02495nas a2200349   4500000000100000008004100001260001300042653001200055653001500067653002000082653002000102653003800122653004200160653003800202653001200240653002800252653000900280653000900289653002400298653002500322653003600347653003200383100001400415700001200429700001400441245019400455856004100649300001000690490000700700520142400707022001402131       1999                            d  c1999 Mar10aAnimals10aArmadillos10aCells, Cultured10aDown-Regulation10aEnzyme-Linked Immunosorbent Assay10aGene Expression Regulation, Bacterial10aIntercellular Adhesion Molecule-110aleprosy10aMacrophages, Peritoneal10aMale10aMice10aMice, Inbred BALB C10aMycobacterium leprae10aTransforming Growth Factor beta10aTumor Necrosis Factor-alpha1 aShimizu T1 aMaw W W1 aTomioka H00aRoles of tumor necrosis factor-alpha and transforming growth factor-beta in regulating intercellular adhesion molecule-1 expression on murine peritoneal macrophages infected with M. leprae.  uhttp://ila.ilsl.br/pdfs/v67n1a06.pdf  a36-450 v673 a<p>Profiles of intercellular adhesion molecule-1 (ICAM-1) expression on murine peritoneal macrophages (M phi s) infected with Mycobacterium leprae during cultivation were examined with special reference to the regulatory effects of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta). When M phi s were infected with M. leprae or stimulated with heat-killed M. leprae at day 0, their ICAM-1 expression, measured in terms of the ratio of M phi s positively stained with anti-ICAM-1 antibody (Ab), rapidly increased, peaking during days 1 to 3 and thereafter fell, returning to the normal level by day 7. The addition of TNF-alpha or anti-TGF-beta Ab inhibited the middle phase (day 7) downregulation of M phi ICAM-1 expression, although the late-phase (day 14) downregulation of ICAM-1 was not prevented by them. M. leprae-infected M phi s released small amounts of TNF-alpha and significant amounts of TGF-beta into the culture medium. This may indicate that M. leprae-infected M phi s produced the majority of TNF-alpha in a membrane-bound form. Alternatively, endogenous TNF-alpha might upregulate M phi ICAM-1 expression even at very low concentrations. In any case, these findings indicate the central roles of TNF-alpha and TGF-beta in the early phase upregulation and the middle-to-late phase downregulation, respectively, of ICAM-1 expression by M. leprae-infected M phi s.</p>  a0148-916X