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Special Issue "Cytoplasmic Sensors: Infection, Inflammation, and Immunity"

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

Deadline for manuscript submissions: closed (31 May 2019).

Special Issue Editor

Dr. Prajwal Gurung
E-Mail Website
Guest Editor
Dept Internal Med, Univ Iowa, Inflammat Program, 429 EMRB, IA 52242 USA
Interests: cytoplasmic sensors; nod-like receptors; inflammasomes; neutrophilic dermatosis; leishmania; endotoxin

Special Issue Information

Dear colleagues,

Cytoplasmic sensors play sentinel roles in detecting intracellular pathogen- or self-derived molecular patterns and initiate a proper healing-immune response. While important for protecting us from invading pathogens and dangers, dysregulated cytoplasmic sensors can promote autoinflammatory disorders. In addition to initiating signalling cascade that results in the production of pro-inflammatory cytokines and antimicrobial peptides, some members of the cytoplasmic sensors (e.g., NLRP1b, NLRP3, NLRC4, AIM2, and PYRIN) assemble a multimeric protein complex known as inflammasomes. The last decade has seen an unprecedented development in our understanding of how these cytoplasmic sensors function within our cells to not only provide immunity but also maintain cellular homeostasis. Manuscripts (articles and reviews) relating to the recent advancement in our understanding of the cellular, molecular, and biochemical pathways that are regulated by cytoplasmic sensors will be given priority and considered for this Special Issue.

Dr. Prajwal Gurung
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

  • pathogen-recognition receptors
  • cytoplasmic sensors
  • inflammasomes
  • nod-like receptors

Published Papers (4 papers)

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Review

Review
Recent Advances in Lipopolysaccharide Recognition Systems
Int. J. Mol. Sci. 2020, 21(2), 379; https://doi.org/10.3390/ijms21020379 - 07 Jan 2020
Cited by 38 | Viewed by 3764
Abstract
Lipopolysaccharide (LPS), commonly known as endotoxin, is ubiquitous and the most-studied pathogen-associated molecular pattern. A component of Gram-negative bacteria, extracellular LPS is sensed by our immune system via the toll-like receptor (TLR)-4. Given that TLR4 is membrane bound, it recognizes LPS in the [...] Read more.
Lipopolysaccharide (LPS), commonly known as endotoxin, is ubiquitous and the most-studied pathogen-associated molecular pattern. A component of Gram-negative bacteria, extracellular LPS is sensed by our immune system via the toll-like receptor (TLR)-4. Given that TLR4 is membrane bound, it recognizes LPS in the extracellular milieu or within endosomes. Whether additional sensors, if any, play a role in LPS recognition within the cytoplasm remained unknown until recently. The last decade has seen an unprecedented unfolding of TLR4-independent LPS sensing pathways. First, transient receptor potential (TRP) channels have been identified as non-TLR membrane-bound sensors of LPS and, second, caspase-4/5 (and caspase-11 in mice) have been established as the cytoplasmic sensors for LPS. Here in this review, we detail the brief history of LPS discovery, followed by the discovery of TLR4, TRP as the membrane-bound sensor, and our current understanding of caspase-4/5/11 as cytoplasmic sensors. Full article
(This article belongs to the Special Issue Cytoplasmic Sensors: Infection, Inflammation, and Immunity)
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Review
Subcellular Localization Signals of bHLH-PAS Proteins: Their Significance, Current State of Knowledge and Future Perspectives
Int. J. Mol. Sci. 2019, 20(19), 4746; https://doi.org/10.3390/ijms20194746 - 24 Sep 2019
Cited by 4 | Viewed by 1588
Abstract
The bHLH-PAS (basic helix-loop-helix/ Period-ARNT-Single minded) proteins are a family of transcriptional regulators commonly occurring in living organisms. bHLH-PAS members act as intracellular and extracellular “signals” sensors, initiating response to endo- and exogenous signals, including toxins, redox potential, and light. The activity of [...] Read more.
The bHLH-PAS (basic helix-loop-helix/ Period-ARNT-Single minded) proteins are a family of transcriptional regulators commonly occurring in living organisms. bHLH-PAS members act as intracellular and extracellular “signals” sensors, initiating response to endo- and exogenous signals, including toxins, redox potential, and light. The activity of these proteins as transcription factors depends on nucleocytoplasmic shuttling: the signal received in the cytoplasm has to be transduced, via translocation, to the nucleus. It leads to the activation of transcription of particular genes and determines the cell response to different stimuli. In this review, we aim to present the current state of knowledge concerning signals that affect shuttling of bHLH-PAS transcription factors. We summarize experimentally verified and published nuclear localization signals/nuclear export signals (NLSs/NESs) in the context of performed in silico predictions. We have used most of the available NLS/NES predictors. Importantly, all our results confirm the existence of a complex system responsible for protein localization regulation that involves many localization signals, which activity has to be precisely controlled. We conclude that the current stage of knowledge in this area is still not complete and for most of bHLH-PAS proteins an experimental verification of the activity of further NLS/NES is needed. Full article
(This article belongs to the Special Issue Cytoplasmic Sensors: Infection, Inflammation, and Immunity)
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Review
The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation
Int. J. Mol. Sci. 2019, 20(13), 3328; https://doi.org/10.3390/ijms20133328 - 06 Jul 2019
Cited by 403 | Viewed by 11544
Abstract
The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with [...] Read more.
The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer’s disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. How NLRP3 responds to those signaling events and initiates the assembly of the NLRP3 inflammasome is not fully understood. In this review, we summarize our current understanding of the mechanisms of NLRP3 inflammasome activation by multiple signaling events, and its regulation by post-translational modifications and interacting partners of NLRP3. Full article
(This article belongs to the Special Issue Cytoplasmic Sensors: Infection, Inflammation, and Immunity)
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Review
Ubiquitination-Mediated Inflammasome Activation during Bacterial Infection
Int. J. Mol. Sci. 2019, 20(9), 2110; https://doi.org/10.3390/ijms20092110 - 29 Apr 2019
Cited by 7 | Viewed by 1581
Abstract
Inflammasome activation is essential for host immune responses during pathogenic infection and sterile signals insult, whereas excessive activation is injurious. Thus, inflammasome activation is tightly regulated at multiple layers. Ubiquitination is an important post-translational modification for orchestrating inflammatory immune responses during pathogenic infection, [...] Read more.
Inflammasome activation is essential for host immune responses during pathogenic infection and sterile signals insult, whereas excessive activation is injurious. Thus, inflammasome activation is tightly regulated at multiple layers. Ubiquitination is an important post-translational modification for orchestrating inflammatory immune responses during pathogenic infection, and a major target hijacked by pathogenic bacteria for promoting their survival and proliferation. This review summarizes recent insights into distinct mechanisms of the inflammasome activation and ubiquitination process triggered by bacterial infection. We discuss the complex regulatory of inflammasome activation mediated by ubiquitination machinery during bacterial infection, and provide therapeutic approaches for specifically targeting aberrant inflammasome activation. Full article
(This article belongs to the Special Issue Cytoplasmic Sensors: Infection, Inflammation, and Immunity)
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