Leishmania amazonensis fails to induce the release of reactive oxygen intermediates by CBA macrophages

被引:22
作者
Almeida, T. F. [1 ]
Palma, L. C. [1 ]
Mendez, L. C. [1 ]
Noronha-Dutra, A. A. [1 ]
Veras, P. S. T. [1 ]
机构
[1] Fiocruz MS, CPqGM, Lab Patol & Biointervencao, BR-40296710 Salvador, BA, Brazil
关键词
Leishmania; macrophage; reactive oxygen intermediates; MECHANISMS IN-VIVO; NITRIC-OXIDE; DONOVANI LIPOPHOSPHOGLYCAN; NAD(P)H OXIDASE; MONONUCLEAR PHAGOCYTES; PKC-ALPHA; SUPEROXIDE; AMASTIGOTES; CELLS; BURST;
D O I
10.1111/j.1365-3024.2012.01384.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CBA mouse macrophages effectively control Leishmania major infection, yet are permissive to Leishmania amazonensis. It has been established that some Leishmania species are destroyed by reactive oxygen species (ROS). However, other species of Leishmania exhibit resistance to ROS or even down-modulate ROS production. We hypothesized that L. amazonensisinfected macrophages reduce ROS production soon after parasitecell interaction. Employing a highly sensitive analysis technique based on chemiluminescence, the production of superoxide (O-2(center dot-)) and hydrogen peroxide (H2O2) by L. major- or L. amazonensis-infected CBA macrophages were measured. L. major induces macrophages to release levels of 3.5 times higher than in uninfected cells. This production is partially dependent on NADPH oxidase (NOX) type 2. The level of accumulated H2O2 is 20 times higher in L. major-than in L. amazonensis-infected cells. Furthermore, macrophages stimulated with L. amazonensis release amounts of ROS similar to uninfected cells. These findings support previous studies showing that CBA macrophages are effective in controlling L. major infection by a mechanism dependent on both production and H2O2 generation. Furthermore, these data reinforce the notion that L. amazonensis survive inside CBA macrophages by reducing ROS production during the phagocytic process.
引用
收藏
页码:492 / 498
页数:7
相关论文
共 42 条
  • [1] Nox4 as the major catalytic component of an endothelial NAD(P)H oxidase
    Ago, T
    Kitazono, T
    Ooboshi, H
    Iyama, T
    Han, YH
    Takada, J
    Wakisaka, M
    Ibayashi, S
    Utsumi, H
    Iida, M
    [J]. CIRCULATION, 2004, 109 (02) : 227 - 233
  • [2] T helper (h)1/Th2 and Leishmania:: paradox rather than paradigm
    Alexander, J
    Bryson, K
    [J]. IMMUNOLOGY LETTERS, 2005, 99 (01) : 17 - 23
  • [3] Helicobacter pylori disrupts NADPH oxidase targeting in human neutrophils to induce extracellular superoxide release
    Allen, LAH
    Beecher, BR
    Lynch, JT
    Rohner, OV
    Wittine, LM
    [J]. JOURNAL OF IMMUNOLOGY, 2005, 174 (06) : 3658 - 3667
  • [4] PRODUCTION OF NITRIC-OXIDE AND SUPEROXIDE BY ACTIVATED MACROPHAGES AND KILLING OF LEISHMANIA-MAJOR
    ASSREUY, J
    CUNHA, FQ
    EPPERLEIN, M
    NORONHADUTRA, A
    ODONNELL, CA
    LIEW, FY
    MONCADA, S
    [J]. EUROPEAN JOURNAL OF IMMUNOLOGY, 1994, 24 (03) : 672 - 676
  • [5] Mechanisms and consequences of persistence of intracellular pathogens: leishmaniasis as an example
    Bogdan, Christian
    [J]. CELLULAR MICROBIOLOGY, 2008, 10 (06) : 1221 - 1234
  • [6] Is the neutrophil reactive oxygen species production measured by luminol and lucigenin chemiluminescence intra or extracellular?: Comparison with DCFH-DA flow cytometry and cytochrome c reduction
    Caldefie-Chézet, F
    Walrand, S
    Moinard, C
    Tridon, A
    Chassagne, J
    Vasson, MP
    [J]. CLINICA CHIMICA ACTA, 2002, 319 (01) : 9 - 17
  • [7] CHANNON JY, 1984, IMMUNOLOGY, V53, P345
  • [8] CHANOCK SJ, 1994, J BIOL CHEM, V269, P24519
  • [9] de Souza VL, 2000, MICROBES INFECT, V2, P1807, DOI 10.1016/S1286-4579(00)01340-X
  • [10] Leishmania mexicana lipophosphoglycan differentially regulates PKCα-induced oxidative burst in macrophages of BALB/c and C57BL/6 mice
    Delgado-Dominguez, J.
    Gonzalez-Aguilar, H.
    Aguirre-Garcia, M.
    Gutierrez-Kobeh, L.
    Berzunza-Cruz, M.
    Ruiz-Remigio, A.
    Robles-Flores, M.
    Becker, I.
    [J]. PARASITE IMMUNOLOGY, 2010, 32 (06) : 440 - 449