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Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders

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Date 2016 Jul 15
PMID 27412959
Citations 92
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Abstract

Major depressive disorder (MDD) and other mood disorders remain difficult to effectively treat, and innovative interventions and therapeutic targets are needed. Psychological stressors and inappropriate inflammation increase the risk and severity of mood disorders; however, only recently have the importance of sterile inflammatory processes in this effect been revealed. This review will introduce the reader to pathogen vs sterile inflammation, inflammatory receptor-ligand interactions, microbial-associated molecular patterns (MAMPs), pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and the more recent discovery of the role of the inflammasome in peripheral and central nervous system cytokine/chemokine inflammatory responses. The review will focus on current preclinical and clinical evidence that sterile inflammation and inflammasome-dependent signaling may contribute to mood disorders. By understanding these inflammatory signaling processes, new approaches for quieting chronic or inappropriate inflammatory states may be revealed and this could serve as novel pharmacological targets for the treatment of mood disorders.

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References
1.
Duewell P, Kono H, Rayner K, Sirois C, Vladimer G, Bauernfeind F . NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010; 464(7293):1357-61. PMC: 2946640. DOI: 10.1038/nature08938. View

2.
Venereau E, Casalgrandi M, Schiraldi M, Antoine D, Cattaneo A, De Marchis F . Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release. J Exp Med. 2012; 209(9):1519-28. PMC: 3428943. DOI: 10.1084/jem.20120189. View

3.
Abulafia D, de Rivero Vaccari J, Diego Lozano J, Lotocki G, Keane R, Dietrich W . Inhibition of the inflammasome complex reduces the inflammatory response after thromboembolic stroke in mice. J Cereb Blood Flow Metab. 2008; 29(3):534-44. DOI: 10.1038/jcbfm.2008.143. View

4.
Pan Y, Chen X, Zhang Q, Kong L . Microglial NLRP3 inflammasome activation mediates IL-1β-related inflammation in prefrontal cortex of depressive rats. Brain Behav Immun. 2014; 41:90-100. DOI: 10.1016/j.bbi.2014.04.007. View

5.
de Rivero Vaccari J, Lotocki G, Alonso O, Bramlett H, Dietrich W, Keane R . Therapeutic neutralization of the NLRP1 inflammasome reduces the innate immune response and improves histopathology after traumatic brain injury. J Cereb Blood Flow Metab. 2009; 29(7):1251-61. PMC: 2846547. DOI: 10.1038/jcbfm.2009.46. View