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Open AccessJournal ArticleDOI

Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β.

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TLDR
By exogenously controlling the replication of Mycobacterium tuberculosis in vivo, the requirement for antimicrobial immunity is obviated and it is discovered that both IL-1 production and infection-induced immunopathology were suppressed by lymphocyte-derived interferon-γ (IFN-γ).
Abstract
Interleukin 1 (IL-1) is an important mediator of innate immunity but can also promote inflammatory tissue damage. During chronic infections such as tuberculosis, the beneficial antimicrobial role of IL-1 must be balanced with the need to prevent immunopathology. By exogenously controlling the replication of Mycobacterium tuberculosis in vivo, we obviated the requirement for antimicrobial immunity and discovered that both IL-1 production and infection-induced immunopathology were suppressed by lymphocyte-derived interferon-γ (IFN-γ). This effect was mediated by nitric oxide (NO), which we found specifically inhibited assembly of the NLRP3 inflammasome via thiol nitrosylation. Our data indicate that the NO produced as a result of adaptive immunity is indispensable in modulating the destructive innate inflammatory responses elicited during persistent infections.

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Comparative in-silico proteomic analysis discerns potential granuloma proteins of Yersinia pseudotuberculosis.

TL;DR: This study has used a computational approach to identify proteins that might be potentially involved in formation of Y. pseudotuberculosis granuloma and can serve as a basis for further studies on Y. Pseudo-Pseudotuber tuberculosis.
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Mycobacterium tuberculosis stimulates IL-1β production by macrophages in an ESAT-6 dependent manner with the involvement of serum amyloid A3

TL;DR: The production of SAA3 is required for Mtb stimulated IL-1β production by macrophages in tuberculosis infection and is identified as one of the highly expressed genes in mouse lungs.
Journal ArticleDOI

Targeting endogenous gaseous signaling molecules as novel host-directed therapies against tuberculosis infection.

TL;DR: In this article, a review of host factors majorly endogenous gaseous signaling molecules which contribute to Mycobacterium tuberculosis survival inside the intracellular environment and highlight the potential therapeutic targets is presented.
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Immunological responses of European badgers (Meles Meles) to infection with Mycobacterium bovis.

TL;DR: Badgers may represent an interesting natural host for M. bovis that can provide a more thorough understanding of efficient immunological responses to tuberculosis.
Journal ArticleDOI

Moonlighting by PPE2 Protein: Focus on Mycobacterial Virulence.

TL;DR: In this paper, the role of Proline-Proline-glutamic acid (PPE) in TB pathogenesis was described and the importance of PPE2 as a novel therapeutic target against TB was discussed.
References
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Journal ArticleDOI

Immunological and Inflammatory Functions of the Interleukin-1 Family

TL;DR: The IL-1 family includes members that suppress inflammation, both specifically within the IL-2 family but also nonspecifically for TLR ligands and the innate immune response.
Journal ArticleDOI

AIM2 recognizes cytosolic dsDNA and forms a caspase-1 activating inflammasome with ASC

TL;DR: Using mouse and human cells, the PYHIN (pyrin and HIN domain-containing protein) family member absent in melanoma 2 (AIM2) is identified as a receptor for cytosolic DNA, which regulates caspase-1.
Journal ArticleDOI

Erratum: NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals (Nature (2010) 464 (1357-1361))

TL;DR: This corrects the article to show that the method used to derive the H2O2 “spatially aggregating force” is a two-step process, not a single step, like in the previous version of this paper.
Journal ArticleDOI

Nitrosylation. the prototypic redox-based signaling mechanism.

TL;DR: Whereas phosphorylation clearly Spain lies at the heart of many signal transduction pathways, has been expanded re-translational modification of proteins, are conserved cently by the discovery of an enzymatic function for throughout evolution and influence most aspects of cel-hemoglobin.
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