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Articles 1 - 6 of 6
Full-Text Articles in Pharmacology, Toxicology and Environmental Health
Exopolysaccharides Regulate Calcium Flow In Cariogenic Biofilms, Monika Astasov-Frauenhoffer, Muth M. Varenganayil, Alan W. Decho, Tuomas Waltimo, Olivier Braissant
Exopolysaccharides Regulate Calcium Flow In Cariogenic Biofilms, Monika Astasov-Frauenhoffer, Muth M. Varenganayil, Alan W. Decho, Tuomas Waltimo, Olivier Braissant
Faculty Publications
Caries-associated biofilms induce loss of calcium from tooth surfaces in the presence of dietary carbohydrates. Exopolysaccharides (EPS) provide a matrix scaffold and an abundance of primary binding sites within biofilms. The role of EPS in binding calcium in cariogenic biofilms is only partially understood. Thus, the aim of the present study is to investigate the relationship between the calcium dissolution rates and calcium tolerance of caries-associated bacteria and yeast as well as to examine the properties of EPS to quantify its binding affinity for dissolved calcium. Calcium dissolution was measured by dissolution zones on Pikovskaya’s agar. Calcium tolerance was assessed …
Hmgb1-Rage Pathway Drives Peroxynitrite Signaling-Induced Ibd-Like Inflammation In Murine Nonalcoholic Fatty Liver Disease, Varun Chandrashekaran, Ratanesh K. Seth, Diptadip Dattaroy, Firas Alhasson, Jacek Ziolenka, James Carson, Franklin G. Berger, Balaraman Kalyanaraman, Anna Mae Diehl, Saurabh Chatterjee
Hmgb1-Rage Pathway Drives Peroxynitrite Signaling-Induced Ibd-Like Inflammation In Murine Nonalcoholic Fatty Liver Disease, Varun Chandrashekaran, Ratanesh K. Seth, Diptadip Dattaroy, Firas Alhasson, Jacek Ziolenka, James Carson, Franklin G. Berger, Balaraman Kalyanaraman, Anna Mae Diehl, Saurabh Chatterjee
Faculty Publications
Recent clinical studies found a strong association of colonic inflammation and Inflammatory bowel disease (IBD)-like phenotype with NonAlcoholic Fatty liver Disease (NAFLD) yet the mechanisms remain unknown. The present study identifies high mobility group box 1 (HMGB1) as a key mediator of intestinal inflammation in NAFLD and outlines a detailed redox signaling mechanism for such a pathway. NAFLD mice showed liver damage and release of elevated HMGB1 in systemic circulation and increased intestinal tyrosine nitration that was dependent on NADPH oxidase. Intestines from NAFLD mice showed higher Toll like receptor 4 (TLR4) activation and proinflammatory cytokine release, an outcome strongly …
Complete Genome Sequence Of Vibrio Gazogenes Atcc 43942, Phani M. Gummadidala, Michael E. Holder, Jacqueline L. O’Brien, Nadim J. Ajami, Joseph F. Petrosino, Chandrani Mitra, Yung Pin Chen, Alan W. Decho, Anindya Chandaa
Complete Genome Sequence Of Vibrio Gazogenes Atcc 43942, Phani M. Gummadidala, Michael E. Holder, Jacqueline L. O’Brien, Nadim J. Ajami, Joseph F. Petrosino, Chandrani Mitra, Yung Pin Chen, Alan W. Decho, Anindya Chandaa
Faculty Publications
Vibrio gazogenes ATCC 43942 has the potential to synthesize a plethora of metabolites which are of clinical and agricultural significance in response to environmental triggers. The complete genomic sequence of Vibrio gazogenes ATCC 43942 is reported herein, contributing to the knowledge base of strains in the Vibrio genus.
