Aim: : Hydrogen sulfide (H2S), together with nitric oxide (NO) and carbon monoxide (CO), belongs to a family of endogenous signaling mediators termed “gasotransmittersâ€. Recent studies suggest that H2S modulates many cellular processes and it has been recognized to play a central role in inflammation, in the cardiovascular and nervous systems.
By infecting monocytes/macrophages with Mycoplasma fermentans (M.F.), a well-known pro-inflammatory agent, we evaluated the effects of H2S.
Methods:
M.F.-infected cells were analyzed by ELISA and real time RT-PCR to detect the M.F. effects on MCP-1 and on MMP-12 expression.
The role of two different H2S donors (NaHS and GYY4137) on MF-infected cells was determined by treating infected cells with H2S and then testing the culture supernatants for MCP-1 and on MMP-12 production by ELISA assay. In order to identify the pathway/s mediating H2S- anti-inflammatory activity, cells were also treated with specific pharmaceutical inhibitors.
Cytoplasmic and nuclear accumulation of NF-kappaB heterodimers was analyzed.
Results:
We show that H2S was able to reduce the production of pro-inflammatory cytokine MCP-1, that was induced in monocytes/macrophages during M.F. infection.
Moreover, MCP-1 was induced by M.F. through Toll-like receptor (TLR)-mediated nuclear factor-kappaB (NF-kappaB) activation, as demonstrated by the fact that TLR inhibitors TIRAP and MyD88 and NF-kappaB inhibitor IKK were able to block the cytokine production.
In contrast H2S treatment of M.F. infected macrophages reduced nuclear accumulation of NF-kappaB heterodimer p65/p52.
Conclusions:
Our data demonstrate that under the present conditions H2S is effective in reducing Mycoplasma-induced inflammation by targeting the NF-kappaB pathway.
This supports further studies for possible clinical applications.
Author: Francesca BenedettiSergio DavinelliSelvi KrishnanRobert C GalloGiovanni ScapagniniDavide ZellaSabrina Curreli
Credits/Source: Journal of Translational Medicine 2014, 12:145
Published on: 2014-05-24
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