Redox stress unbalances the inflammatory cytokine network: role in autoinflammatory patients and healthy subjects. Issue 1 (21st July 2015)

• Record Type: Journal Article
• Authors: Lavieri, Rosa; Rubartelli, Anna; Carta, Sonia
• Is Part Of: Journal of leukocyte biology. Volume 99:Issue 1(2016)
• Page Start: 79
• Page End: 86
• Publication Date: 2015-07-21
• Subjects: interleukin-1 family -- ATP secretion -- TLR agonist -- NLRP3 inflammasome; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.3MR0415-159R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : Review on the interplay between stress and cytokine dysregulation in inflammation, in both healthy individuals and CAPS patients. Abstract: The cell stress and redox responses are increasingly acknowledged as factors contributing to the generation and development of the inflammatory response. Several inflammation-inducing stressors have been identified, inside and outside of the cell. Furthermore, many hereditary diseases associate with inflammation and oxidative stress, suggesting a role for mutated proteins as stressors. The nucleotide-binding oligomerization domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasome is an important node at the crossroad between redox response and inflammation. Remarkably, monocytes from patients with mutations in the NLRP3 gene undergo oxidative stress after stimulation with minute amounts of TLR agonists, resulting in unbalanced production of IL-1β and regulatory cytokines. Similar alterations in cytokine production are found in healthy monocytes upon TLR overstimulation. This mini-review summarizes recent progress in this field, discusses the molecular mechanisms underlying the loss of control of the cytokine network following oxidative stress, and proposes new therapeutic opportunities.