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Presumed hydrogen sulfide-mediated neurotoxicity after streptococcus anginosus group meningitis.

ABSTRACT: Hydrogen sulfide is an environmental toxicant and gaseous neurotransmitter. It is produced enterically by sulfur-reducing bacteria and invasive pathogens including Streptococcus anginosus group, Salmonella and Citrobacter. We describe putative focal hydrogen sulfide neurotoxicity after Streptococcus constellatus meningitis, treated with adjunctive sodium nitrite and hyperbaric oxygen therapy.

SUBMITTER: Verma S

PROVIDER: S-EPMC3548939 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature

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Presumed hydrogen sulfide-mediated neurotoxicity after streptococcus anginosus group meningitis.

Verma Sumit S Landisch Rachel R Quirk Brendan B Schmainda Kathleen K Prah Melissa M Whelan Harry T HT Willoughby Rodney E RE

The Pediatric infectious disease journal 20130201 2

Hydrogen sulfide is an environmental toxicant and gaseous neurotransmitter. It is produced enterically by sulfur-reducing bacteria and invasive pathogens including Streptococcus anginosus group, Salmonella and Citrobacter. We describe putative focal hydrogen sulfide neurotoxicity after Streptococcus constellatus meningitis, treated with adjunctive sodium nitrite and hyperbaric oxygen therapy. ...[more]

PMID: 23014355

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Hydrogen sulfide, endoplasmic reticulum stress and alcohol mediated neurotoxicity.

Project description:Alcohol is one of the most socially accepted addictive drugs in modern society. Its abuse affects virtually all organ systems with the central nervous system (CNS) being particularly vulnerable to excessive alcohol exposure. Alcohol exposure also causes profound damage to both the adult and developing brain. Excessive alcohol consumption induces numerous pathophysiological stress responses, one of which is the endoplasmic reticulum (ER) stress response. Potential mechanisms that trigger the alcohol induced ER stress response are either directly or indirectly related to alcohol metabolism, which include toxic levels of acetaldehyde and homocysteine, oxidative stress and abnormal epigenetic modifications. Growing evidence suggests that H2S is the most recently recognized gasotransmitter with tremendous physiological protective functions against oxidative stress induced neurotoxicity. In this review we address the alcohol induced oxidative stress mediated ER stress and the role of H2S in its mitigation in the context of alcohol neurotoxicity. Interruption of ER stress triggers is anticipated to have therapeutic benefits for alcohol mediated diseases and disorders.

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An unusual case of Streptococcus anginosus group pyomyositis diagnosed using direct 16S ribosomal DNA sequencing.

Project description:Bacteria belonging to the Streptococcus anginosus group (Streptococcus intermedius, Streptococcus constellatus and Streptococcus anginosus) are capable of causing serious pyogenic infections, with a tendency for abscess formation. The present article reports a case of S anginosus group pyomyositis in a 47-year-old man. The pathogen was recovered from one of two blood cultures obtained from the patient, but speciation was initially not performed because the organism was considered to be a contaminant (viridans streptococci group). The diagnosis was ultimately confirmed using 16S ribosomal DNA sequencing of purulent fluid obtained from a muscle abscess aspirate. The present case serves to emphasize that finding even a single positive blood culture of an organism belonging to the S anginosus group should prompt careful evaluation of the patient for a pyogenic focus of infection. It also highlights the potential utility of 16S ribosomal DNA amplification and sequencing in direct pathogen detection from aspirated fluid in cases of pyomyositis in which antimicrobial therapy was initiated before specimen collection.

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Angicin, a novel bacteriocin of Streptococcus anginosus.

