01886nas a2200289   4500000000100000008004100001260001300042653001400055653002000069653001100089653001200100653002400112653002500136653001600161653003200177100001700209700001500226700001700241700001400258700001300272700001600285245010900301300001100410490000700421520115400428022001401582       1999                            d  c1999 Mar10aApoptosis10aCells, Cultured10aHumans10aleprosy10aLipopolysaccharides10aMycobacterium leprae10aNeutrophils10aTumor Necrosis Factor-alpha1 aOliveira R B1 aMoraes M O1 aOliveira E B1 aSarno E N1 aNery J A1 aSampaio E P00aNeutrophils isolated from leprosy patients release TNF-alpha and exhibit accelerated apoptosis in vitro.  a364-710 v653 a<p>This study demonstrated that polymorphonuclear neutrophils (PMN) participate in the acute inflammatory response in leprosy as effector cells. Lepromatous patients present intense infiltrate of neutrophils in reactional (ENL) lesions. Circulating PMN of nonreactional patients, healthy donors, and reactional patients were purified and analyzed in vitro. The study confirmed the short lifespan of these cells in culture with progressive changes characteristic of apoptosis. Apoptosis was greatly accelerated in ENL patients as shown by cellular morphology, later confirmed by qualitative and quantitative analysis of fragmented DNA. It was observed that neutrophils stimulated with lipopolysaccharide, Mycobacterium leprae, and lipoarabinomannan secrete interleukin-8 and tumor necrosis factor alpha (TNF-alpha). Thalidomide, a drug known to inhibit TNF-alpha synthesis on monocytes, also exerted an inhibitory effect on TNF-alpha secretion in neutrophils. These data suggest that PMN can participate in the regulation of the immune response in leprosy and can contribute to the amplification of TNF-alpha production at the site of ENL lesion.</p>  a0741-5400