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Special Issue "Inflammasome"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 15 June 2020.

Special Issue Editor

Prof. Kuo-Feng Hua
E-Mail Website
Guest Editor
Department of Biotechnology and Animal Science, National Ilan University, Ilan, Taiwan, Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
Interests: Molecular Immunology; Cell Signaling; Inflammation

Special Issue Information

Dear Colleagues,

Inflammasomes are cytosolic caspase-1-containing protein complexes which recognize and respond to pathogen infection and diverse sterile host-derived or environmental danger signals to promote inflammatory disease development. Activation of inflammasomes leads to caspase-1-dependent maturation and release of proinflammatory cytokines IL-1β and IL-18 and promotes Gasdermin D-dependent pyroptotic cell death. Dysregulation of inflammasomes is associated with a number of inflammatory conditions. such as metabolic disorders, diabetes, cardiovascular diseases, neurodegenerative diseases, inflammatory bowel disease, kidney injury, and infectious diseases. As inflammasomes respond to a board range of medically relevant stimuli, inflammasomes become a highly desirable drug target to treat a wide range of human diseases. Small molecule inhibitors targeting inflammasomes offer a new therapeutic strategy in new drug development. This Special Issue, “Inflammasome”, welcomes original research and review articles in the field, with a focus on but not limited to the molecular and mechanistic basis for the inflammasome activation, inflammasome-associated pathogenesis, inflammasome inhibitor development, and inflammasome-specific therapeutics.

Prof. Kuo-Feng Hua
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • Inflammasome
  • Inflammatory disease
  • Caspase-1
  • Cytokines
  • Pyroptosis
  • NLRP3
  • Inflammasome inhibitor
  • Sterile inflammation

Published Papers (2 papers)

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Research

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Open AccessArticle
Microtubule-Mediated NLRP3 Inflammasome Activation Is Independent of Microtubule-Associated Innate Immune Factor GEF-H1 in Murine Macrophages
Int. J. Mol. Sci. 2020, 21(4), 1302; https://doi.org/10.3390/ijms21041302 (registering DOI) - 14 Feb 2020
Abstract
Inflammasomes are intracellular multiple protein complexes that mount innate immune responses to tissue damage and invading pathogens. Their excessive activation is crucial in the development and pathogenesis of inflammatory disorders. Microtubules have been reported to provide the platform for mediating the assembly and [...] Read more.
Inflammasomes are intracellular multiple protein complexes that mount innate immune responses to tissue damage and invading pathogens. Their excessive activation is crucial in the development and pathogenesis of inflammatory disorders. Microtubules have been reported to provide the platform for mediating the assembly and activation of NLRP3 inflammasome. Recently, we have identified the microtubule-associated immune molecule guanine nucleotide exchange factor-H1 (GEF-H1) that is crucial in coupling microtubule dynamics to the initiation of microtubule-mediated immune responses. However, whether GEF-H1 also controls the activation of other immune receptors that require microtubules is still undefined. Here we employed GEF-H1-deficient mouse bone marrow-derived macrophages (BMDMs) to interrogate the impact of GEF-H1 on the activation of NLRP3 inflammasome. NLRP3 but not NLRC4 or AIM2 inflammasome-mediated IL-1β production was dependent on dynamic microtubule network in wild-type (WT) BMDMs. However, GEF-H1 deficiency did not affect NLRP3-driven IL-1β maturation and secretion in macrophages. Moreover, α-tubulin acetylation and mitochondria aggregations were comparable between WT and GEF-H1-deficient BMDMs in response to NLRP3 inducers. Further, GEF-H1 was not required for NLRP3-mediated immune defense against Salmonella typhimurium infection. Collectively, these findings suggest that the microtubule-associated immune modulator GEF-H1 is dispensable for microtubule-mediated NLRP3 activation and host defense in mouse macrophages. Full article
(This article belongs to the Special Issue Inflammasome)

Review

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Open AccessReview
Inflammasome and Cognitive Symptoms in Human Diseases: Biological Evidence from Experimental Research
Int. J. Mol. Sci. 2020, 21(3), 1103; https://doi.org/10.3390/ijms21031103 - 07 Feb 2020
Abstract
Cognitive symptoms are prevalent in the elderly and are associated with an elevated risk of developing dementia. Disease-driven changes can cause cognitive disabilities in memory, attention, and language. The inflammasome is an innate immune intracellular complex that has a critical role in the [...] Read more.
Cognitive symptoms are prevalent in the elderly and are associated with an elevated risk of developing dementia. Disease-driven changes can cause cognitive disabilities in memory, attention, and language. The inflammasome is an innate immune intracellular complex that has a critical role in the host defense system, in that it senses infectious pathogen-associated and endogenous danger-associated molecular patterns. An unbalanced or dysregulated inflammasome is associated with infectious, inflammatory, and neurodegenerative diseases. Due to its importance in such pathological conditions, the inflammasome is an emerging drug target for human diseases. A growing number of studies have revealed links between cognitive symptoms and the inflammasome. Several studies have shown that reducing the inflammasome component mitigates cognitive symptoms in diseased states. Therefore, understanding the inflammasome regulatory mechanisms may be required for the prevention and treatment of cognitive symptoms. The purpose of this review is to discuss the current understanding of the inflammasome and its relationships with cognitive symptoms in various human diseases. Full article
(This article belongs to the Special Issue Inflammasome)
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