Mechanisms of sterile inflammation.

Rubartelli A, Lotze MT, Latz E, Manfredi A
Frontiers in immunology · 2013 · doi:10.3389/fimmu.2013.00398 · PMID:24319446 · PMC3837241
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This special topic review explores molecular mechanisms of sterile inflammation, highlighting DAMPs and IL-1 family cytokines, while illustrating their roles in pathologies including endometriosis.

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This editorial review outlines the molecular mechanisms underlying sterile inflammation, emphasizing how persistent physical, chemical, or metabolic stressors trigger immune responses through damage-associated molecular patterns and cytokines like IL-1β. The authors highlight the roles of various immune cells, including myelomonocytic and innate lymphoid cells, in perpetuating this inflammatory cycle, which contributes to the pathophysiology of numerous chronic diseases. While the text broadly addresses general inflammatory pathways, it explicitly cites endometriosis as one of the key pathologies illustrated by these mechanisms of disease. Relevance to endometriosis: listed as one indication for understanding macrophage-driven inflammation, though the paper's main focus is the general biology of sterile inflammation.

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References

1 GombaultABaronLCouillinI. ATP release and purinergic signaling in NLRP3 inflammasome activation. Front Immunol (2013) 3:414.10.3389/fimmu.2012.00414 2 RivaFBonavitaEBarbatiEMuzioMMantovaniAGarlandaC. TIR8/SIGIRR is an interleukin-1 receptor/toll like receptor family member with regulatory functions in inflammation and immunity. Front Immunol (2012) 3:322.10.3389/fimmu.2012.00322 3 RiderPKaplanovIRomzovaMBernardisLBraimanAVoronovEet alThe transcription of the alarmin cytokine interleukin-1 alpha is controlled by hypoxia inducible factors 1 and 2 alpha in hypoxic cells. Front Immunol (2012) 3:290.10.3389/fimmu.2012.00290 4 LukensJRGrossJMKannegantiT-D. IL-1 family cytokines trigger sterile inflammatory disease. Front Immunol (2012) 3:315.10.3389/fimmu.2012.00315 5 LiGLiangXLotzeMT. HMGB1: the central cytokine for all lymphoid cells. Front Immunol (2013) 4:68.10.3389/fimmu.2013.00068 6 RussellSEWalshPT. Sterile inflammation – do innate lymphoid cell subsets play a role?Front Immunol (2012) 3:246.10.3389/fimmu.2012.00246 7 SchornCJankoCLatzkoMChaurioRSchettGHerrmannM. Monosodium urate crystals induce extracellular DNA traps in neutrophils, eosinophils, and basophils but not in mononuclear cells. Front Immunol (2012) 3:277.10.3389/fimmu.2012.00277 8 SavageCLopez-CastejonGDenesABroughD. NLRP3-inflammasome activating DAMPs stimulate an inflammatory response in glia in the absence of priming which contributes to brain inflammation after injury. Front Immunol (2012) 3:288.10.3389/fimmu.2012.00288 9 GrantRWDixitWD. Mechanisms of disease: inflammasome activation and the development of type 2 diabetes. Front Immunol (2013) 4:50.10.3389/fimmu.2013.00050 10 CapobiancoARovere-QueriniP. Endometriosis, a disease of the macrophage. Front Immunol (2013) 4:9.10.3389/fimmu.2013.00009 11 CunhaCCarvalhoAEspositoABistoniFRomaniL. DAMP signaling in fungal infections and diseases. Front Immunol (2012) 3:286.10.3389/fimmu.2012.00286 12 KobayashiH. The entry of fetal and amniotic fluid components into the uterine vessel circulation leads to sterile inflammatory processes during parturition. Front Immunol (2012) 3:321.10.3389/fimmu.2012.00321 Summary

Keywords

stress, inflammasome activation, HMGB1, IL-1, DAMPs, PRR, acute inflammation, chronic inflammation Citation Rubartelli A, Lotze MT, Latz E and Manfredi A (2013) Mechanisms of Sterile Inflammation. Front. Immunol. 4:398. doi: 10.3389/fimmu.2013.00398 Received 25 October 2013 Accepted 07 November 2013 Published 22 November 2013 Volume 4 - 2013 Edited by Kendall A. Smith, Cornell University, USA Copyright © 2013 Rubartelli, Lotze, Latz and Manfredi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. *Correspondence: [email protected] This article was submitted to Inflammation, a section of the journal Frontiers in Immunology. Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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