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Interferon-epsilon, an estrogen-induced type I interferon, is uniquely exploited by Neisseria gonorrhoeae via effects on sialic acid metabolism.干扰素-ε是一种雌激素诱导的I型干扰素，淋病奈瑟菌通过对唾液酸代谢的影响独特地利用了它。
Cell Host Microbe. 2025 Jul 9;33(7):1133-1145.e4. doi: 10.1016/j.chom.2025.05.015. Epub 2025 Jun 9.
2
Type I interferons give gonococci a sweet treat and a chance at survival.I型干扰素为淋球菌提供了甜蜜的馈赠以及生存的机会。
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Efficacy of Antigonococcal CMP-Nonulosonate Therapeutics Require Cathelicidins.抗淋病奈瑟球菌 CMP-非乳糖苷治疗的疗效需要抗菌肽。
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α-2,3-sialyltransferase expression level impacts the kinetics of lipooligosaccharide sialylation, complement resistance, and the ability of Neisseria gonorrhoeae to colonize the murine genital tract.α-2,3-唾液酸转移酶的表达水平会影响脂寡糖的唾液酸化动力学、补体抗性以及淋病奈瑟菌在小鼠生殖道中定殖的能力。
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scavenges host sialic acid for Siglec-mediated, complement-independent suppression of neutrophil activation.它从宿主中摄取唾液酸，通过 Siglec 介导的、补体非依赖的方式抑制中性粒细胞的激活。
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Utilizing CMP-Sialic Acid Analogs to Unravel Neisseria gonorrhoeae Lipooligosaccharide-Mediated Complement Resistance and Design Novel Therapeutics.利用CMP-唾液酸类似物解析淋病奈瑟菌脂寡糖介导的补体抗性并设计新型疗法。
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IFN-I promotes T-cell-independent immunity and RBC autoantibodies via modulation of B-1 cell subsets in murine SCD.在小鼠镰状细胞病中，I型干扰素通过调节B-1细胞亚群促进非T细胞依赖性免疫和红细胞自身抗体。
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The Lst Sialyltransferase of Neisseria gonorrhoeae Can Transfer Keto-Deoxyoctanoate as the Terminal Sugar of Lipooligosaccharide: a Glyco-Achilles Heel That Provides a New Strategy for Vaccines to Prevent Gonorrhea.淋病奈瑟菌的最后一个唾液酸转移酶可以将酮-脱氧辛酮酸作为脂寡糖的末端糖转移：这是一个聚糖阿喀琉斯之踵，为预防淋病的疫苗提供了新策略。
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本文引用的文献

1
scavenges host sialic acid for Siglec-mediated, complement-independent suppression of neutrophil activation.它从宿主中摄取唾液酸，通过 Siglec 介导的、补体非依赖的方式抑制中性粒细胞的激活。
mBio. 2024 May 8;15(5):e0011924. doi: 10.1128/mbio.00119-24. Epub 2024 Apr 9.
2
Higher bacterial load in coinfections with compared with single infections does not lead to more symptoms.与单一感染相比，合并感染时更高的细菌载量不会导致更多症状。
Sex Transm Infect. 2024 Feb 19;100(2):127-128. doi: 10.1136/sextrans-2023-055977.
3
Comparison of lipooligosaccharides from human challenge strains of .来自人类攻击菌株的脂寡糖的比较。 （原文中“of.”后面似乎内容不完整）
Front Microbiol. 2023 Sep 15;14:1215946. doi: 10.3389/fmicb.2023.1215946. eCollection 2023.
4
Interferon-ε is a tumour suppressor and restricts ovarian cancer.干扰素-ε 是一种肿瘤抑制因子，可限制卵巢癌的发展。
Nature. 2023 Aug;620(7976):1063-1070. doi: 10.1038/s41586-023-06421-w. Epub 2023 Aug 16.
5
Increase in Multidrug Resistant FC428-Like Isolates Harboring the Mosaic penA 60.001 Gene, in Nanjing, China (2017-2020).中国南京（2017 - 2020年）携带嵌合型penA 60.001基因的多重耐药FC428样分离株增加。
Infect Drug Resist. 2023 Jun 23;16:4053-4064. doi: 10.2147/IDR.S408896. eCollection 2023.
6
Neisseria gonorrhoeae Infection in Women Increases With Rising Gonococcal Burdens in Partners: Chlamydia Coinfection in Women Increases Gonococcal Burden.淋病奈瑟菌感染在女性中增加，随着伴侣中淋球菌负担的增加而增加：衣原体合并感染在女性中增加淋球菌负担。
J Infect Dis. 2022 Dec 13;226(12):2192-2203. doi: 10.1093/infdis/jiac408.
7
Detection of Sialic Acids on the Cell Surface Using Flow Cytometry.使用流式细胞术检测细胞表面的唾液酸。
Methods Mol Biol. 2022;2556:31-35. doi: 10.1007/978-1-0716-2635-1_3.
8
Spatiotemporal regulation of human IFN-ε and innate immunity in the female reproductive tract.人干扰素-ε在女性生殖道中的时空调节及固有免疫。
JCI Insight. 2022 Sep 22;7(18):e135407. doi: 10.1172/jci.insight.135407.
9
WHO global antimicrobial resistance surveillance for Neisseria gonorrhoeae 2017-18: a retrospective observational study.世界卫生组织2017 - 18年淋病奈瑟菌全球抗菌药物耐药性监测：一项回顾性观察研究。
Lancet Microbe. 2021 Nov;2(11):e627-e636. doi: 10.1016/S2666-5247(21)00171-3. Epub 2021 Sep 2.
10
Effectiveness of a serogroup B outer membrane vesicle meningococcal vaccine against gonorrhoea: a retrospective observational study.B 群脑膜炎球菌外膜囊泡疫苗预防淋病的效果：一项回顾性观察研究。
Lancet Infect Dis. 2022 Jul;22(7):1021-1029. doi: 10.1016/S1473-3099(21)00812-4. Epub 2022 Apr 12.

