Anaerobic Methane Oxidizers

The anaerobic oxidation of methane (AOM) with sulfate as the final electron acceptor according to (CH4 + SO4 2− → HCO3 − + HS− + H2O) is the major sink of methane in the oceans and hence a significant process in the global carbon cycle and methane budget. Anaerobic methane oxidizing archaea (ANME) and sulfate-reducing bacteria (SRB) are assumed to act as a syntrophic consortium where the archaeal partner activates and metabolizes methane, leading to an intermediate that is scavenged as electron donor by the sulfate-reducing partner. All known anaerobic methanotrophs are related to the methanogenic Euryarchaeota. Recently, much has been learned about the distribution, activity, and physiology of the ANME, however, not a single member of these groups has been obtained in culture and the biochemical functioning of AOM remains unknown

Anaerobic Methane Oxidizers

The anaerobic oxidation of methane (AOM) with sulfate as the final electron acceptor according to the net reaction CH4 + SO42- -> HCO3- -> HS- + H2O is the major sink of methane in the ocean floor and hence a significant process in the marine methane budget and the global carbon cycle. Since its discovery, much has been learned about the distribution of the AOM process, its activity in different settings, and connections to other metabolic reactions in the seafloor. AOM is performed by consortia of anaerobic methane-oxidizing archaea (ANME) and sulfate-reducing bacteria (SRB). Since all known ANME and most of their partner bacteria have so far resisted isolation, the physiology of both organisms has been largely inferred from culture-independent approaches on natural enrichments or enrichment cultures. All known ANME are related to methanogenic Euryarchaeota, and as such they reverse the methanogenesis pathway to activate and completely oxidize methane. The reducing equivalents are shuttled to the partner bacteria, which use them for sulfate reduction. Recently, evidence has been found for ANME that can use nitrate or iron as electron acceptors. The exact mechanisms for the required exchange of reducing equivalents in AOM and their genetic codes are yet poorly understood, but recently discovered accumulations of cytochromes and nanowire connections in the intercellular space of the consortia suggest direct electron transfer between both partners

The human cytomegalovirus glycoprotein pUL11 acts via CD45 to induce T cell IL-10 secretion.

Human Cytomegalovirus (HCMV) is a widespread pathogen, infection with which can cause severe disease for immunocompromised individuals. The complex changes wrought on the host's immune system during both productive and latent HCMV infection are well known. Infected cells are masked and manipulated and uninfected immune cells are also affected; peripheral blood mononuclear cell (PBMC) proliferation is reduced and cytokine profiles altered. Levels increase of the anti-inflammatory cytokine IL-10, which may be important for the establishment of HCMV infections and is required for the development of high viral titres by murine cytomegalovirus. The mechanisms by which HCMV affects T cell IL-10 secretion are not understood. We show here that treatment of PBMC with purified pUL11 induces IL-10 producing T cells as a result of pUL11 binding to the CD45 phosphatase on T cells. IL-10 production induced by HCMV infection is also in part mediated by pUL11. Supernatants from pUL11 treated cells have anti-inflammatory effects on untreated PBMC. Considering the mechanism, CD45 can be a positive or negative regulator of TCR signalling, depending on its expression level, and we show that pUL11 also has concentration dependent activating or inhibitory effects on T cell proliferation and on the kinase function of the CD45 substrate Lck. pUL11 is therefore the first example of a viral protein that can target CD45 to induce T cells with anti-inflammatory properties. It is also the first HCMV protein shown to induce T cell IL-10 secretion. Understanding the mechanisms by which pUL11-induced changes in signal strength influence T cell development and function may provide the basis for the development of novel antiviral treatments and therapies against immune pathologies