This muted Th17 response led to dissemination of Salmonella from the gut to the peripheral blood, Dandekar said.
The team of researchers also used mice that lacked the IL-17 receptor, an arm of the mucosal immune response, to confirm that IL-17 deficiency leads to increased systemic dissemination of Salmonella.
We believe IL-17 deficiency causes defects in the mucosal barrier of the gut, Dandekar said.
Both Bumler and Dandekar agreed that the results of their collaboration have exciting implications for both HIV and Salmonella research and, more importantly, get scientists closer to finding treatments for HIV and the deadly form of Salmonella.
In terms of HIV, the results suggest that Th17 may make a good biomarker for monitoring HIV infection and testing the efficacy of vaccines and other therapies. They also suggest that efforts to enhance Th17 function may improve existing antiretroviral treatments.
We are interested in looking at different molecules and compounds to see if we can boost mucosal immune defenses in the gut, she said.
Dandekar is also interested in looking at Th17 function in those who respond well to treatment and in long-term non-progressors, those individuals who carry HIV for years without going onto develop AIDS.
Now we know these cells are playing a big role, but we need to better understand how they are contributing to immune inactivation and inflammation, Dandekar said.
In terms of Salmonella, Bumlers next step is to discover the mechanisms by which non-immunocompromised patients are able to rid themselves of the infections.
We now know which cytokines orchestrate the mucosal barrier function, but we still dont know what kills these bacteria, he said.
|Contact: David Ong|
University of California - Davis - Health System