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      Anti-inflammatory effects of H 2S during acute bacterial infection: a review

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          Abstract

          Hydrogen sulfide (H 2S), previously only considered a toxic environmental air pollutant, is now increasingly recognized as an important signaling molecule able to modulate several cellular pathways in many human tissues. As demonstrated in recent studies, H 2S is produced endogenously in response to different cellular stimuli and plays different roles in controlling a number of physiological responses. The precise role of H 2S in inflammation is still largely unknown. In particular, the role of H 2S in the regulation of the inflammatory response in acute and chronic infections is being actively investigated because of its potential therapeutic use. To study the effect of H 2S as an anti-inflammatory mediator during bacterial infections, we developed an ex vivo model of primary cells and cell lines infected with Mycoplasma. Our data demonstrate a dichotomic effect of H 2S on the NF-kB and Nrf-2 molecular pathways, which were inhibited and stimulated, respectively.

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          The vasorelaxant effect of H(2)S as a novel endogenous gaseous K(ATP) channel opener.

          W Zhao, J ZHANG, Y. Lu … (2001)
          Hydrogen sulfide (H(2)S) has been traditionally viewed as a toxic gas. It is also, however, endogenously generated from cysteine metabolism. We attempted to assess the physiological role of H(2)S in the regulation of vascular contractility, the modulation of H(2)S production in vascular tissues, and the underlying mechanisms. Intravenous bolus injection of H(2)S transiently decreased blood pressure of rats by 12- 30 mmHg, which was antagonized by prior blockade of K(ATP) channels. H(2)S relaxed rat aortic tissues in vitro in a K(ATP) channel-dependent manner. In isolated vascular smooth muscle cells (SMCs), H(2)S directly increased K(ATP) channel currents and hyperpolarized membrane. The expression of H(2)S-generating enzyme was identified in vascular SMCs, but not in endothelium. The endogenous production of H(2)S from different vascular tissues was also directly measured with the abundant level in the order of tail artery, aorta and mesenteric artery. Most importantly, H(2)S production from vascular tissues was enhanced by nitric oxide. Our results demonstrate that H(2)S is an important endogenous vasoactive factor and the first identified gaseous opener of K(ATP) channels in vascular SMCs.
          Article 0 comments Cited 397 times – based on 0 reviews     Review now
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            Molecular mechanisms activating the Nrf2-Keap1 pathway of antioxidant gene regulation.

            Makoto Kobayashi, Masayuki Yamamoto (2005)
            Several years have passed since NF-E2-related factor 2 (Nrf2) was demonstrated to regulate the induction of genes encoding antioxidant proteins and phase 2 detoxifying enzymes. Following a number of studies, it was realized that Nrf2 is a key factor for cytoprotection in various aspects, such as anticarcinogenicity, neuroprotection, antiinflammatory response, and so forth. These widespread functions of Nrf2 spring from the coordinated actions of various categories of target genes. The activation mechanism of Nrf2 has been studied extensively. Under normal conditions, Nrf2 localizes in the cytoplasm where it interacts with the actin binding protein, Kelch-like ECH associating protein 1 (Keap1), and is rapidly degraded by the ubiquitin-proteasome pathway. Signals from reactive oxygen species or electrophilic insults target the Nrf2-Keap1 complex, dissociating Nrf2 from Keap1. Stabilized Nrf2 then translocates to the nuclei and transactivates its target genes. Interestingly, Keap1 is now assumed to be a substrate-specific adaptor of Cul3-based E3 ubiquitin ligase. Direct participation of Keap1 in the ubiquitination and degradation of Nrf2 is plausible. The Nrf2-Keap1 system is present not only in mammals, but in fish, suggesting that its roles in cellular defense are conserved throughout evolution among vertebrates. This review article recounts recent knowledge of the Nrf2-Keap1 system, focusing especially on the molecular mechanism of Nrf2 regulation.
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              Hydrogen sulfide and cell signaling.

              Ling Li, Peter Rose, Philip Moore (2011)
              Hydrogen sulfide (H₂S) is a gaseous mediator synthesized from cysteine by cystathionine γ lyase (CSE) and other naturally occurring enzymes. Pharmacological experiments using H₂S donors and genetic experiments using CSE knockout mice suggest important roles for this vasodilator gas in the regulation of blood vessel caliber, cardiac response to ischemia/reperfusion injury, and inflammation. That H₂S inhibits cytochrome c oxidase and reduces cell energy production has been known for many decades, but more recently, a number of additional pharmacological targets for this gas have been identified. H₂S activates K(ATP) and transient receptor potential (TRP) channels but usually inhibits big conductance Ca²(+)-sensitive K(+) (BK(Ca)) channels, T-type calcium channels, and M-type calcium channels. H₂S may inhibit or activate NF-κB nuclear translocation while affecting the activity of numerous kinases including p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt. These disparate effects may be secondary to the well-known reducing activity of H₂S and/or its ability to promote sulfhydration of protein cysteine moieties within the cell.
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                Author and article information

                Contributors
                Francesca Benedetti:
                ORCID: http://orcid.org/0000-0001-8720-090X
                FBenedetti@ihv.umaryland.edu
                Sabrina Curreli: SCurreli@ihv.umaryland.edu
                Selvi Krishnan: SKrishnan@ihv.umaryland.edu
                Sergio Davinelli: sergio.davinelli@unimol.it
                Fiorenza Cocchi: FCocchi@ihv.umaryland.edu
                Giovanni Scapagnini: g.scapagnini@gmail.com
                Robert C. Gallo: RGallo@ihv.umaryland.edu
                Davide Zella: DZella@ihv.umaryland.edu
                Journal
                Journal ID (nlm-ta): J Transl Med
                Journal ID (iso-abbrev): J Transl Med
                Title: Journal of Translational Medicine
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1479-5876
                Publication date (Electronic): 10 May 2017
                Publication date PMC-release: 10 May 2017
                Publication date Collection: 2017
                Volume: 15
                Electronic Location Identifier: 100
                Affiliations
                [1 ]ISNI 0000 0001 2175 4264, GRID grid.411024.2, Institute of Human Virology, , University of Maryland School of Medicine, ; Baltimore, MD 21201 USA
                [2 ]ISNI 0000000122055422, GRID grid.10373.36, Department of Medicine and Health Sciences, , University of Molise, ; 86100 Campobasso, Italy
                Author information
                http://orcid.org/0000-0001-8720-090X
                Article
                Publisher ID: 1206
                DOI: 10.1186/s12967-017-1206-8
                PMC ID: 5424385
                PubMed ID: 28490346
                SO-VID: de94e835-ec15-4e26-b8ff-80e66382109b
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 31 January 2017
                Date accepted : 3 May 2017
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Medicine
                Keywords: mycoplasma,hydrogen sulfide,nahs,gyy4137,nf-kb,nrf2,ros,inflammation,u937
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: mycoplasma, hydrogen sulfide, nahs, gyy4137, nf-kb, nrf2, ros, inflammation, u937

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