2009, Number 3
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Rev Inst Nal Enf Resp Mex 2009; 22 (3)
Infection with Mycobacterium tuberculosis increases the nitric oxide and TNF-α production in alveolar macrophages from household contacts of tuberculous patients
Carranza C, Juárez E, Sarabia C, Escobedo D, Sada E, Torres M
Language: Spanish
References: 22
Page: 163-170
PDF size: 102.21 Kb.
ABSTRACT
Household contacts of patients with tuberculosis seem to be a protected population that develops specific memory against
Mycobacterium tuberculosis. In this work, alveolar macrophages from household contacts and control individuals from community were evaluated for their capability to produce nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) in response to the infection with strains H37Ra (non-virulent) and H37Rv (virulent) of
M. tuberculosis. Our results showed that production of NO and TNF-a in supernatants of alveolar macrophages cultures from household contacts increased on days 4 and 7. By contrast, NO and TNF-α production was lower in alveolar macrophages from community controls. These results suggest that local production of NO and TNF-α plays an important role in the control of tuberculosis in individuals exposed to the infection.
REFERENCES
The World Health Organization. Global Tuberculosis Control. Surveillance, Planning. WHO report, 2004:7-9.
Grybowski S, Allen E. The challeng of tuberculosis in decline. Am Rev Respir Dis 1974;90:707-720.
Schwander S, Torres M, Carranza CC, et ál. Pulmonary mononuclear cell responses to antigens of Mycobacterium tuberculosis in healthy household contacts of patients with active tuberculosis and healthy controls from the community. J Immunol 2000;165:1479-1485.
Mohan VP, Scanga CA, Yu K, et ál. Effects of tumor necrosis factor alpha on host immune response in chronic persistent tuberculosis: possible role for limiting pathology. Infect Immun 2001;69:1847-1855.
Giacomini E, Iona E, Ferroni L, et ál. Infection of human macrophages and dendritic cells with Mycobacterium tuberculosis induces a differential cytokine gene expression that modulates T cell response. J Immunol 2001;166:7033-7041.
MacMiking JD, North RJ, LaCourse R, Mudgett JS, Shah SK, Nathan CF. Identification of nitric oxide synthese as a protective locus against tuberculosis. Proc Natl Acad Sci 1997;94:5243-5248.
Scanga CA, Mohan VP, Tanaka K, Alland D, Flynn JL, Chan J. The inducible nitric oxide synthase locus confers protection against aerogenic challenge of both clinical and laboratory strains of Mycobacterium tuberculosis in mice. Infect Immun 2001;69:7711-7717.
Nozaki Y, Hasegawa Y, Ichiyama S, Nakashima I, Shimokata K. Mechanism of nitric oxide-dependent killing of Mycobacterium bovis BCG in human alveolar macrophages. Infect Immun 1997;65:3644-3647.
Wang CH, Liu CY, Lin HC, Yu CT, Chung KF, Kuo HP. Increased exhaled nitric oxide in active pulmonary tuberculosis due to inducible NO synthase upregulation in alveolar macrophages. Eur Respir J 1998;11:809-815.
Chan ED, Chan J, Schluger NW. What is the role of nitric oxide in murine and human host defense against tuberculosis? Current knowledge. Am J Respir Cell Mol Biol 2001;25:606-612.
De Maio J, Zhang Y, Ko C, Young DB, Bishai WR. A stationary-phase stress-response s factor from Mycobacterium tuberculosis. Proc Natl Acad Sci USA 1996;93:2790-2794.
Green LC, Wagner DA, Glogowski J, Skipper PL, Wishnok JS, Tannenbaum SR. Analysis of nitrate, nitrite, and [15N] nitrate in biological fluids. Anal Biochem 1982;126:131-138.
Rich EA, Torres M, Sada E, Finegan CK, Hamilton BD, Tossi Z. Mycobacterium tuberculosis (MTB)-stimulated production of nitric oxide by human alveolar macrophages and relationship of nitric oxide production to growth inhibition of MTB. Tuber Lung Dis 1997;78: 247-255.
Nicholson S, Bonecini-Almeida Mda G, Lapa e Silva J, et ál. Inducible nitric oxide synthase in pulmonary alveolar macrophages from patients with tuberculosis. J Exp Med 1996;183:2293-2302.
Jung YL, Ryan L, LaCourse R, North RJ. Properties and protective value of the secondary versus primary T helper type 1 response to airborne Mycobacterium tuberculosis infection in mice. J Exp Med 2005;201: 1915-1924.
Kim HC, Kim JH, Park JW, et ál. Difference of nitric oxide production in peripheral blood mononuclear cells and airway epithelial cells between healthy volunteer and patients with tuberculosis. Tubercul Respir Dis 1997;44:72.
Lee J, Remold HG, Ieong MH, Kornfeld H. Macrophage apoptosis in response to high intracellular burden of Mycobacterium tuberculosis is mediated by a novel caspase-independent pathway. J Immunol 2006; 176:4267-4274.
Davis AS, Vergne I, Master SS, Kyei GB, Chua J, Deretic V. Mechanism of inducible nitric oxide synthase exclusion from mycobacterial phagosomes. PLoS Pathog 2007;3:e186.
Aston C, Rom WN, Talbot AT, Reibman J. Early inhibition of mycobacterial growth by human alveolar macrophages is not due to nitric oxide. Am J Respir Crit Care Med 1998;157(6 Pt 1):1943-1950.
Hortelano S, Través PG, Zeini M, Alvarez AM, Boscá L. Sustained nitric oxide delivery delays nitric oxide-dependent apoptosis in macrophages: contribution to the physiological function of activated macrophages. J Immunol 2003;171:6059-6064.
Beisiegel M, Kursar M, Koch M, et ál. Combination of host susceptibility and virulence of Mycobacterium tuberculosis determines dual role of nitric oxide in the protection and control of inflammation. J Infect Dis 2009;199:1222-1232.
Axelrod S, Oschkinat H, Enders J, et ál. Delay of phagosome maturation by a mycobacterial lipid is reversed by nitric oxide. Cell Microbiol 2008;10:1530-1545.