Maksouri Hasnaa, Darif Dounia, Estaquier Jerome, Riyad Myriam, Desterke Christophe, Lemrani Meryem, Dang Pham My-Chan, Akarid Khadija
Research Team on Immunopathology of Infectious and Systemic Diseases, Laboratory of Cellular and Molecular Pathology, Faculty of Medicine and Pharmacy (FMPC), Hassan II University of Casablanca (UH2C), 20000 Casablanca, Morocco.
Molecular Genetics and Immunophysiopathology Research Team, Health and Environment Laboratory, Aïn Chock Faculty of Sciences, UH2C, 20000 Casablanca, Morocco.
Microorganisms. 2021 May 10;9(5):1025. doi: 10.3390/microorganisms9051025.
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.
多形核中性粒细胞(PMNs)是最早被招募并感染的吞噬细胞。它们在NADPH氧化酶复合物的控制下合成超氧阴离子(O)。在摩洛哥,[具体寄生虫名称1]和[具体寄生虫名称2]是引起皮肤利什曼病(CL)的主要病原体。这些寄生虫对人类PMN功能的影响仍不清楚。我们评估了摩洛哥原发性[具体寄生虫名称1]和[具体寄生虫名称2]菌株在体外调节PMN O产生以及NADPH氧化酶复合物p47磷酸化状态的能力。从健康献血者中分离出PMNs,并通过显微镜测量其感染率。通过超氧化物歧化酶抑制的细胞色素C还原法测量O的产生。使用针对Ser328和Ser345位点的特异性抗体通过蛋白质免疫印迹法分析p47磷酸化。虽然我们没有观察到PMN感染率有任何差异,但我们的结果表明,只有[具体寄生虫名称1]前鞭毛体独立于p47磷酸化抑制fMLF和PMA介导的O产生。来自这两种寄生虫的可溶性抗原(SLAs)均显著抑制fMLF或PMA诱导的O产生。然而,它们仅降低PMA诱导的p47phox磷酸化。[具体寄生虫名称1]和[具体寄生虫名称2]独立于p47磷酸化对人类PMN产生的O有不同的调节作用。[具体寄生虫名称1]对ROS产生的抑制可能是其在PMN内存活的一种机制,这可能解释了所报道的[具体寄生虫名称1] CL的慢性致病性。
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