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MINI REVIEW article
Front. Immunol.
Sec. Microbial Immunology
Volume 15 - 2024 |
doi: 10.3389/fimmu.2024.1436676
This article is part of the Research Topic Community Series in The Immunological Consequences of Regulated Cell Death in Infection and Inflammation: Volume II View all 5 articles
The role of Inflammasomes as central inflammatory hubs in Mycobacterium tuberculosis infection
Provisionally accepted- University Hospital of Cologne, Cologne, Germany
Mycobacterium tuberculosis (Mtb) infection represents a global health problem and is characterized by formation of granuloma with a necrotic center and a systemic inflammatory response. Inflammasomes have a crucial role in the host immune response towards Mtb. These intracellular multi-protein complexes are assembled in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs). Inflammasome platforms activate caspases, leading to the maturation of the proinflammatory cytokines interleukin (IL)-1 and 18 and the cleavage of gasdermin D (GSDMD), a pore-forming protein responsible for cytokine release and pyroptotic cell death. Recent in vitro and in vivo findings have highlighted the importance of inflammasome signaling and subsequent necrotic cell death in Mtb-infected innate immune cells. However, we are just beginning to understand how inflammasomes contribute to disease or to a protective immune response in tuberculosis (TB). A detailed molecular understanding of inflammasome-associated pathomechanisms may foster the development of novel host-directed therapeutics or vaccines with improved activity. In this mini-review, we discuss the regulatory and molecular aspects of inflammasome activation and the associated immunological consequences for Mtb pathogenesis.
Keywords: Mycobacterium tuberculosis, Inflammasome, Tuberculosis, Drug Resistance, Interleukin-1, NLRP3 inflammasome, AIM2 inflammasome, gasdermin
Received: 22 May 2024; Accepted: 26 Aug 2024.
Copyright: © 2024 Theobald, Müller, Lange, Keck and Rybniker. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Jan Rybniker, University Hospital of Cologne, Cologne, Germany
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