The villain team-up or how Trichomonas vaginalis and bacterial vaginosis alter innate immunity in concert.
The villain team-up or how Trichomonas vaginalis and bacterial vaginosis alter innate immunity in concert.
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DOI：
10.1136/sextrans-2013-051052
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发表时间：
2013-09
影响因子：
3.6
通讯作者：
Onderdonk AB
中科院分区：
文献类型：
--
作者：
Fichorova RN;Buck OR;Yamamoto HS;Fashemi T;Dawood HY;Fashemi B;Hayes GR;Beach DH;Takagi Y;Delaney ML;Nibert ML;Singh BN;Onderdonk AB
阴道微生物与生殖道上皮的复杂相互作用形成了粘膜先天免疫，这是性健康和生殖健康的关键。细菌性阴道病（BV）是一种在育龄妇女中普遍存在的微生物组紊乱综合征，通常与滴虫病同时发生，两者都与不良生殖结果和病毒感染的风险增加相关，主要归因于炎症。为了研究炎症、BV和滴虫病之间的因果关系，我们建立了一个人宫颈阴道上皮细胞模型，该模型由阴道乳杆菌分离株（在健康女性中占优势）和常见的BV物种（阴道变形菌、阴道加德纳菌和两维普雷沃菌）定殖。定植的上皮细胞感染阴道毛滴虫（TV）或暴露于纯化的TV毒力因子（膜脂磷酸聚糖（LPG）、其神经酰胺-磷酸肌醇-聚糖核心（CPI-GC）或内共生体迷走毛滴虫病毒（TVV）），然后评估细菌菌落形成单位、粘膜抗炎杀微生物剂分泌性白细胞蛋白酶抑制剂（SLPI）和驱动促炎的趋化因子，抗原呈递和T细胞。TV减少了乳酸杆菌的定植，但没有减少BV种类的定植，BV在上皮细胞内发现。TV增加白细胞介素（IL）-8和抑制SLPI，可能通过LPG/CPI-GC，上调IL-8和RANTES，可能通过TVV使用纯化的致病决定簇。BV种类A vaginae和G vaginae诱导IL-8和RANTES，并且还放大了对LPG/CPI-GC和TVV的促炎反应，而P bivia抑制TV/TVV诱导的趋化因子。这些分子宿主-寄生虫-内共生菌-细菌相互作用解释了流行病学的关联，并提出了一种用于恢复阴道免疫力和预防女性BV/TV归因的炎症后遗症的修正范例。
Complex interactions of vaginal microorganisms with the genital tract epithelium shape mucosal innate immunity, which holds the key to sexual and reproductive health. Bacterial vaginosis (BV), a microbiome-disturbance syndrome prevalent in reproductive-age women, occurs commonly in concert with trichomoniasis, and both are associated with increased risk of adverse reproductive outcomes and viral infections, largely attributable to inflammation. To investigate the causative relationships among inflammation, BV and trichomoniasis, we established a model of human cervicovaginal epithelial cells colonised by vaginal Lactobacillus isolates, dominant in healthy women, and common BV species (Atopobium vaginae, Gardnerella vaginalis and Prevotella bivia). Colonised epithelia were infected with Trichomonas vaginalis (TV) or exposed to purified TV virulence factors (membrane lipophosphoglycan (LPG), its ceramide-phosphoinositol-glycan core (CPI-GC) or the endosymbiont Trichomonas vaginalis virus (TVV)), followed by assessment of bacterial colony-forming units, the mucosal anti-inflammatory microbicide secretory leucocyte protease inhibitor (SLPI), and chemokines that drive pro-inflammatory, antigen-presenting and T cells. TV reduced colonisation by Lactobacillus but not by BV species, which were found inside epithelial cells. TV increased interleukin (IL)-8 and suppressed SLPI, likely via LPG/CPI-GC, and upregulated IL-8 and RANTES, likely via TVV as suggested by use of purified pathogenic determinants. BV species A vaginae and G vaginalis induced IL-8 and RANTES, and also amplified the pro-inflammatory responses to both LPG/CPI-GC and TVV, whereas P bivia suppressed the TV/TVV-induced chemokines. These molecular host–parasite–endosymbiont–bacteria interactions explain epidemiological associations and suggest a revised paradigm for restoring vaginal immunity and preventing BV/TV-attributable inflammatory sequelae in women.
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影响因子：
--
作者：
Novak, Richard M.;Donoval, Betty A.;Landay, Alan
通讯作者：
Landay, Alan
影响因子：
3.4
作者：
Fichorova, Raina N.
通讯作者：
Fichorova, Raina N.
影响因子：
4.2
作者：
Verhelst R;Verstraelen H;Claeys G;Verschraegen G;Delanghe J;Van Simaey L;De Ganck C;Temmerman M;Vaneechoutte M
通讯作者：
Vaneechoutte M
影响因子：
4.2
作者：
Yamamoto HS;Xu Q;Fichorova RN
通讯作者：
Fichorova RN
影响因子：
17.1
作者：
Gajer P;Brotman RM;Bai G;Sakamoto J;Schütte UM;Zhong X;Koenig SS;Fu L;Ma ZS;Zhou X;Abdo Z;Forney LJ;Ravel J
通讯作者：
Ravel J