Rada Balázs, Hably Csilla, Meczner András, Timár Csaba, Lakatos Gergely, Enyedi Péter, Ligeti Erzsébet
Laboratory of Host Defenses, Molecular Defenses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA.
Semin Immunopathol. 2008 Jul;30(3):237-53. doi: 10.1007/s00281-008-0126-3. Epub 2008 Jun 24.
NADPH oxidase of the phagocytic cells (Nox2) transfers electrons from cytosolic NADPH to molecular oxygen in the extracellular or intraphagosomal space. The produced superoxide anion (O2) provides the source for formation of all toxic oxygen derivatives, but continuous O2 generation depends on adequate charge compensation. The vital role of Nox2 in efficient elimination of microorganisms is clearly indicated by human pathology as insufficient activity of the enzyme results in severe, recurrent bacterial infections, the typical symptoms of chronic granulomatous disease. The goals of this contribution are to provide critical review of the Nox2-dependent cellular processes that potentially contribute to bacterial killing and degradation and to indicate possible targets of pharmacological interventions.
吞噬细胞的NADPH氧化酶(Nox2)将胞质NADPH中的电子转移到细胞外或吞噬体内空间的分子氧上。产生的超氧阴离子(O₂⁻)为所有有毒氧衍生物的形成提供了来源,但持续产生O₂⁻取决于足够的电荷补偿。人类病理学清楚地表明了Nox2在有效清除微生物中的重要作用,因为该酶活性不足会导致严重的复发性细菌感染,这是慢性肉芽肿病的典型症状。本文的目的是对可能有助于细菌杀伤和降解的Nox2依赖性细胞过程进行批判性综述,并指出可能的药物干预靶点。