Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 13, Issue 4, Pages 641-645Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2013.06.007
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Funding
- Mallinckrodt Scholar Award
- Searle Scholar Award
- Duke University Center for AIDS Research
- NIH
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There is a growing appreciation of the diverse roles that lipid mediators play in modulating inflammatory responses during infection. In the case of tuberculosis, virulent mycobacteria induce host production of anti-inflammatory mediators, including lipoxins, which limit the host inflammatory response and lead to necrotic cell death of infected macrophages. Recent work using the zebrafish model suggests that, while excess anti-inflammatory lipoxins are host detrimental during mycobacterial infections, excess pro-inflammatory lipids also drive host susceptibility. The balance of these inflammatory states is influenced by common human genetic variation in Asia. Fuller understanding of the mechanisms of eicosanoid-mediated inflammatory imbalance during tuberculosis infection has important implications for the development of adjunctive theraples.
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