An enzyme that inactivates the inflammatory mediator leukotriene b4 restricts mycobacterial infection.
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While tuberculosis susceptibility has historically been ascribed to failed inflammation, it is now known that an excess of leukotriene A4 hydrolase (LTA4H), which catalyzes the final step in leukotriene B4 (LTB4) synthesis, produces a hyperinflammatory state and tuberculosis susceptibility. Here we show that the LTB4-inactivating enzyme leukotriene B4 dehydrogenase/prostaglandin reductase 1 (LTB4DH/PTGR1) restricts inflammation and independently confers resistance to tuberculous infection. LTB4DH overexpression counters the susceptibility resulting from LTA4H excess while ltb4dh-deficient animals can be rescued pharmacologically by LTB4 receptor antagonists. These data place LTB4DH as a key modulator of TB susceptibility and suggest new tuberculosis therapeutic strategies.
Amino Acid Sequence
Molecular Sequence Data
Receptors, Leukotriene B4
Published Version (Please cite this version)10.1371/journal.pone.0067828
Publication InfoKo, Dennis; Ramakrishnan, L; Ray, JP; Roca, FJ; & Tobin, DM (2013). An enzyme that inactivates the inflammatory mediator leukotriene b4 restricts mycobacterial infection. PLoS One, 8(7). pp. e67828. 10.1371/journal.pone.0067828. Retrieved from http://hdl.handle.net/10161/11197.
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Assistant Professor in Molecular Genetics and Microbiology
Using Pathogens to Decipher Genetic Variation Connecting Cell Biology and Disease SusceptibilityDespite improvements in public health, advancements in vaccines, and the development of many classes of antibiotics, infectious disease is still responsible for over a quarter of all deaths worldwide. However, even for the most devastating of pandemics, individuals demonstrate a large variability in the severity of infection. The long-term goal of the lab is to understand the ge