TNF-α failed to reverse the M. leprae-induced defective chemiluminescence response of human mononuclear cells

Abstract

The effect of phagocyte activation by TNF‐α on the ability to trigger a chemiluminescence (CL) response, associated with the release of oxidizing species was evaluated in healthy human mononuclear cells in the presence of Mycobacterium leprae. Recombinant TNF‐α (r‐TNF‐α) increased the CL response of unstimulated M. bovis BCG‐ and PMA‐stimulated cells but did not reverse the M. leprae defective activation of the human phagocyte oxidative burst. M. leprae was less well phagocytosed than M. bovis BCG but phagocytosis of mycobacteria was not altered by addition of r‐TNF‐α. The failure of activation of oxygen‐free radical production might have some relevance to the pathogenesis of leprosy.

Lipids from Mycobacterium leprae cell wall are endowed with an anti‐inflammatory property and inhibit macrophage function in vivo

“…26 There is evidence from some authors describing macrophage deactivation caused by mycobacteria structures. 8,[18][19][20][21][22][23][24][25] Further in the mice pleurisy model we showed that delipidation of Mycobacteria led to a distinct profile of cellular accumulation. Delipidated BCG recruited lower numbers of leucocytes to the cavity than BCG itself.…”