Inflammasome Biology and Molecular Pathology

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: closed (15 October 2022) | Viewed by 1311

Special Issue Editor


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Guest Editor
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Interests: innate immune sensing during infection; inflammasome; pyroptosis; gram- infection

Special Issue Information

Dear Colleagues, 

Inflammasomes are cytosolic sensors that detect microbial molecules and endogenous danger signals to promote inflammation. When triggered, inflammasomes recruit and activate caspase-1 or caspase-11, and its human homologs caspase-4 and 5. Active caspase-1 cleaves pro-IL-1b and pro-IL-18 to mature, secreted forms. Additionally, caspase-1 or 11 cleave gasdermin D (GSDMD), liberating an N-terminal pore-forming domain (PFD) to promote pyroptosis, a form of lytic cell death. The GSDMD-PFD inserts into the plasma membrane and forms large pores that facilitate the release of IL-1b and other small molecules, and subsequently drives plasma membrane rupture (PMR), permitting the release of damage-associated molecular patterns (DAMPs). While inflammasomes can play a protective role against various infections, the hyperactivation or dysregulation of inflammasomes is associated with a number of immunopathologies, such as septic shock, inflammatory bowel disease, type I and II diabetes, and spontaneous allelic mutation-associated inflammatory disorders. To comprehend disease pathogenesis with the objective of novel therapeutic development, it is imperative to first understand the molecular and physiological roles of immune sensors during infection. Recent advances in the field of inflammasome biology suggest roles for inflammasomes in multiple cell processes to mediate defense or inflammatory pathology. In this Special Issue on inflammasome biology and molecular pathology, we solicit original research and review articles that address the molecular mechanisms of inflammasome activation, inflammasome-associated defense, pathogenesis, and therapeutics.

Dr. Youssef Aachoui
Guest Editor

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Keywords

  • inflammasome
  • pyroptosis
  • cell-specific inflammasome
  • inflammatory caspases
  • gasdermin D
  • apoptosis
  • defense against infection
  • inflammatory pathology

Published Papers (1 paper)

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Research

10 pages, 867 KiB  
Article
Serial Increases in Human Leukocyte Antigen-DR Expression and Decreases in Interleukin-10 Expression in Alveolar Monocytes of Survivors of Pneumonia-Related Acute Respiratory Distress Syndrome
by Chien-Ming Chu, Chia-Jung Chung, Chih-Yu Huang, Chung-Chieh Yu, Chao-Hung Wang, Li-Fu Li and Huang-Pin Wu
Biology 2022, 11(12), 1793; https://doi.org/10.3390/biology11121793 - 9 Dec 2022
Viewed by 1018
Abstract
ARDS is a potentially lethal syndrome. HLA-DR expression in monocytes reflects their activation and antigen-presenting capacity. However, the correlation between clinical outcomes and HLA-DR expression in alveolar monocytes/macrophages in patients with pneumonia-related ARDS remains unclear. Thus, we determined the trends of HLA-DR and [...] Read more.
ARDS is a potentially lethal syndrome. HLA-DR expression in monocytes reflects their activation and antigen-presenting capacity. However, the correlation between clinical outcomes and HLA-DR expression in alveolar monocytes/macrophages in patients with pneumonia-related ARDS remains unclear. Thus, we determined the trends of HLA-DR and cytokine expressions in alveolar monocytes using repeated measurements to answer this question. Thirty-one pneumonia patients with respiratory failure and ARDS without coronavirus disease 2019 between November 2019 and November 2021 were enrolled in our intensive care unit and three without complete data were excluded. Interleukin (IL)-10, IL-12, and HLA-DR expression in bronchoalveolar lavage (BAL) monocytes were determined on days one and eight. Monocyte HLA-DR expression (mHLA-DR) and CD4 T lymphocytes percentages in BAL cells of survivors increased remarkably after seven days. Monocyte IL-10 expression and monocytes percentages in BAL cells of survivors decreased substantially after seven days. The mHLA-DR was negatively correlated with disease severity scores on day one and eight. In conclusion, serial increases in HLA-DR expression and decreases in IL-10 expression were observed in BAL monocytes of survivors of pneumonia-related ARDS. More studies are needed to confirm this point of view, and then development of a therapeutic agent restoring mHLA-DR and preventing IL-10 production can be considered. Full article
(This article belongs to the Special Issue Inflammasome Biology and Molecular Pathology)
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