The Inflammasome and Type-2 Immunity in Clostridium difficile Infection
The Inflammasome and Type-2 Immunity in Clostridium difficile Infection
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DOI：
10.1055/s-0040-1701231
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发表时间：
2020-03-01
影响因子：
1.4
通讯作者：
Petri, William A., Jr.
中科院分区：
文献类型：
--
作者：
Donlan, Alexandra;Petri, William A., Jr.
艰难梭菌（重新分类为“梭菌”）是美国医院获得性感染的主要原因，与高患者死亡率和高复发率相关。炎症小体被细菌毒素TcdA、TcdB和艰难梭菌转移酶（CDT）启动和激活，启动以白细胞介素- (IL) 8、IL-1 β和中性粒细胞募集为特征的有效免疫反应，这是杀死病原体所必需的。然而，越来越清楚的是，艰难梭菌感染期间强烈的炎症反应可导致宿主组织损伤，并与较差的患者预后相关。最近的研究已经开始表明，2型免疫反应（通常与蠕虫感染、过敏和哮喘有关）可能在艰难梭菌感染期间具有保护作用。虽然这种反应保护的机制尚不清楚，但有证据表明它是通过嗜酸性粒细胞活性介导的。本章将回顾艰难梭菌的免疫反应，感染过程中的炎性体信号如何对宿主有害，以及目前对保护性2型免疫的理解。了解宿主免疫反应可能有助于洞察预后标志物的新方法，以及如何在没有或除了抗生素之外治疗患者艰难梭菌感染。
Clostridium difficile (reclassified as "Clostridioides") is the leading cause of hospital-acquired infections in the United States, and is associated with high-patient mortality and high rates of recurrence. Inflammasome priming and activation by the bacterial toxins, TcdA, TcdB, and C. difficile transferase (CDT), initiates a potent immune response that is characterized by interleukin- (IL) 8, IL-1 beta, and neutrophil recruitment, and is required for pathogen killing. However, it is becoming clearer that a strong inflammatory response during C. difficile infection can result in host tissue damage, and is associated with worse patient outcome. Recent work has begun to show that a type-2 immune response, most often associated with helminth infections, allergy, and asthma, may be protective during C. difficile infection. While the mechanisms through how this response protect are still unclear, there is evidence that it is mediated through eosinophil activity. This chapter will review the immune response to C. difficile, how the inflammasome signaling during infection can deleterious to the host, as well as the current understanding of a protective type-2 immunity. Understanding the host immune response may help to provide insight into novel approaches to prognosis markers, as well as how treat patient C. difficile infection without, or in addition to, antibiotics.