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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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Nitric Oxide Engages an Anti-inflammatory Feedback Loop Mediated by Peroxiredoxin 5 in Phagocytes.

TL;DR: It is demonstrated that engaging the antioxidant response is sufficient to suppress Toll-like receptor (TLR)-induced cytokine production in dendritic cells and that Prdx5 is required for attenuation of inflammatory cytokineproduction.
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Targeting immunometabolism in host defence against Mycobacterium tuberculosis

TL;DR: This review aims to examine the metabolic demands of the immune cells involved in both host resistance and disease tolerance, chiefly the macrophage and T‐lymphocyte, and discusses how baseline metabolic heterogeneity and inflammation‐driven metabolic reprogramming during infection are linked to their key immune functions.
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Research Progress on the Role of Inflammasomes in Kidney Disease.

TL;DR: The research progress oninflammasomes and the key pathogenic roles of inflammasome in the development and progression of kidney diseases are focused on and the potential of this intracellular inflammation to further prevent or block the development of the kidney disease is explored.
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Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation.

TL;DR: Conversion of cultured human macrophages into foam cells suppresses their proinflammatory responses to M1-polarizing factors, which may locally weaken the macrophage-dependent inflammatory component of atherogenesis.
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Phosphodiesterase 3B (PDE3B) regulates NLRP3 inflammasome in adipose tissue.

TL;DR: A role for PDE3B in modulating inflammatory response is established, which may contribute to a reduced inflammatory state in adipose tissue.
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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