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Int. J. Mol. Sci. 2018, 19(7), 1959; https://doi.org/10.3390/ijms19071959

Transmembrane TNF and Partially TNFR1 Regulate TNFR2 Expression and Control Inflammation in Mycobacterial-Induced Pleurisy

1
Department of Pathology and Immunology, Centre Medical Universitaire (CMU), Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland
2
Centre National de la Recherche Scientifique, UMR7355, and Experimental and Molecular Immunology and Neurogenetics, University of Orléans, 45100 Orléans, France
Present address: Laboratory of Integrative Immunology, National Institute of Respiratory Diseases “Ismael Cosio Villegas”, Mexico City 14080, Mexico.
*
Author to whom correspondence should be addressed.
Received: 13 April 2018 / Revised: 15 June 2018 / Accepted: 30 June 2018 / Published: 4 July 2018
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
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Abstract

Pleural tuberculosis is one of the most frequent forms of extra-pulmonary tuberculosis observed in patients infected with Mycobacterium tuberculosis. Tumor Necrosis Factor (TNF) is a crucial cytokine needed to control tuberculosis infection that remains a leading cause of morbidity and mortality worldwide. TNF blockade compromises host immunity and may increase the risk of reactivation of latent infection resulting in overt pulmonary, pleural and extra-pulmonary tuberculosis. While TNF signaling is mainly considered pro-inflammatory, its requirement for the anti-inflammation process involved in the resolution of infection and tissue repair is less explored. Our study analyzes the role of TNF and TNF receptors in the control of the inflammatory process associated with Bacillus Calmette-Guérin (BCG)-induced pleurisy. This study shows that the absence of TNF causes exacerbated inflammation in the pleural cavity of BCG-infected mice which is controlled by the transmembrane TNF (tmTNF) expression. The lack of TNF is associated with an impaired cellular expression and shedding of TNFR2 in the pleural cavity. The presence of tmTNF restores the normal expression of TNFR2 on myeloid cells during BCG-induced pleurisy. We also show that absence of TNFR1 affects the expression of TNFR2 on pleural cells and inflammation in the pleural cavity of BCG-infected mice. In conclusion, tmTNF but not soluble TNF prevents pleural cavity inflammation leading to attenuation and the resolution of the inflammatory process caused by mycobacterial pleurisy in association with the expression of TNFR2 on myeloid cells. View Full-Text
Keywords: TNF; TNF receptors; BCG-induced pleurisy; inflammation TNF; TNF receptors; BCG-induced pleurisy; inflammation
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Uysal, H.; Chavez-Galan, L.; Vesin, D.; Blaser, G.; Benkhoucha, M.; Ryffel, B.; Quesniaux, V.F.J.; Garcia, I. Transmembrane TNF and Partially TNFR1 Regulate TNFR2 Expression and Control Inflammation in Mycobacterial-Induced Pleurisy. Int. J. Mol. Sci. 2018, 19, 1959.

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