Suppr超能文献

不止一个孔:补体的非裂解性抗菌功能和细菌逃避的策略。

More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.

机构信息

Division of Host-Microbe Systems and Therapeutics, Department of Pediatrics, UC San Diego, La Jolla, California, USA

Skaggs School of Pharmacy and Pharmaceutical Sciences, UC San Diego, La Jolla, California, USA.

出版信息

Microbiol Mol Biol Rev. 2021 Jan 27;85(1). doi: 10.1128/MMBR.00177-20. Print 2021 Feb 17.

Abstract

The complement system is an evolutionarily ancient defense mechanism against foreign substances. Consisting of three proteolytic activation pathways, complement converges on a common effector cascade terminating in the formation of a lytic pore on the target surface. The classical and lectin pathways are initiated by pattern recognition molecules binding to specific ligands, while the alternative pathway is constitutively active at low levels in circulation. Complement-mediated killing is essential for defense against many Gram-negative bacterial pathogens, and genetic deficiencies in complement can render individuals highly susceptible to infection, for example, invasive meningococcal disease. In contrast, Gram-positive bacteria are inherently resistant to the direct bactericidal activity of complement due to their thick layer of cell wall peptidoglycan. However, complement also serves diverse roles in immune defense against all bacteria by flagging them for opsonization and killing by professional phagocytes, synergizing with neutrophils, modulating inflammatory responses, regulating T cell development, and cross talk with coagulation cascades. In this review, we discuss newly appreciated roles for complement beyond direct membrane lysis, incorporate nonlytic roles of complement into immunological paradigms of host-pathogen interactions, and identify bacterial strategies for complement evasion.

摘要

补体系统是一种古老的防御机制,可抵御外来物质。它由三种蛋白水解激活途径组成,补体汇集到一个共同的效应级联反应,最终在靶表面形成一个溶解孔。经典途径和凝集素途径是由模式识别分子与特定配体结合启动的,而替代途径在循环中以低水平持续激活。补体介导的杀伤对于防御许多革兰氏阴性细菌病原体至关重要,补体的遗传缺陷可使个体极易感染,例如侵袭性脑膜炎球菌病。相比之下,革兰氏阳性细菌由于其厚厚的细胞壁肽聚糖层,天生对补体的直接杀菌活性具有抗性。然而,补体还通过标记它们进行调理和专业吞噬细胞的杀伤、与中性粒细胞协同作用、调节炎症反应、调节 T 细胞发育以及与凝血级联反应的相互作用,在针对所有细菌的免疫防御中发挥多种作用。在这篇综述中,我们讨论了补体除了直接膜溶解之外的新作用,将补体的非溶血性作用纳入宿主-病原体相互作用的免疫学范例,并确定了细菌逃避补体的策略。

相似文献

1
More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.
Microbiol Mol Biol Rev. 2021 Jan 27;85(1). doi: 10.1128/MMBR.00177-20. Print 2021 Feb 17.
2
Utilization of complement receptors in immune cell-microbe interaction.
FEBS Lett. 2020 Aug;594(16):2695-2713. doi: 10.1002/1873-3468.13743. Epub 2020 Feb 12.
3
Hijacking Factor H for Complement Immune Evasion.
Front Immunol. 2021 Feb 25;12:602277. doi: 10.3389/fimmu.2021.602277. eCollection 2021.
4
Complement resistance mechanisms of Klebsiella pneumoniae.
Immunobiology. 2016 Oct;221(10):1102-9. doi: 10.1016/j.imbio.2016.06.014. Epub 2016 Jun 16.
5
Bacteria under stress by complement and coagulation.
FEMS Microbiol Rev. 2014 Nov;38(6):1146-71. doi: 10.1111/1574-6976.12080. Epub 2014 Sep 3.
7
Complement and bacteria: chemistry and biology in host defense.
Annu Rev Immunol. 1984;2:461-91. doi: 10.1146/annurev.iy.02.040184.002333.
9
Autophagy as a macrophage response to bacterial infection.
IUBMB Life. 2012 Sep;64(9):740-7. doi: 10.1002/iub.1070. Epub 2012 Jul 20.
10
Pseudomonas aeruginosa alkaline protease blocks complement activation via the classical and lectin pathways.
J Immunol. 2012 Jan 1;188(1):386-93. doi: 10.4049/jimmunol.1102162. Epub 2011 Nov 30.