干扰素-ε是一种雌激素诱导的I型干扰素，淋病奈瑟菌通过对唾液酸代谢的影响独特地利用了它。

Interferon-epsilon, an estrogen-induced type I interferon, is uniquely exploited by Neisseria gonorrhoeae via effects on sialic acid metabolism.

作者信息

Kurt-Jones Evelyn A, Gulati Sunita, King Michael, de Oliveira Rosane B, Rice Peter A, Zheng Bo, Shaughnessy Jutamas, Edwards Jennifer L, Hertzog Paul J, Ram Sanjay, Golenbock Douglas T

机构信息

Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, USA.

Department of Pediatrics, The Research Institute at Nationwide Children's Hospital and The Ohio State University, Columbus, OH, USA.

出版信息

Cell Host Microbe. 2025 Jul 9;33(7):1133-1145.e4. doi: 10.1016/j.chom.2025.05.015. Epub 2025 Jun 9.

DOI:10.1016/j.chom.2025.05.015
PMID:40494348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12303037/
Abstract

The female genital mucosa expresses the hormone-dependent type I interferon (IFN), IFN-epsilon (IFN-ε), which protects against chlamydia and herpes infection. Surprisingly, we found that IFN-ε knockout (Ifnε) mice and type I IFN receptor knockout (Ifnar1) mice exhibited enhanced clearance of Neisseria gonorrhoeae (Ng). This result was phenocopied using blocking anti-IFNAR monoclonal antibody (mAb). Ng colonization of the Ifnε urogenital tract was restored by exogenous recombinant IFN-ε or IFN-β. Clearance of Ng in anti-IFNAR-treated mice required the expression of the cathelicidin mCRAMP. Ng deploys a unique mechanism to evade cathelicidins and other innate defenses by sialylating its lipooligosaccharide (LOS) using host-derived cytidine-5'-monophospho-N-acetylneuraminic acid (CMP-Neu5Ac or CMP-sialic acid). Ifnε mice expressed reduced levels of CMP-sialic acid synthetase mRNA in genital tissues. Accordingly, Ng recovered from IFN-deficient mice were hyposialylated. In conclusion, Ng exploits type I IFNs to obtain CMP-sialic acid for LOS sialylation, resulting in innate immune evasion and enhanced colonization.

摘要

女性生殖黏膜表达激素依赖性I型干扰素（IFN），即IFN-ε，它可抵御衣原体和疱疹感染。令人惊讶的是，我们发现IFN-ε基因敲除（Ifnε）小鼠和I型干扰素受体基因敲除（Ifnar1）小鼠对淋病奈瑟菌（Ng）的清除能力增强。使用抗IFNAR单克隆抗体（mAb）阻断可模拟这一结果。Ifnε泌尿生殖道中的Ng定植可通过外源性重组IFN-ε或IFN-β恢复。抗IFNAR处理的小鼠中Ng的清除需要cathelicidin mCRAMP的表达。Ng通过利用宿主来源的胞苷-5'-单磷酸-N-乙酰神经氨酸（CMP-Neu5Ac或CMP-唾液酸）对其脂寡糖（LOS）进行唾液酸化，从而部署了一种独特的机制来逃避cathelicidin和其他固有防御。Ifnε小鼠生殖组织中CMP-唾液酸合成酶mRNA的表达水平降低。因此，从IFN缺陷小鼠中分离出的Ng唾液酸化程度较低。总之，Ng利用I型干扰素获取CMP-唾液酸用于LOS唾液酸化，从而导致固有免疫逃避和定植增强。