Chlamydial plasmid-encoded virulence factor Pgp3 interacts with human cathelicidin peptide LL-37 to modulate immune response.

Chlamydial plasmid-encoded virulence factor Pgp3 interacts with human cathelicidin peptide LL-37 to modulate immune response.
复制标题

衣原体质粒编码的毒力因子 Pgp3 与人抗菌素肽 LL-37 相互作用调节免疫反应

DOI:
10.1016/j.micinf.2018.06.003
复制
发表时间:
2019-01
影响因子:
5.8
通讯作者:
Zhong G
Zhong G
中科院分区:
医学3区
文献类型:
--
作者:
Hou S;Sun X;Dong X;Lin H;Tang L;Xue M;Zhong G

文献摘要

参考文献

被引文献

相似文献

We have previously reported that Chlamydia trachomatis plasmid-encoded Pgp3 is able to neutralize anti-chlamydial activity of human cathelicidin peptide LL-37 by binding to and forming stable complex with LL-37. Besides its microbicidal activity, LL-37 also modulates immune response, including inducing cytokine/chemokine production in fibroblast/epithelial cells and recruitment of inflammatory cells. We now report that LL-37 was significantly induced in the genital tracts of women diagnosed positive for C. trachomatis. Both the LL-37-stimulated IL-6/8 production in human endometrial epithelial cells and the LL-37-induced neutrophil chemotaxis were blocked by Pgp3. Interestingly, although Pgp3 itself alone could not induce cytokines in epithelial cell cells, it did so in neutrophils. Importantly, the Pgp3 proinflammatory activity in neutrophils was significantly enhanced by forming complex with LL-37 although LL-37 alone failed to induce cytokine production in neutrophils. Thus, we have demonstrated that Pgp3 can modulate the proinflammatory activities of LL-37 on epithelial cells by forming stable complex with LL-37 but the Pgp3’s own proinflammatory activity on myeloid cells is enhanced by forming the same complex. We hypothesize that Chlamydia may use Pgp3 to both block detrimental inflammation for improving its own fitness in the genital tract epithelial tissue and activate myeloid cell-mediated inflammation for potentially promoting spreading between the hosts, the latter of which may inevitably contribute to the development of inflammatory sequelae such as tubal fibrosis.
DOI: 10.1186/1471-2180-8-90
发表时间: 2008-06-09
期刊: BMC microbiology
影响因子: 4.2
作者:
Li Z;Zhong Y;Lei L;Wu Y;Wang S;Zhong G
通讯作者: Zhong G
DOI: 10.1128/iai.01257-10
发表时间: 2011-05-01
影响因子: 3.1
作者:
Lacy, H. Marie;Bowlin, Anne K.;Rank, Roger G.
通讯作者: Rank, Roger G.
DOI: 10.1128/iai.01543-13
发表时间: 2014-03-01
影响因子: 3.1
作者:
Lei, Lei;Chen, Jianlin;Zhong, Guangming
通讯作者: Zhong, Guangming
DOI: 10.1128/iai.00746-15
发表时间: 2015-12-01
影响因子: 3.1
作者:
Hou, Shuping;Dong, Xiaohua;Zhong, Guangming
通讯作者: Zhong, Guangming
DOI: 10.1128/iai.05535-11
发表时间: 2011-10-01
影响因子: 3.1
作者:
Frazer, Lauren C.;O'Connell, Catherine M.;Darville, Toni
通讯作者: Darville, Toni