引用本文的文献

2
PgtE protease enables virulent to evade C3-mediated serum and neutrophil killing.
mBio. 2025 Aug 13;16(8):e0380224. doi: 10.1128/mbio.03802-24. Epub 2025 Jul 14.
3
Therapeutic strategies targeting complement in myasthenia gravis patients.
J Neurol. 2025 Jul 2;272(8):489. doi: 10.1007/s00415-025-13225-7.
4
From gingiva to multiple organs in mice: The trace of via imaging.
J Dent Sci. 2025 Jan;20(1):292-301. doi: 10.1016/j.jds.2024.07.009. Epub 2024 Jul 20.
6
PgtE protease enables virulent to evade C3-mediated serum and neutrophil killing.
bioRxiv. 2024 Nov 5:2024.11.05.622138. doi: 10.1101/2024.11.05.622138.
7
The complement system: A key player in the host response to infections.
Eur J Immunol. 2024 Nov;54(11):e2350814. doi: 10.1002/eji.202350814. Epub 2024 Aug 27.
8
Novel insights: crosstalk with non-puerperal mastitis and immunity.
Front Immunol. 2024 Aug 1;15:1431681. doi: 10.3389/fimmu.2024.1431681. eCollection 2024.
9
Clinical features and multiomics profiles indicate coagulation and platelet dysfunction in COVID-19 viral sepsis.
iScience. 2024 May 25;27(6):110110. doi: 10.1016/j.isci.2024.110110. eCollection 2024 Jun 21.
10
Plasmid-encoded toxin of cleaves complement system proteins and inhibits complement-mediated lysis .
Front Cell Infect Microbiol. 2024 Feb 2;14:1327241. doi: 10.3389/fcimb.2024.1327241. eCollection 2024.

本文引用的文献

1
Complement C1q Enhances Primary Hemostasis.
Front Immunol. 2020 Jul 16;11:1522. doi: 10.3389/fimmu.2020.01522. eCollection 2020.
2
Viral Evasion of the Complement System and Its Importance for Vaccines and Therapeutics.
Front Immunol. 2020 Jul 9;11:1450. doi: 10.3389/fimmu.2020.01450. eCollection 2020.
3
Poly-γ-D-Glutamate Capsule Inhibits Opsonic Phagocytosis by Impeding Complement Activation.
Front Immunol. 2020 Mar 31;11:462. doi: 10.3389/fimmu.2020.00462. eCollection 2020.
4
Regulation of anti-microbial autophagy by factors of the complement system.
Microb Cell. 2020 Mar 19;7(4):93-105. doi: 10.15698/mic2020.04.712.
5
Complement as a Major Inducer of Harmful Events in Infectious Sepsis.
Shock. 2020 Nov;54(5):595-605. doi: 10.1097/SHK.0000000000001531.
6
Neutralizing Complement C5a Protects Mice with Pneumococcal Pulmonary Sepsis.
Anesthesiology. 2020 Apr;132(4):795-807. doi: 10.1097/ALN.0000000000003149.
7
C4BP-IgM protein as a therapeutic approach to treat Neisseria gonorrhoeae infections.
JCI Insight. 2019 Dec 5;4(23):131886. doi: 10.1172/jci.insight.131886.
8
How the Membrane Attack Complex Damages the Bacterial Cell Envelope and Kills Gram-Negative Bacteria.
Bioessays. 2019 Oct;41(10):e1900074. doi: 10.1002/bies.201900074. Epub 2019 Aug 26.
9
The hijackers guide to escaping complement: Lessons learned from pathogens.
Mol Immunol. 2019 Oct;114:49-61. doi: 10.1016/j.molimm.2019.07.018. Epub 2019 Jul 20.
10
Role of Pneumococcal NanA Neuraminidase Activity in Peripheral Blood.
Front Cell Infect Microbiol. 2019 Jun 26;9:218. doi: 10.3389/fcimb.2019.00218. eCollection 2019.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验