01899nas a2200301   4500000000100000008004100001260001300042653001500055653001000070653002400080653001600104653001600120653001100136653001200147653000900159653002500168653003200193100001400225700001300239700001600252700001600268245008600284856006800370300000800438490000700446050001600453520112800469       2008                            d  c2008 Mar10aAdolescent10aAdult10aAntigens, Bacterial10aBlood Cells10aGlycolipids10aHumans10aleprosy10aMale10aMycobacterium leprae10aTumor Necrosis Factor-alpha1 aDhungel S1 aRanjit C1 aSapkota B R1 aMacdonald M00aRole of PGL-I of M. leprae in TNF-alpha production by in vitro whole blood assay.  uhttp://www.nmcth.edu/images/gallery/Editorial/YHmCDsdhungel.pdf  a1-30 v10  aDHUNGEL20083 a<p>Phenolic glycolipid-I (PGL-I) is known to be a major antigen of Mycobacterium leprae. We have studied the influence of PGL-I on the production of Tumour Necrosis Factor alpha (TNF-alpha) using the in vitro whole blood assay. Armadillo-derived M. leprae (ADML) are thought to be depleted of PGL-I during the purification process. M. leprae obtained from mouse foot pad material (MFPML) has been subjected to a less rigorous purification process; their PGL-I coating is therefore believed to be more intact than that of ADML. PGL-I or ADML alone induced the secretion of minimal levels of TNF-alpha in whole blood assay; when added in combination, higher levels of this cytokine were observed. The highest TNF-alpha response was seen following stimulation with MFPML. MFP material not infected with ML did not elicit any response. The difference in TNF-alpha response shown by ADML and MFPML was postulated to be largely due to the presence of higher levels of PGL-I in MFPML. This increase in TNF-alpha production suggests that PGL-I may play a significant role in the induction of TNF-alpha during natural infection.</p>