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刺激Dectin-1的β-葡聚糖在体外和体内均能抑制衣原体感染。

Dectin-1 stimulating β-glucans inhibit Chlamydia infections both in vitro and in vivo.

作者信息

Kintner Jennifer, Callaghan Morgan, Bulawa Lillith, Chu Angela, Ma Zuchao, Williams David L, Schoborg Robert V, Kruppa Michael D, Hall Jennifer V

机构信息

Department of Biomedical Sciences, East Tennessee State University, Johnson City, TN 37614, USA.

Center for Infectious Disease, Inflammation and Immunity, East Tennessee State University, Johnson City, TN 37614, USA.

出版信息

Pathog Dis. 2025 Jan 30;83. doi: 10.1093/femspd/ftaf002.

DOI:10.1093/femspd/ftaf002
PMID:39886876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11840957/
Abstract

Chlamydia trachomatis and Candida albicans are common inhabitants of the female genital tract. Candida albicans can impact the viability and pathogenesis of some bacteria. Previously, we investigated physical interactions between Ch. trachomatis elementary bodies (EBs) and Ca. albicans. This work indicated that EBs bind to Ca. albicans and become noninfectious by 24 h post-binding. Here, we continue our investigation of these interkingdom, polymicrobial interactions. Candida albicans adheres to bacteria or host surfaces via agglutinin-like sequence or heat shock 70 (Ssa) proteins. Chlamydia trachomatis EBs did not bind Ca. albicans Ssa2 deficient strains as efficiently as wild-type or complemented strains, indicating a role for this protein in chlamydial adherence to Candida. Additionally, Ca. albicans β-glucans inhibit chlamydial infection when exposure occurs during EB adsorption onto cervical cells. Laminarin, a β-glucan agonist of the C-type lectin receptor Dectin-1, inhibited chlamydial infection in both cervical epithelial cells and mice when exposure occurred prior to, during, or immediately following EB inoculation. Conversely, a Dectin-1 antagonist laminarin did not inhibit infection in vitro, suggesting that β-glucan inhibition of Ch. trachomatis requires C-type lectin receptor signaling. Overall, our data demonstrate that β-glucans from multiple species, including Ca. albicans, inhibit Chlamydia via stimulation of host-signaling pathways.

摘要

沙眼衣原体和白色念珠菌是女性生殖道的常见寄居菌。白色念珠菌可影响某些细菌的生存能力和致病性。此前,我们研究了沙眼衣原体原体(EBs)与白色念珠菌之间的物理相互作用。这项工作表明,EBs与白色念珠菌结合,并在结合后24小时失去感染性。在此,我们继续研究这些跨物种、多微生物间的相互作用。白色念珠菌通过凝集素样序列或热休克70(Ssa)蛋白粘附于细菌或宿主表面。沙眼衣原体EBs与白色念珠菌Ssa2缺陷菌株的结合效率不如野生型或互补菌株,表明该蛋白在衣原体粘附白色念珠菌中起作用。此外,当在EB吸附到宫颈细胞的过程中暴露时,白色念珠菌的β-葡聚糖会抑制衣原体感染。海带多糖,一种C型凝集素受体Dectin-1的β-葡聚糖激动剂,在EB接种前、接种期间或接种后立即暴露时,均可抑制宫颈上皮细胞和小鼠中的衣原体感染。相反,一种Dectin-1拮抗剂海带多糖在体外不抑制感染,这表明β-葡聚糖对沙眼衣原体的抑制作用需要C型凝集素受体信号传导。总体而言,我们的数据表明,包括白色念珠菌在内的多种物种的β-葡聚糖通过刺激宿主信号通路来抑制衣原体。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/c1758b146eed/ftaf002fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/c487654fd458/ftaf002fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/2bbd10d12850/ftaf002fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/a37078e46929/ftaf002fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/c1758b146eed/ftaf002fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/c487654fd458/ftaf002fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/2bbd10d12850/ftaf002fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/a37078e46929/ftaf002fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce73/11840957/c1758b146eed/ftaf002fig4.jpg

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