The anti-inflammatory activity of curcumin protects the genital mucosal epithelial barrier from disruption and blocks replication of HIV-1 and HSV-2.
The anti-inflammatory activity of curcumin protects the genital mucosal epithelial barrier from disruption and blocks replication of HIV-1 and HSV-2.
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DOI：
10.1371/journal.pone.0124903
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Kaushic C
中科院分区：
文献类型：
--
作者：
Ferreira VH;Nazli A;Dizzell SE;Mueller K;Kaushic C
炎症是一种已知的促进HIV获取和感染传播的机制。在这项研究中，我们评估了姜黄素，一种有效和安全的抗炎化合物，是否可以用来消除炎症过程，促进HIV-1在女性生殖道（FGT）获得和促进HIV扩增。用姜黄素预处理原代人生殖器上皮细胞（GECs）并暴露于HIV-1或HIV糖蛋白120 （gp120）中，这两种细胞都被证明可以破坏上皮紧密连接蛋白，包括ZO-1和occludin。姜黄素预处理通过维持ZO-1和occludin的表达和维持生殖器上皮的跨上皮电阻来防止粘膜屏障的破坏。姜黄素预处理还消除了gp120介导的促炎细胞因子肿瘤坏死因子-α和白细胞介素(IL)-6的上调，这些细胞介导屏障破坏，以及能够将HIV靶细胞募集到FGT的趋化因子IL-8、RANTES和干扰素γ诱导蛋白-10 （IP-10）。用姜黄素处理的gec暴露于性传播的共同感染微生物HSV-1、HSV-2和淋病奈瑟菌中，无法引发间接诱导HIV启动子激活的先天炎症反应，姜黄素阻断了慢性感染t细胞中toll样受体（TLR）介导的HIV复制诱导。最后，姜黄素治疗分别显著降低了慢性感染t细胞和原代gec中HIV-1和HSV-2的复制。总之，我们的研究结果表明，姜黄素等抗炎化合物的使用可能为预防和/或控制HIV在FGT中的复制提供了一种可行的替代方案。
Inflammation is a known mechanism that facilitates HIV acquisition and the spread of infection. In this study, we evaluated whether curcumin, a potent and safe anti-inflammatory compound, could be used to abrogate inflammatory processes that facilitate HIV-1 acquisition in the female genital tract (FGT) and contribute to HIV amplification. Primary, human genital epithelial cells (GECs) were pretreated with curcumin and exposed to HIV-1 or HIV glycoprotein 120 (gp120), both of which have been shown to disrupt epithelial tight junction proteins, including ZO-1 and occludin. Pre-treatment with curcumin prevented disruption of the mucosal barrier by maintaining ZO-1 and occludin expression and maintained trans-epithelial electric resistance across the genital epithelium. Curcumin pre-treatment also abrogated the gp120-mediated upregulation of the proinflammatory cytokines tumor necrosis factor-α and interleukin (IL)-6, which mediate barrier disruption, as well as the chemokines IL-8, RANTES and interferon gamma-induced protein-10 (IP-10), which are capable of recruiting HIV target cells to the FGT. GECs treated with curcumin and exposed to the sexually transmitted co-infecting microbes HSV-1, HSV-2 and Neisseria gonorrhoeae were unable to elicit innate inflammatory responses that indirectly induced activation of the HIV promoter and curcumin blocked Toll-like receptor (TLR)-mediated induction of HIV replication in chronically infected T-cells. Finally, curcumin treatment resulted in significantly decreased HIV-1 and HSV-2 replication in chronically infected T-cells and primary GECs, respectively. All together, our results suggest that the use of anti-inflammatory compounds such as curcumin may offer a viable alternative for the prevention and/or control of HIV replication in the FGT.
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影响因子：
3.3
作者：
Berginc, Katja;Skalko-Basnet, Natasa;Kristl, Albin
通讯作者：
Kristl, Albin
DOI：
10.1073/pnas.86.7.2365
发表时间：
1989-04-01
影响因子：
11.1
作者：
FOLKS, TM;CLOUSE, KA;FAUCI, AS
通讯作者：
FAUCI, AS
使用细胞因子的组合在潜在感染的CD4+ T细胞中诱导HIV-1复制。
DOI：
10.1084/jem.188.1.83
发表时间：
1998-07-06
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
通讯作者：
--
影响因子：
1
作者：
Barnabas RV;Celum C
通讯作者：
Celum C
影响因子：
5.4
作者：
Gillgrass, AE;Tang, VA;Kaushic, C
通讯作者：
Kaushic, C