFU were expressed as mean ± standard deviation of the mean (SD) of several determinations, each conducted on a different animal in an independent experiment. Differences in cytokine levels and organ CFUs were assessed by one-way analysis of variance and the Student’s-Keuls-Newman test. Survival data were analyzed check details with Kaplan–Meier survival plots followed by the log rank test (JMP Software; SAS Institute, Cary, NC) on an Apple Macintosh computer. When p values of < 0.05 were obtained, differences were considered statistically significant. We thank S. Akira, G. Brown, B. Beutler, S. Bauer, and T. Taniguchi for providing KO mice. This work was partially supported by the Programma Operativo Nazionale PON01_00117/8 from the Ministero dell'Istruzione,

dell’Università e della Ricerca of Italy and by Progetti di Ricerca d’Ateneo A.013.BIO200809 and A.013.MAN200809 from the University of Messina granted

to CBi and C-X-C chemokine receptor type 7 (CXCR-7) GM, respectively. The authors declare no financial or commercial conflict of interest Disclaimer: EPZ-6438 purchase Supplementary materials have been peer-reviewed but not copyedited. “
“Deposition of Schistosoma mansoni eggs in the intestinal mucosa is associated with recruitment of mucosal mast cells (MMC) expressing mouse mast cell protease-1 (mMCP-1). We investigated the involvement of mMCP-1 in intestinal barrier disruption and egg excretion by examining BALB/c mice lacking mMCP-1 (Mcpt-1−/−). Tissue and faecal egg counts from 6 weeks until 12 weeks post-infection (w p.i.) revealed no differences between wild type (WT) and Mcpt-1−/−mice. Using chamber experiments on ileal tissue revealed that at 8 w p.i., the epithelial barrier and secretory capacity were severely impaired, whereas no difference was found between WT and Mcpt-1−/−mice in this respect. However, a fragmented distribution of the tight junction (TJ) protein occludin, but not of claudin-3 or ZO-1, was observed in WT mice at 8 w p.i., while no changes in TJ integrity were seen in Mcpt-1−/−mice. Therefore, we conclude that in contrast to the situation in Trichinella spiralis-infected mice, in schistosomiasis, mMCP-1 is not a key mediator in egg excretion or impairment of the intestinal barrier. The marked decrease in ileal secretory capacity during S.