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The Modulation of NADPH Oxidase Activity in Human Neutrophils by Moroccan Strains of Leishmania major and Leishmania tropica Is Not Associated with p47 phox Phosphorylation

Polymorphonuclear neutrophils (PMNs) are the first phagocyte recruited and infected by . They synthetize superoxide anions (O ) under the control of the NADPH oxidase complex. In Morocco, and are the main species responsible for cutaneous leishmaniasis (CL). The impact of these parasites on human PM...

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Bibliographic Details
Published in:Microorganisms (Basel) 2021-05, Vol.9 (5)
Main Authors: Maksouri, Hasnaa, Darif, Dounia, Estaquier, Jerome, Riyad, Myriam, Desterke, Christophe, Lemrani, Meryem, Dang, Pham My-Chan, Akarid, Khadija
Format: Article
Language:English
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Summary:Polymorphonuclear neutrophils (PMNs) are the first phagocyte recruited and infected by . They synthetize superoxide anions (O ) under the control of the NADPH oxidase complex. In Morocco, and are the main species responsible for cutaneous leishmaniasis (CL). The impact of these parasites on human PMN functions is still unclear. We evaluated the in vitro capacity of primary Moroccan strains of and to modulate PMN O production and p47 phosphorylation status of the NADPH oxidase complex. PMNs were isolated from healthy blood donors, and their infection rate was measured by microscopy. O production was measured by superoxide dismutase-inhibitable reduction of cytochrome C. P47 phosphorylation was analyzed by Western blot using specific antibodies against Ser328 and Ser345 sites. Whereas we did not observe any difference in PMN infectivity rate, our results indicated that only promastigotes inhibited both fMLF- and PMA-mediated O production independently of p47 phosphorylation. soluble antigens (SLAs) from both species significantly inhibited O induced by fMLF or PMA. However, they only decreased PMA-induced p47phox phosphorylation. and modulated differently O production by human PMNs independently of p47 phosphorylation. The inhibition of ROS production by could be a mechanism of its survival within PMNs that might explain the reported chronic pathogenicity of CL.
ISSN:2076-2607
2076-2607
DOI:10.3390/microorganisms9051025