Antihistoplasma effect of activated mouse splenic macrophages involves production of reactive nitrogen intermediates.

Abstract:

:The mechanism by which recombinant murine gamma interferon (rMuIFN-gamma) and bacterial lipopolysaccharide (LPS) activate mouse resident splenic macrophages to inhibit the intracellular growth of the fungus Histoplasma capsulatum was examined. Growth inhibition depended on L-arginine metabolism. The growth inhibitory state normally induced by rMuIFN-gamma and LPS in resident splenic macrophages did not occur when the macrophages were cultured in the presence of NG-monomethyl-L-arginine, a competitive inhibitor of L-arginine metabolism. Resident splenic macrophages treated with rMuIFN-gamma and LPS produced nitrite (NO2-), an end product of L-arginine metabolism. When macrophages were cultured in the presence of NG-monomethyl-L-arginine together with rMuIFN-gamma and LPS, only baseline levels of NO2- were detected. Spleen cells from H. capsulatum-infected mice produced high levels of NO2- in culture. The production of NO2- correlated with in vitro inhibition of the intracellular growth of H. capsulatum. Anti-tumor necrosis factor alpha antibody did not block NO2- production by the immigrant splenic macrophages and did not abolish the antihistoplasma activity.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Lane TE,Wu-Hsieh BA,Howard DH

doi

10.1128/IAI.62.5.1940-1945.1994

subject

Has Abstract

pub_date

1994-05-01 00:00:00

pages

1940-5

issue

5

eissn

0019-9567

issn

1098-5522

journal_volume

62

pub_type

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