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精液补体对HIV-1的调理作用增强了人类上皮细胞的感染。

Opsonization of HIV-1 by semen complement enhances infection of human epithelial cells.

作者信息

Bouhlal Hicham, Chomont Nicolas, Haeffner-Cavaillon Nicole, Kazatchkine Michel D, Belec Laurent, Hocini Hakim

机构信息

Institut National de la Santé et de la Recherche Médicale, Unité 430, and Université Pierre et Marie Curie, Paris, France.

出版信息

J Immunol. 2002 Sep 15;169(6):3301-6. doi: 10.4049/jimmunol.169.6.3301.

Abstract

In the present study we demonstrate that both X4- and R5-tropic HIV-1 strains are able to infect the human epithelial cell line HT-29. Infection was enhanced 2-fold when HIV was added to semen before contact with the cell cultures. The enhancing effect of semen was complement dependent, as evidenced by blockage of generation of C3a/C3a(desArg) in semen by heat or EDTA treatment of semen and suppression of semen-dependent enhancement with mAbs directed to complement receptor type 3 (CD11b/CD18) and soluble CD16. Infection of HT-29 cells was assessed by the release of p24 Ag in cultures and semiquantitative PCR of the HIV-1 pol gene. Inhibition of infection of HT-29 by stromal cell-derived factor 1 was decreased in the case of semen-opsonized X4- and R5-tropic virus compared with unopsonized virus. In contrast, inhibition of infection by RANTES was increased for opsonized X4-tropic HIV-1 compared with unopsonized virus. Taken together these observations indicate that activation of complement in semen may play an enhancing role in mucosal transmission of HIV-1 by facilitating infection of epithelial cells and/or enhancing infection of complement receptor-expressing target cells in the mucosa.

摘要

在本研究中,我们证明X4嗜性和R5嗜性的HIV-1毒株均能够感染人上皮细胞系HT-29。在HIV与细胞培养物接触之前将其添加到精液中时,感染增强了2倍。精液的增强作用依赖补体,这可通过对精液进行加热或EDTA处理来阻断精液中C3a/C3a(去精氨酸)的产生以及用针对补体受体3型(CD11b/CD18)和可溶性CD16的单克隆抗体抑制精液依赖性增强作用来证明。通过培养物中p24抗原的释放以及HIV-1 pol基因的半定量PCR来评估HT-29细胞的感染情况。与未调理的病毒相比,在精液调理的X4嗜性和R5嗜性病毒的情况下,基质细胞衍生因子1对HT-29感染的抑制作用降低。相反,与未调理的病毒相比,调理的X4嗜性HIV-1对RANTES感染的抑制作用增强。综上所述,这些观察结果表明,精液中补体的激活可能通过促进上皮细胞感染和/或增强粘膜中表达补体受体的靶细胞感染,在HIV-1的粘膜传播中发挥增强作用。

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