Exogenous hydrogen sulfide induces functional inhibition and cell death of cytotoxic lymphocytes subsets

Authors: Mirandola P (1) , Gobbi G (1) , Sponzilli I (1) , Pambianco M (2) , Malinverno C (1) , Cacchioli A (3) , De Panfilis G (4) , Vitale M (1)

Affiliations:

(1) Department of Anatomy, Pharmacology & Forensic Medicine, Human Anatomy Section, University of Parma (2) Terme di Sirmione, Cell Biology Laboratory (3) Department of Animal Health, University of Parma (4) Department of Surgery, Section of Dermatology, University of Parma

Source: J Cell Physiol. 2007 Dec;213(3):826-33

DOI: 10.1002/jcp.21151 Publication date: 2007 Dec E-Publication date: May 21, 2007 Availability: abstract Copyright: 2007 Wiley-Liss, Inc.

Language: English Countries: Italy Location: Not specified Correspondence address: Marco Vitale (marco.vitale@unipr.it)

Department of Anatomy, Pharmacology & Forensic Medicine, Human Anatomy Section, University of Parma, Ospedale Maggiore, Via Gramsci, 14, I-43100 Parma, Italy.

Keywords

Article abstract

The toxic effects of exogenous hydrogen sulfide on peripheral blood lymphocytes have been investigated in detail. Hydrogen sulfide is now considered as a gasotransmitter with specific functional roles in different cell types, like neurons and vascular smooth muscle. Here we show that exogenous hydrogen sulfide induces a caspase-independent cell death of peripheral blood lymphocytes that depends on their intracellular glutathione levels, with a physiologically relevant subset specificity for CD8+ T cells and NK cells. Although lymphocyte activation does not modify their sensitivity to HS-, after 24 h exposure to hydrogen sulfide surviving lymphocyte subsets show a dramatically decreased proliferation in response to mitogens and a reduced IL-2 production. Overall, our data demonstrate that HS- reduces the cellular cytotoxic response of peripheral blood lymphocytes as well as their production of IL-2, therefore de-activating the major players of local inflammatory responses, adding new basic knowledge to the clinically well known anti-inflammatory effects of sulfur compounds.

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