Administration of p60 before a sublethal infection with L. monocytogenes enhanced innate host resistance in naive mice. Mouse macrophage RAW264.7 cells produced tumor necrosis factor (TNF)-alpha in response to stimulation with recombinant p60. Toll-like receptor 4 may be involved in TNF-alpha production from RAW264.7 cells and enhanced host resistance induced by p60 administration. Our findings demonstrated that p60 modulates NSC 136476 innate immune responses against L. monocytogenes infection.”
“Background: We investigated the epidemic of cholera that occurred in Kashipur and Dasmantpur blocks of Orissa, reported during July-September 2007.

Methods: Sixty-two rectal swabs and 28 water samples

collected from diarrhea patients at different hospitals and villages were bacteriologically analyzed for the identification, antibiogram, and detection of toxic genes of Vibrio Apoptosis inhibitor cholerae.

Results: The cholera outbreaks were caused by V. cholerae O1 Ogawa biotype El Tor in both Kashipur and Dasmantpur blocks. All the V. cholerae isolates from the clinical and environmental samples were sensitive to tetracycline, gentamicin, azithromycin, and chloramphenicol, but were resistant to ampicillin, ciprofloxacin, norfloxacin,

co-trimoxazole, nalidixic acid, neomycin, and furazolidone, except the water isolates, which were sensitive to ciprofloxacin and norfloxacin. The multiplex PCR

assay revealed that all the clinical Emricasan and environmental V. cholerae isolates were positive for the ctxA and tcpA genes, showing biotype El Tor. Interestingly, 88% of the clinical and environmental isolates of V. cholerae were El Tor biotype with mutation at the ctxB gene of the classical strain, as confirmed by mismatch amplification of mutation (MAMA)-PCR assay.

Conclusions: This is the first report of the El Tor variant of V. cholerae O1 Ogawa having the ctxB gene of the classical strain with altered antibiogram causing epidemics of cholera in Orissa, India. (C) 2009 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.”
“Vigorous acute inflammatory responses accompany Chlamydia muridarum infections in mice and are positively correlated with adverse urogenital and respiratory tract infection outcomes in the mouse model. Thus, we tested the hypothesis that neutrophils induce an acute inflammatory insult that, in the repair phase, leads to the chronic sequelae of hydrosalpinx – a surrogate marker of infertility in the mouse model. To this end, we induced neutropenia in mice using a neutrophil-depleting monoclonal antibody during acute phases of C. muridarum urogenital infection only (days 2-21 postinfection). To prove induced neutropenia, peripheral blood was monitored for neutrophils during the treatment regimen.