Linked Life Data

16448800

Source:http://linkedlifedata.com/resource/pubmed/id/16448800

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-14
pubmed:abstractText
The involvement of nitric oxide (NO) in host defense and cytoprotective functions in murine salmonellosis has been reported. Salmonella mutants with the altered sigma factor RpoS (sigmaS) are less virulent and are susceptible to various stresses. This study investigated the role of the rpoS gene of Salmonella enterica serovar Typhi in NO-dependent host defense in vitro and in vivo. Wild-type mice and mice deficient in inducible NO synthase (iNOS) were infected intraperitoneally or orally with serovar Typhi strains. iNOS-deficient mice were more susceptible to infection by both wild-type and rpoS mutant strains of serovar Typhi and showed extensive apoptotic liver damage compared with wild-type mice. Intracellular killing of Salmonella was analyzed with RAW 264 macrophage-like cells and primary peritoneal macrophages from wild-type and iNOS-deficient mice after cells were infected with the serovar Typhi parent or rpoS mutant strain. The rpoS mutant was more susceptible to killing by macrophages than was the wild-type strain. Also, the wild-type strain produced more extensive apoptotic changes in macrophages than did rpoS mutant. These effects were nullified in RAW 264 cells treated with an NOS inhibitor and in iNOS-deficient primary macrophages. Peroxynitrite susceptibility assays of these strains were also performed. The rpoS mutant Typhi strain was more sensitive to in vitro peroxynitrite treatment than was the parent strain. Together these data show that NO has a significant host defense function during serovar Typhi infection, and that Salmonella RpoS, because it reacts to the presence of NO or its reactive derivatives, is thought to have a role in the pathogenicity of serovar Typhi.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0882-4010
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
116-25
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16448800-Animals, pubmed-meshheading:16448800-Anti-Bacterial Agents, pubmed-meshheading:16448800-Apoptosis, pubmed-meshheading:16448800-Bacterial Proteins, pubmed-meshheading:16448800-Body Weight, pubmed-meshheading:16448800-Cell Line, pubmed-meshheading:16448800-Cells, Cultured, pubmed-meshheading:16448800-Colony Count, Microbial, pubmed-meshheading:16448800-Disease Models, Animal, pubmed-meshheading:16448800-In Situ Nick-End Labeling, pubmed-meshheading:16448800-Liver, pubmed-meshheading:16448800-Macrophages, pubmed-meshheading:16448800-Macrophages, Peritoneal, pubmed-meshheading:16448800-Mice, pubmed-meshheading:16448800-Mice, Knockout, pubmed-meshheading:16448800-Nitric Oxide, pubmed-meshheading:16448800-Nitric Oxide Synthase Type II, pubmed-meshheading:16448800-Peroxynitrous Acid, pubmed-meshheading:16448800-Salmonella Infections, Animal, pubmed-meshheading:16448800-Salmonella typhi, pubmed-meshheading:16448800-Sigma Factor, pubmed-meshheading:16448800-Survival Analysis
pubmed:year
2006
pubmed:articleTitle
Involvement of Salmonella enterica serovar Typhi RpoS in resistance to NO-mediated host defense against serovar Typhi infection.
pubmed:affiliation
Department of Microbiology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't