Microbial Extracellular Polymeric Substances (Epss) In Ocean Systems, Alan W. Decho, Tony Gutierrez
Microbial Extracellular Polymeric Substances (Epss) In Ocean Systems, Alan W. Decho, Tony Gutierrez
Faculty Publications
Microbial cells (i.e., bacteria, archaea, microeukaryotes) in oceans secrete a diverse array of large molecules, collectively called extracellular polymeric substances (EPSs) or simply exopolymers. These secretions facilitate attachment to surfaces that lead to the formation of structured ‘biofilm’ communities. In open-water environments, they also lead to formation of organic colloids, and larger aggregations of cells, called ‘marine snow.’ Secretion of EPS is now recognized as a fundamental microbial adaptation, occurring under many environmental conditions, and one that influences many ocean processes. This relatively recent realization has revolutionized our understanding of microbial impacts on ocean systems. EPS occur in a range …
Tgf-Beta Triggers Rapid Fibrillogenesis Via A Novel T Beta Rii-Dependent Fibronectin-Trafficking Mechanism, Archana Varadaraj, Laura M. Jenkins, Priyanka Singh, Anindya Chanda, John Snider, N.Y. Lee, Ayelet R. Amsalem-Zafran, Marcelo Ehrlich, Yoav I. Henis, Karthikeyan Mythreye
Tgf-Beta Triggers Rapid Fibrillogenesis Via A Novel T Beta Rii-Dependent Fibronectin-Trafficking Mechanism, Archana Varadaraj, Laura M. Jenkins, Priyanka Singh, Anindya Chanda, John Snider, N.Y. Lee, Ayelet R. Amsalem-Zafran, Marcelo Ehrlich, Yoav I. Henis, Karthikeyan Mythreye
Faculty Publications
Fibronectin (FN) is a critical regulator of extracellular matrix (ECM) remodeling through its availability and stepwise polymerization for fibrillogenesis. Availability of FN is regulated by its synthesis and turnover, and fibrillogenesis is a multistep, integrin-dependent process essential for cell migration, proliferation, and tissue function. Transforming growth factor β (TGF-β) is an established regulator of ECM remodeling via transcriptional control of ECM proteins. Here we show that TGF-β, through increased FN trafficking in a transcription- and SMAD-independent manner, is a direct and rapid inducer of the fibrillogenesis required for TGF-β–induced cell migration. Whereas TGF-β signaling is dispensable for rapid fibrillogenesis, stable …
Altered Gut Microbiome In A Mouse Model Of Gulf War Illness Causes Neuroinflammation And Intestinal Injury Via Leaky Gut And Tlr4 Activation, Firas Alhasson, Suvarthi Das, Ratanesh K. Seth, Diptadip Dattaroy, Varun Chandrashekaran, Caitlin N. Ryan, Luisa S. Chan, Traci Testerman, James Burch, Lorne J. Hofseth, Ronnie Horner, Mitzi Nagarkatti, Prakash Nagarkatti, Stephen M. Lasley, Saurabh Chatterjee
Altered Gut Microbiome In A Mouse Model Of Gulf War Illness Causes Neuroinflammation And Intestinal Injury Via Leaky Gut And Tlr4 Activation, Firas Alhasson, Suvarthi Das, Ratanesh K. Seth, Diptadip Dattaroy, Varun Chandrashekaran, Caitlin N. Ryan, Luisa S. Chan, Traci Testerman, James Burch, Lorne J. Hofseth, Ronnie Horner, Mitzi Nagarkatti, Prakash Nagarkatti, Stephen M. Lasley, Saurabh Chatterjee
Faculty Publications
Many of the symptoms of Gulf War Illness (GWI) that include neurological abnormalities, neuroinflammation, chronic fatigue and gastrointestinal disturbances have been traced to Gulf War chemical exposure. Though the association and subsequent evidences are strong, the mechanisms that connect exposure to intestinal and neurological abnormalities remain unclear. Using an established rodent model of Gulf War Illness, we show that chemical exposure caused significant dysbiosis in the gut that included increased abundance of phylum Firmicutes and Tenericutes, and decreased abundance of Bacteroidetes. Several gram negative bacterial genera were enriched in the GWI-model that included Allobaculum sp. Altered microbiome caused significant decrease …