Affiliation:
1. Division of Infectious Diseases
2. Department of Molecular Biology, Massachusetts General Hospital
3. Department of Genetics
4. Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts
Abstract
ABSTRACT
Staphylococcus aureus
, an important pathogen of humans and other warm-blooded animals, is also capable of killing the nematode
Caenorhabditis elegans
. Here, we show that
C. elegans
organisms that are fed
S. aureus
die over the course of several days in a process that is correlated with the accumulation of bacteria within the nematode digestive tract. Several
S. aureus
virulence determinants known or speculated to be important in mammalian pathogenesis, including the quorum-sensing global virulence regulatory system
agr
and the global virulence regulator
sarA
, the alternative sigma factor σ
B
, alpha-hemolysin, and V8 serine protease, are required for full pathogenicity in nematodes. In addition, several defined
C. elegans
mutants were examined for susceptibility to
S. aureus
infection. Enhanced susceptibility to
S. aureus
killing was observed with loss-of-function mutations in the
C. elegans
genes
esp-2
/
sek-1
and
esp-8
/
nsy-1
, which encode components of a conserved p38 MAP kinase signaling pathway involved in nematode defense against multiple pathogens. These results suggest that key aspects of
S. aureus
pathogenesis have been conserved, irrespective of the host, and that specific
C. elegans
host factors can alter susceptibility to this gram-positive human pathogen.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
284 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献