Project description:As a conserved defense mechanism, many bacteria produce antimicrobial peptides, called bacteriocins, which provide a colonization advantage in a multispecies environment. Here the first bacteriocin of Streptococcus anginosus, designated Angicin, is described. S. anginosus is commonly described as a commensal, however it also possesses a high pathogenic potential. Therefore, understanding factors contributing to its host colonization and persistence are important. A radial diffusion assay was used to identify S. anginosus BSU 1211 as a potent bacteriocin producer. By genetic mutagenesis the background of bacteriocin production and the bacteriocin gene itself were identified. Synthetic Angicin shows high activity against closely related streptococci, listeria and vancomycin resistant enterococci. It has a fast mechanism of action and causes a membrane disruption in target cells. Angicin, present in cell free supernatant, is insensitive to changes in temperature from - 70 to 90 °C and pH values from 2 to 10, suggesting that it represents an interesting compound for potential applications in food preservation or clinical settings.

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CC17 group B Streptococcus exploits integrins for neonatal meningitis development.

Project description:Group B Streptococcus (GBS) is the major cause of human neonatal infections. A single clone, designated CC17-GBS, accounts for more than 80% of meningitis cases, the most severe form of the infection. However, the events allowing blood-borne GBS to penetrate the brain remain largely elusive. In this study, we identified the host transmembrane receptors α5β1 and αvβ3 integrins as the ligands of Srr2, a major CC17-GBS-specific adhesin. Two motifs located in the binding region of Srr2 were responsible for the interaction between CC17-GBS and these integrins. We demonstrated in a blood-brain-barrier cellular model that both integrins contributed to the adhesion and internalization of CC17-GBS. Strikingly, both integrins were overexpressed during the postnatal period in the brain vessels of the blood-brain barrier and blood-cerebrospinal fluid barrier and contributed to juvenile susceptibility to CC17 meningitis. Finally, blocking these integrins decreased the ability of CC17-GBS to cross into the CNS of juvenile mice in an in vivo model of meningitis. Our study demonstrated that CC17-GBS exploits integrins in order to cross the brain vessels, leading to meningitis. Importantly, it provides host molecular insights into neonate's susceptibility to CC17-GBS meningitis, thereby opening new perspectives for therapeutic and prevention strategies of GBS-elicited meningitis.

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Group A Streptococcus strains causing meningitis without distinct invasive phenotype

Project description: Not available

| S-EPMC10765256 | biostudies-literature

Horizontal transfer of segments of the 16S rRNA genes between species of the Streptococcus anginosus group.

Project description:The nature in variation of the 16S rRNA gene of members of the Streptococcus anginosus group was investigated by hybridization and DNA sequencing. A collection of 708 strains was analyzed by reverse line blot hybridization. This revealed the presence of distinct reaction patterns representing 11 different hybridization groups. The 16S rRNA genes of two strains of each hybridization group were sequenced to near-completion, and the sequence data confirmed the reverse line blot hybridization results. Closer inspection of the sequences revealed mosaic-like structures, strongly suggesting horizontal transfer of segments of the 16S rRNA gene between different species belonging to the Streptococcus anginosus group. Southern blot hybridization further showed that within a single strain all copies of the 16S rRNA gene had the same composition, indicating that the apparent mosaic structures were not PCR-induced artifacts. These findings indicate that the highly conserved rRNA genes are also subject to recombination and that these events may be fixed in the population. Such recombination may lead to the construction of incorrect phylogenetic trees based on the 16S rRNA genes.

| S-EPMC296235 | biostudies-literature

Hydrogen Sulfide-Mediated Polyamines and Sugar Changes Are Involved in Hydrogen Sulfide-Induced Drought Tolerance in Spinacia oleracea Seedlings.

