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Therapeutic Methods and Therapies TCIM
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1.
Gut Microbes ; 16(1): 2297872, 2024.
Article in English | MEDLINE | ID: mdl-38165200

ABSTRACT

Hyperbaric oxygen (HBO) therapy is a well-established method for improving tissue oxygenation and is typically used for the treatment of various inflammatory conditions, including infectious diseases. However, its effect on the intestinal mucosa, a microenvironment known to be physiologically hypoxic, remains unclear. Here, we demonstrated that daily treatment with hyperbaric oxygen affects gut microbiome composition, worsening antibiotic-induced dysbiosis. Accordingly, HBO-treated mice were more susceptible to Clostridioides difficile infection (CDI), an enteric pathogen highly associated with antibiotic-induced colitis. These observations were closely linked with a decline in the level of microbiota-derived short-chain fatty acids (SCFAs). Butyrate, a SCFA produced primarily by anaerobic microbial species, mitigated HBO-induced susceptibility to CDI and increased epithelial barrier integrity by improving group 3 innate lymphoid cell (ILC3) responses. Mice displaying tissue-specific deletion of HIF-1 in RORγt-positive cells exhibited no protective effect of butyrate during CDI. In contrast, the reinforcement of HIF-1 signaling in RORγt-positive cells through the conditional deletion of VHL mitigated disease outcome, even after HBO therapy. Taken together, we conclude that HBO induces intestinal dysbiosis and impairs the production of SCFAs affecting the HIF-1α-IL-22 axis in ILC3 and worsening the response of mice to subsequent C. difficile infection.


Subject(s)
Clostridioides difficile , Clostridium Infections , Gastrointestinal Microbiome , Hyperbaric Oxygenation , Mice , Animals , Nuclear Receptor Subfamily 1, Group F, Member 3 , Immunity, Innate , Hyperbaric Oxygenation/adverse effects , Interleukin-22 , Dysbiosis/therapy , Lymphocytes , Butyrates/pharmacology , Fatty Acids, Volatile/pharmacology , Anti-Bacterial Agents/pharmacology
2.
J Neuroimmunol ; 267(1-2): 28-34, 2014 Feb 15.
Article in English | MEDLINE | ID: mdl-24360909

ABSTRACT

We investigated whether inflammatory mediators during cecal ligation and puncture (CLP)-induced sepsis may diminish copeptin expression in magnocellular neurons, thus affecting arginine-vasopressin (AVP) synthesis. The transcript abundance of IL-1ß, IL-1R1, iNOS and HIF-1α was continuously elevated. IL-1ß, iNOS and cytochrome c protein levels progressively increased until 24h. Immunostaining for these proteins was higher at 6 and 24h, as also seen in the annexin-V assay, while copeptin was continuously decreased. This suggests that increased IL-1ß and NO levels may cause significant bioenergetics changes in magnocellular neurons, affecting copeptin expression and compromising AVP synthesis and secretion in the late phase of sepsis.


Subject(s)
Energy Metabolism/physiology , Gene Expression Regulation/physiology , Glycopeptides/metabolism , Hypothalamus/pathology , Neurons/metabolism , Sepsis/metabolism , Sepsis/pathology , Animals , Annexin A5/metabolism , Arginine Vasopressin/genetics , Arginine Vasopressin/metabolism , Cecum , Disease Models, Animal , Hypoxia-Inducible Factor 1, alpha Subunit/genetics , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Male , Nitric Oxide Synthase Type II/genetics , Nitric Oxide Synthase Type II/metabolism , Optic Chiasm/metabolism , RNA, Messenger/metabolism , Rats , Rats, Wistar , Receptors, Interleukin-1 Type I/genetics , Receptors, Interleukin-1 Type I/metabolism , Sepsis/etiology , Statistics, Nonparametric , Time Factors
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