Rodrigues-Bastos Ana Paula M, Nascimento Camila X, Werneck-Barroso Eduardo, Cordeiro Renato S B, Henriques Maria das Graças M O, Moura Aparecida Cristina N
Department of Cell Biology and Genetics, IBRAG, Universidade do Estado do Rio de Janeiro (UERJ), R. São Francisco Xavier 524-PHLC, 20550-013-Rio de Janeiro, Brazil.
Inflammopharmacology. 2004;12(4):353-72. doi: 10.1163/1568560043696236.
Mycobacterium bovis-BCG (BCG) and Mycobacterium leprae (ML) have opposite inflammatory properties. Mycobacteria-induced pleurisy in C57Bl/6 and C57Bl/10 mice was evaluated to establish if their innate responses could be comparable, verifying cellular migration and nitrite production. Kinetic responses after ML or BCG intrathoracic injection were compared in those mice, sharing the H-2(b) MHC haplotype. BCG led to acute eosinophilia and late neutrophilia in both mice. In C57Bl/6 late pleurisy, monocytes and neutrophil recruitment was dose- and iNOS-dependent, inhibited by methotrexate but not by indomethacin. Pleural macrophages released nitrites ex vivo after 7 days of BCG stimulus, without "priming" and blocked by the nitrite inhibitor L-N5-(1-iminoethyl)-ornithine (L-NIO). ML did not induce cellular migration or nitrite production, independent of the mouse strain, timing, or number of bacilli. Although these mycobacteria have high homology, there was no effect of ML on BCG-evoked secondary cellular recruitment. Both C57Black mice trigger similar onset of inflammatory responses to these mycobacteria, so far can alternatively be used in experimental studies.