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Nitric oxide induces SOCS-1 expression in human monocytes in a TNF--dependent manner

Research Unit, "La Paz' Hospital, Madrid, Spain

Alessandra Soares-Schanoski

Research Unit, "La Paz' Hospital, Madrid, Spain

Carlos del Fresno

Research Unit, "La Paz' Hospital, Madrid, Spain

Agata Cimadevila

Research Unit, "La Paz' Hospital, Madrid, Spain

Vanesa Goméz-Piña

Research Unit, "La Paz' Hospital, Madrid, Spain

Elena Mendoza-Barberá

Research Unit, "La Paz' Hospital, Madrid, Spain

Felipe García

Discover Unit, EMPIREO Molecular Diagnostic, Madrid, Spain

Elvira Marín

National Center for Biotechnology, Spain

Francisco Arnalich

Department of Medicine, "La Paz' Hospital Medical School, Universidad Autónoma de Madrid, Madrid, Spain

Pablo Fuentes-Prior

Cardiovascular Research Center, ICCC-CSIC, Sant Antoni Ma, Barcelona, Spain

Eduardo López-Collazo

Research Unit, "La Paz' Hospital, Madrid, Spain, elopezc.hulp{at}salud.madrid.org

In contrast to the thoroughly characterized mechanisms of positive regulation within cytokine signaling pathways, our knowledge of negative feedback loops is comparatively sparse. We and others have previously reported that IRAK-M down-regulates inflammatory responses to multiple stimuli. In particular, we could show that the nitric oxide (NO) donor, GSNO, induces IRAK-M overexpression in human monocytes. Here we study the expression of another important negative regulator of cytokine signaling, SOCS-1, in human monocytes exposed to GSNO. The NO donor induced significant levels of SOCS-1 mRNA and protein, 6 h and 16 h after stimulation, respectively. Monocytes stimulated with GSNO for longer periods (24 h and 48 h) failed to express IL-6 and IP-10 upon LPS challenge. In addition, and in line with previous reports of NO-mediated induction of TNF-, we have found that exposure to this cytokine induces SOCS-1 mRNA in human monocytes. A blocking antibody against TNF- impaired SOCS-1 expression upon GSNO treatment and re-instated IL-6 and IP-10 mRNA levels after LPS challenge in cultures pretreated with the NO donor. We conclude that NO stimulates SOCS-1 overexpression in a pathway at least partially regulated by TNF-.

Key Words: Nitric oxide • SOCS-1 • TNF- • monocyte • inflammation

Journal of Endotoxin Research, Vol. 12, No. 5, 296-306 (2006)
DOI: 10.1177/09680519060120050501


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