Leprosy is caused by the microbe Mycobacterium leprae, which lives inside cells and survives by both evading the immune system and using human fat molecules (lipids) to promote its growth and virulence.
A link between these two factors influencing M. leprae survival in the lesions that characterize disease in individuals with the lepromatous form of human leprosy (L-lep) has now been uncovered by Robert Modlin and colleagues, at UCLA David Geffen School of Medicine, Los Angeles.
In the study, expression of genes containing the information for making proteins involved in lipid metabolism (the production and breakdown of lipids) was observed in human L-lep lesions. Consistent with this, the lipid-laden cells (specifically macrophages) in human L-lep lesions that are known to harbor M. leprae were found to accumulate human lipids known as oxidized phospholipids.
Further in vitro analysis indicated that some of these oxidized phospholipids inhibited innate immune responses. The accumulation of macrophages laden with human oxidized phospholipids in L-lep lesions is strikingly similar to what is observed in the lesions that narrow the blood vessels in the disease atherosclerosis -- a common disease of the major arterial blood vessels that can result in heart attack or stroke.
These similarities have led the authors to suggest that in both microbial infection and atherosclerosis there is a link between innate immunity and human lipid metabolism.
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