Database : HANSEN
Search on : OXIDO NITRICO [Subject descriptor]
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Id:19497
Author:Park, Eunkyue; Levis, Willian R; Quinn, Michael R; Park, Seung Yong; Schuller-Levis, Georgia B.
Title:Regulation of nitric oxide induced by mycobacterial lipoarabinomannan in murine macrophages: effects of interferon-B and taurine-chloramine.
Source:Int. J. Lepr;68(4):444-451, Dec., 2000. graf.
Abstract:We examined the effects of interferon beta (IFN-beta) 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-gamma) or IFN-beta in both high- and low-responder mice. In contrast to IFN-gamma, both high- and low-responder mice failed to induce nitrite production when IFN-beta was added, except at a high concentration of IFN-beta. 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-beta or IFN-gamma, 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-gamma or IFN-beta 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-gamma and IFN-beta for the production of LPS and LAM initiated NO in peritoneal macrophages from low-responder (C3H/HeJ) mice. (AU)^ien.
Descriptors:Macrófagos/imunol
Micobactérias Atípicas/imunol
Óxido Nítrico/imunol
Interferon beta/imunol
Limits:Camundongos
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2000/pdf/v68n4/v68n4a06.pdf / en
Location:BR191.1


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Id:13617
Author:Visca, Paolo; Fabozzi, Giulia; Milani, Mario; Bolognesi, Martino; Ascenzi, Paolo
Title:Nitric oxide and mycobacterium leprae pathogenicity ..-
Source:s.l; s.n; 2002. 5 p. ilus.
Abstract:Leprosy is an old, still dreaded infectious disease caused by the obligate intracellular bacterium Mycobacterium leprae. During the infectious process, M. leprae is faced with the host macrophagic environment, where the oxidative stress and NO release, combined with low pH, low pO2, and high pCO2, contribute to limit the growth of the bacilli. Comparative genomics has unraveled massive gene decay in M. leprae, linking the strictly parasitic lifestyle with the reductive genome evolution. Compared with Mycobacterium tuberculosis and Mycobacterium bovis, the leprosy bacillus has lost most of the genes involved in the detoxification of reactive oxygen and nitrogen species. The very low reactivity of the unique truncated hemoglobin retained by M. leprae could account for the susceptibility of this exceptionally slow-growing microbe to NO. (AU).
Descriptors:MYCOBACTERIUM LEPRAE/patogen
OXIDO NITRICO/fisiol
Limits:SUPPORT, NON-U.S. GOV'T
Location:BR191.1; 09036/s


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Id:12281
Author:Cooper, Andrea M; Adams, Linda B; Dalton, Dyana K; Appelberg, Rui; Ehlers, Stefan
Title:IFN-gamma and NO in mycobacterial disease: new jobs for old hands ..-
Source:s.l; s.n; May 2002. 6 p. ilus.
Descriptors:GRANULOMA
GRANULOMA
INTERFERON TIPO II
HANSENIASE
MACROFAGOS
CAMUNDONGOS
MODELOS IMUNOLOGICOS
MICOBACTERIOSE
MYCOBACTERIUM AVIUM
MYCOBACTERIUM BOVIS
OXIDO NITRICO
SINTASE DE OXIDO NITRICO
TUBERCULOSE PULMONAR
TUBERCULOSE PULMONAR
Limits:ESTUDO COMPARATIVO
Location:BR191.1; 08649/s



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