Experimental infection in tumor necrosis factor alpha receptor, interferon gamma and interleukin 4 deficient mice by pathogenic Leptospira interrogans.
Only recently, knockout mouse models were applied in studies on the pathogenesis of leptospirosis. Current data suggest an important role of innate immunity receptors and interferon gamma dependant cellular response on protection. It is not clear, however, whether T helper cell polarization influences on outcome of leptospiral infection. We report findings of experimental infection of C57BL/6 (interferon gamma or tumor necrosis factor alpha receptor deficient) and BALB/c (interleukin 4 deficient) mice infected by pathogenic Leptospira interrogans serovar Copenhageni. Specific cytokine gene deficiency had no impact on outcome since all animals survived. TNFR knockout mice, however, exhibited more severe residual renal inflammation during convalescence thus suggesting this cytokine is important in early control of infection, protecting kidneys from relevant pathology.
Athanazio
Daniel A
DA
Gonçalo Moniz Research Centre, Oswaldo Cruz Foundation, Ministry of Health, Salvador, Brazil.
Santos
Cleiton S
CS
Santos
Andréia C
AC
McBride
Flávia W C
FW
Reis
Mitermayer G
MG
D000818:Animals; D007249:Inflammation / Q000473:pathology; D007371:Interferon-gamma / Q000172:deficiency*; D015847:Interleukin-4 / Q000172:deficiency*; D007668:Kidney / Q000473:pathology; D007921:Leptospira interrogans / Q000276:immunology*; D007922:Leptospirosis / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018124:Receptors, Tumor Necrosis Factor / Q000172:deficiency*; D016019:Survival Analysis
D018124:Receptors, Tumor Necrosis Factor; D015847:Interleukin-4; D007371:Interferon-gamma