IL-26 Is Overexpressed in Rheumatoid Arthritis and Induces Proinflammatory Cytokine Production and Th17 Cell Generation

Interleukin-26 (IL-26), a member of the IL-10 cytokine family, induces the production of proinflammatory cytokines by epithelial cells. IL-26 has been also reported overexpressed in Crohn\u27s disease, suggesting that it may be involved in the physiopathology of chronic inflammatory disorders. Here, we have analyzed the expression and role of IL-26 in rheumatoid arthritis (RA), a chronic inflammatory disorder characterized by joint synovial inflammation. We report that the concentrations of IL-26 are higher in the serums of RA patients than of healthy subjects and dramatically elevated in RA synovial fluids compared to RA serums. Immunohistochemistry reveals that synoviolin+ fibroblast-like synoviocytes and CD68+ macrophage-like synoviocytes are the main IL-26-producing cells in RA joints. Fibroblast-like synoviocytes from RA patients constitutively produce IL-26 and this production is upregulated by IL-1-beta and IL-17A. We have therefore investigated the role of IL-26 in the inflammatory process. Results show that IL-26 induces the production of the proinflammatory cytokines IL-1-beta, IL-6, and tumor necrosis factor (TNF)-alpha by human monocytes and also upregulates the expression of numerous chemokines (mainly CCL20). Interestingly, IL-26-stimulated monocytes selectively promote the generation of RORgamma t+ Th17 cells, through IL-1-beta secretion by monocytes. More precisely, IL-26-stimulated monocytes switch non-Th17 committed (IL-23R− or CCR6− CD161−) CD4+ memory T cells into Th17 cells. Finally, synovial fluids from RA patients also induce Th17 cell generation and this effect is reduced after IL-26 depletion. These findings show that IL-26 is constitutively produced by RA synoviocytes, induces proinflammatory cytokine secretion by myeloid cells, and favors Th17 cell generation. IL-26 thereby appears as a novel proinflammatory cytokine, located upstream of the proinflammatory cascade, that may constitute a promising target to treat RA and chronic inflammatory disorders

Simulation of ignition of unburnt gases in the extraction vent of a room fire

International audienc

Heat feedback to the fuel surface of a pool fire in an enclosure

International audienceAs a part of an effort to determine the energy balance at the pool fire surface in compartments, a series of fire experiments were conducted to study heat flux of the flame in a vitiated environment formed with air and combustion products gases. This paper presents experimental results of the burning behaviour of a heptane pool fire in a reduced scale compartment equipped with a mechanical ventilation network. Measurements of heat fluxes, fuel mass loss rate, oxygen concentration and temperature are performed for heptane fires of 0.26 and 0.3 m diameter pans at different ventilation flow rates. An original method to separate effects of the radiant heat flux of the flame and of the external heat feedback to the fuel surface is developed. This was achieved by using an additional heat flux measurement located under the pool fire. A correlation was also developed to determine the temperature rise on the plume centerline in the compartment as a function of the heat release rate. The results indicate a decrease in the fuel mass loss rate, flame temperature and heat fluxes to the fuel surface as the oxygen concentration measured near the fuel decreases by varying the air refresh rate of the compartment. The flame radiation fraction shows a similar behaviour, whereas the convective fraction of the flame heat flux increases when oxygen concentration decreases. Based on these experimental findings, it was discussed that any classification of the burning regime of a pool fire should consider both the effects of pan diameter and the burning response to vitiated air. © 2013 Elsevier Ltd. All rights reserved