Killing non-invasive bacteria?
Nuruddeen Lewis
Saturday, 12 July 2008 05:31 UTC
Hi there. I am hoping to spark some discussion about host defense and would like to hear some ideas from the great people at Nature Network. Here’s the question:
How does our immune system kill non-invasive bacteria, such as bacteria in our stomach and intestines? I work on H. pylori which evades the immune response in the stomach for the life of its host. However, I’m not sure what an effective immune response would look like against this bacteria, given its colonizing niche. Any ideas?
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Replies
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Killing such bacteria is not necessary to prevent infection by them. Simply suppressing quorum sensing, which suppresses the expression of virulence factors is sufficient to prevent infection by most bacteria.
I am not familiar enough with H. pylori to appreciate how it regulates its own virulence. Presumably it does because most people carrying it remain asymptomatic most of the time.
Some commensals are close enough to pathogenic species that there is interference between the quorum sensing of the pathogen. That might be an important factor in how antibiotic resistant bacteria may be present but not a problem until a course of antibiotics wipe out the susceptible commensals that are suppressing the pathogen.
I think that is the mechanism by which the bacteria I am working with (autotrophic ammonia oxidizing bacteria) suppress heterotrophic bacteria on the skin. By blocking quorum sensing and biofilm formation, the heterotrophic bacteria can’t get a foot hold, can’t form a biofilm, and can’t express virulence factors to cause an infection.
I think that may be an important reason behind the expression of iNOS during sepsis. It is to suppress the quorum sensing and to suppress biofilm formation of the bacteria that are floating around in the blood stream. If those bacteria deposit and form a biofilm, they become much more difficult to kill and the prognosis becomes much worse. It is “worth” a significant risk of death to try and suppress biofilm formation because if that happens death becomes much more likely.
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Hi Nuruddeen,
There are evidence available which shows that DCs can be induced by inserting dendrites between the epithelial cells that form the protecting barrier and make contact with the non-invasive bacteria.
Check this article out.. might be helpful..
How do DCs interact with intestinal antigens?
Simon W.F. Milling, Lesley Cousins and G. Gordon MacPherson
Sir William Dunn School of Pathology, South Parks Road, Oxford, UK OX1 3RE -
Thanks for the replies.
@ David: I am not very familiar with quorum sensing. With HP infection, although most people are asymptomatic, there is active adaptive and innate gastritis during infection. However, this response is just not enough to eradicate the bug. That’s interesting that you mentioned iNOS, because my project is focused on that.
@ Amit: Thanks for directing me to that article. I am familiar with this, as we think this may is one of the ways the immune response gets activated in response to HP. However, I want to know what happens next. Once the immune response gets charged up and all the cells migrate to the site of infection (the stomach for HP), how are they supposed to kill the bug. If the bacteria are sitting above the epithelial cells, how does the immune system deal with them? I’ve heard that neutrophils, and possibly macrophages can get across this epithelial barrier. This may be a possible way. Are there any articles which outline a successful response to a non-invasive bacteria?
Thanks for the advice and insight.
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