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ShareMar. 15, 2011 — Scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have shown how the O157:H7 strain of Escherichia coli causes infection and thrives by manipulating the host immune response.
The bacterium secretes a protein called NleH1 that directs the host immune enzyme IKK-beta to alter specific immune responses. This process not only helps the bacterium evade elimination by the immune system, it also works to prolong the survival of the infected host, enabling the bacterium to persist and ultimately spread to unaffected individuals. This finely balanced mechanism, observed in both laboratory and animal models, could be relevant to other pathogens involved in foodborne diseases.
While most E. coli strains help check the growth of harmful bacteria in the guts of animals and humans, a few E. coli strains, such as O157:H7, can cause severe diarrhea, abdominal cramps and, in rare cases, death. Human cases of E. coli O157:H7 have been linked to consumption of raw, undercooked, or spoiled meat.
NIAID researchers plan to use the new information to further study how the host immune system mounts a response to E. coli O157:H7 when infection begins and how the bacterium selectively blocks these defenses. Several foodborne pathogens, including Shigella and Salmonella, use a similar secretion system to disrupt host immune responses and infect gut cells.
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The above story is reprinted from materials provided by NIH/National Institute of Allergy and Infectious Diseases, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Fengyi Wan, Amanda Weaver, Xiaofei Gao, Michael Bern, Philip R Hardwidge, Michael J Lenardo. IKKβ phosphorylation regulates RPS3 nuclear translocation and NF-κB function during infection with Escherichia coli strain O157:H7. Nature Immunology, 2011; DOI: 10.1038/ni.2007
Note: If no author is given, the source is cited instead.
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