Author:
Fierer Joshua,Okamoto Sharon,Banerjee Ananya,Guiney Donald G.
Abstract
ABSTRACTWe investigated the roles ofSalmonellapathogenicity island 2 (SPI-2) and two SPI-2 effectors inSalmonellacolitis and diarrhea in genetically resistant BALB/c.D2Slc11a1congenic mice with the wild-type Nramp1 locus. Wild-typeSalmonella entericaserovar Typhimurium 14028s caused a pan-colitis, and the infected mice developed frank diarrhea with a doubling of the fecal water content. AnssaVmutant caused only a 26% increase in fecal water content, without producing the pathological changes of colitis, and it did not cause weight loss over a 1-week period of observation. However, two SPI-2 effector mutants, thespvBandsifAmutants, and a doublespvB sifAmutant caused diarrhea and colitis, even though thesifAmutant was sensitive to killing by bone marrow-derived macrophages from BALB/c.D2 mice and was severely impaired in extraintestinal growth but not in growth in the cecum. These results demonstrate that systemicS. entericainfection and diarrhea/colitis are distinct pathogenic processes and that only the former requiresspvBandsifA.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
16 articles.
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