Project description:Hydrogen sulfide (H2S) is a newly appreciated participant in physiological and biochemical regulation in plants. However, whether H2S is involved in the regulation of plant responses to drought stress remains unclear. Here, the role of H2S in the regulation of drought stress response in Spinacia oleracea seedlings is reported. First, drought stress dramatically decreased the relative water content (RWC) of leaves, photosynthesis, and the efficiency of PSII. Moreover, drought caused the accumulation of ROS and increased the MDA content. However, the application of NaHS counteracted the drought-induced changes in these parameters. Second, NaHS application increased the water and osmotic potential of leaves. Additionally, osmoprotectants such as proline and glycinebetaine (GB) content were altered by NaHS application under drought conditions, suggesting that osmoprotectant contributes to H2S-induced drought resistance. Third, the levels of soluble sugars and polyamines (PAs) were increased differentially by NaHS application in S. oleracea seedlings. Moreover, several genes related to PA and soluble sugar biosynthesis, as well as betaine aldehyde dehydrogenase (SoBADH), choline monooxygenase (SoCMO), and aquaporin (SoPIP1;2), were up-regulated by H2S under drought stress. These results suggest that H2S contributes to drought tolerance in S. oleracea through its effect on the biosynthesis of PAs and soluble sugars. Additionally, GB and trehalose also play key roles in enhancing S. oleracea drought resistance.

| S-EPMC4972840 | biostudies-literature

Characterizing a mouse model for evaluation of countermeasures against hydrogen sulfide-induced neurotoxicity and neurological sequelae.

Project description:Hydrogen sulfide (H2 S) is a highly neurotoxic gas. It is the second most common cause of gas-induced deaths. Beyond mortality, surviving victims of acute exposure may suffer long-term neurological sequelae. There is a need to develop countermeasures against H2 S poisoning. However, no translational animal model of H2 S-induced neurological sequelae exists. Here, we describe a novel mouse model of H2 S-induced neurotoxicity for translational research. In paradigm I, C57/BL6 mice were exposed to 765 ppm H2 S for 40 min on day 1, followed by 15-min daily exposures for periods ranging from 1 to 6 days. In paradigm II, mice were exposed once to 1000 ppm H2 S for 60 minutes. Mice were assessed for behavioral, neurochemical, biochemical, and histopathological changes. H2 S intoxication caused seizures, dyspnea, respiratory depression, knockdowns, and death. H2 S-exposed mice showed significant impairment in locomotor and coordinated motor movement activity compared with controls. Histopathology revealed neurodegenerative lesions in the collicular, thalamic, and cortical brain regions. H2 S significantly increased dopamine and serotonin concentration in several brain regions and caused time-dependent decreases in GABA and glutamate concentrations. Furthermore, H2 S significantly suppressed cytochrome c oxidase activity and caused significant loss in body weight. Overall, male mice were more sensitive than females. This novel translational mouse model of H2 S-induced neurotoxicity is reliable, reproducible, and recapitulates acute H2 S poisoning in humans.

| S-EPMC6383676 | biostudies-literature

Gene Expression Analysis of Carbonyl Sulfide Neurotoxicity

Project description:To gain insight into the pathogenesis of carbonyl sulfide induced neurotoxicity, we examined the gene expression profile of exposed rats before the onset of morphological changes (days 1 and 2) using the most consistently affected brain region, the posterior colliculus.

2009-07-07 | GSE12018 | GEO

Hydrogen Sulfide in Pharmacotherapy, Beyond the Hydrogen Sulfide-Donors.

Project description:Hydrogen sulfide (H2S) is one of the important biological mediators involved in physiological and pathological processes in mammals. Recently developed H2S donors show promising effects against several pathological processes in preclinical and early clinical studies. For example, H2S donors have been found to be effective in the prevention of gastrointestinal ulcers during anti-inflammatory treatment. Notably, there are well-established medicines used for the treatment of a variety of diseases, whose chemical structure contains sulfur moieties and may release H2S. Hence, the therapeutic effect of these drugs may be partly the result of the release of H2S occurring during drug metabolism and/or the effect of these drugs on the production of endogenous hydrogen sulfide. In this work, we review data regarding sulfur drugs commonly used in clinical practice that can support the hypothesis about H2S-dependent pharmacotherapeutic effects of these drugs.

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