%A Park E
%A Levis WR
%A Quinn MR
%A Park SY
%A Schuller-Levis GB


%T Regulation of nitric oxide induced by  mycobacterial lipoarabinomannan in murine macrophages: effects of interferon-β and Taurine-chloramine

%0 Journal Article

%D 2000

%J International Journal of Leprosy and other Mycobacterial Diseases

%P 0148-916X

%V 68

%N 4

%X We examined the effects of interferon beta  (IFN-β) on the production of liporabinomannan (LAM)-induced nitric oxide (NO)  in peritoneal macrophages from low- responder and high-responder (C3H/HeJ and  C3H/OuJ) mice. NO was produced in a dose response when induced by lipo-  polysaccharide (LPS) or LAM plus interferon gamma (IFN-γ) or IFN-β in both  high- and low-responder mice. In contrast to IFN-γ, both high- and  low-responder mice failed to induce nitrite production when IFN-β was added,  except at a high concentration of IFN-β. Tau-Cl (0.5 mM) inhibited NO production about 50%  in the high-responder strain when  cells were activated with LPS or LAM in combination with either IFN-β or  IFN-γ, and almost abolished NO production at 1.0 mM. In the low-responder strain, Tau-Cl (0.5 mM) significantly inhibited NO production  when cells were activated with IFN-γ or IFN-β in addition to LPS or LAM, but  did not completely inhibit NO production at 1.0 mM. Tau-Cl appears to play a potent role in regulating inflammatory  reaction-induced bacterial or mycobacterial organisms. These data indicate a  pivotal role for IFN-γ and IFN-β for the production of LPS and LAM initiated NO  in peritoneal macrophages from low-responder (C3H/HeJ) mice.