Laboratoire de Bactériologie Moléculaire, Université Libre de Bruxelles (ULB), Campus Erasme, Route de Lennik 808, B-1070 Brussels, Belgium.
Trends Mol Med. 2009 Dec;15(12):571-9. doi: 10.1016/j.molmed.2009.10.003. Epub 2009 Nov 11.
Among the host defense mechanisms against bacteria, leukocyte phagocytosis leads to their hydrogen peroxide (H(2)O(2))-mediated destruction. The recent discovery of dual oxidase (DUOX)-dependent H(2)O(2) generation associated with peroxidase and thiocyanate secretion at the apex of mucosal cells has been similarly interpreted as a killing mechanism. However, the rapid degradation of H(2)O(2) would be expected to reduce the efficiency of this system. It has been demonstrated that H(2)O(2) acts as a chemorepellent for bacteria, and such an effect might be sufficient to block cellular infection. Therefore, H(2)O(2) generation might represent one of the mechanisms that allows the coexistence of mucosae with potentially harmful bacteria. Here, we discuss the possible role of DUOXes and H(2)O(2) in interactions between host mucosae and bacteria to maintain mucosal homeostasis.
在针对细菌的宿主防御机制中，白细胞吞噬作用导致其过氧化氢 (H₂O₂) 介导的破坏。最近发现，双氧化酶 (DUOX) 依赖性 H₂O₂ 生成与黏膜细胞顶端的过氧化物酶和硫氰酸盐分泌有关，同样被解释为一种杀伤机制。然而，H₂O₂ 的快速降解预计会降低该系统的效率。已经证明 H₂O₂ 是细菌的趋化抑制剂，这种作用足以阻止细胞感染。因此，H₂O₂ 的生成可能是允许黏膜与潜在有害细菌共存的机制之一。在这里，我们讨论了 DUOX 酶和 H₂O₂ 在宿主黏膜与细菌相互作用中维持黏膜内稳态的可能作用。
