Oral on mice endometritis through uterine microbiome and metabolic alternations.

Endometritis occurs frequently in humans and animals, which can negatively affect fertility and cause preterm parturition syndrome. Orally administered , a butyrate-producing gram-positive anaerobe, exhibits anti-inflammatory effects. However, the precise mechanism by which attenuates endometritis remains unclear.

Association between the gut microbiome and organic acid profiles in a Japanese population with HIV infection.

Introduction: An increased incidence of metabolic syndrome has been observed in human immunodeficiency virus (HIV)-infected individuals. In contrast, gut dysbiosis is involved in various pathogeneses, including vascular endothelial disorders. Organic acids, including short-chain fatty acids (SCFAs), are essential for maintaining gut homeostasis.

Mycobiome and Mycobiome-Associated Diseases.

The human body is host to a large number of commensal microbial species such as bacteria, fungi, and viruses. Among these, the human mycobiome is often neglected as a potential cause of disease, as it is thought to be comparatively much less abundant and less diverse than the human bacteriome. Additionally, most fungi are not easily cultured, even in specific media.

First case of bacteremia caused by Cetobacterium somerae following necrotizing cholecystitis.

Cetobacterium somerae, a gram-negative anaerobic rod, first identified in the feces of children with autism, also colonize freshwater fish intestinal tract. However there have been no reports of human C. somerae infection.

Clostridium butyricum-induced ω-3 fatty acid 18-HEPE elicits anti-influenza virus pneumonia effects through interferon-λ upregulation.

The precise mechanism by which butyrate-producing bacteria in the gut contribute to resistance to respiratory viral infections remains to be elucidated. Here, we describe a gut-lung axis mechanism and report that orally administered Clostridium butyricum (CB) enhances influenza virus infection resistance through upregulation of interferon (IFN)-λ in lung epithelial cells. Gut microbiome-induced ω-3 fatty acid 18-hydroxy eicosapentaenoic acid (18-HEPE) promotes IFN-λ production through the G protein-coupled receptor (GPR)120 and IFN regulatory factor (IRF)-1/-7 activations.

Effect of on Gastrointestinal Infections.

is a human commensal bacterium with beneficial effects including butyrate production, spore formation, increasing levels of beneficial bacteria, and inhibition of pathogenic bacteria. Owing to its preventive and ameliorative effects on gastrointestinal infections, MIYAIRI 588 (CBM 588) has been used as a probiotic in clinical and veterinary medicine for decades. This review summarizes the effects of , including CBM 588, on bacterial gastrointestinal infections.

MIYAIRI 588 Modifies Bacterial Composition under Antibiotic-Induced Dysbiosis for the Activation of Interactions via Lipid Metabolism between the Gut Microbiome and the Host.

The gut microbiome is closely related to gut metabolic functions, and the gut microbiome and host metabolic functions affect each other. MIYAIRI 588 (CBM 588) upregulates protectin D1 production in host colon tissue following G protein-coupled receptor (GPR) 120 activation to protect gut epithelial cells under antibiotic-induced dysbiosis. However, how CBM 588 enhances polyunsaturated fatty acid (PUFA) metabolites remains unclear.

Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation.

Clostridioides difficile infection (CDI) represents the leading cause of nosocomial diarrhea worldwide and is associated with gut dysbiosis and intestinal damage. Clostridium butyricum MIYAIRI 588 (CBM 588) contributes significantly to reduce epithelial damage. However, the impacts of CBM 588 on antibacterial therapy for CDI are not clear.

MIYAIRI 588-Induced Protectin D1 Has an Anti-inflammatory Effect on Antibiotic-Induced Intestinal Disorder.

Metabolites are thought as the end products in cellular regulatory processes and their levels show the strongest relationships with the phenotype. Previously, we showed that the administration of MIYAIRI 588 (CBM 588) upregulated protectin D1, an anti-inflammatory lipid metabolite, in colon tissue under antibiotic therapy. However, how CBM 588 induces protectin D1 expression and whether the metabolite has anti-inflammatory effects on antibiotic-induced inflammation are unclear.

Clostridium butyricum Modulates the Microbiome to Protect Intestinal Barrier Function in Mice with Antibiotic-Induced Dysbiosis.

Clostridium butyricum MIYAIRI 588 (CBM 588) is a probiotic bacterium that has previously been used to prevent antibiotic-associated diarrhea. However, the underlying mechanism by which CBM 588 protects the gut epithelial barrier remains unclear. Here, we show that CBM 588 increased the abundance of Bifidobacterium, Lactobacillus, and Lactococcus species in the gut microbiome and also enhanced the intestinal barrier function of mice with antibiotic-induced dysbiosis.

Comparative toxicities of silver nitrate, silver nanocolloids, and silver chloro-complexes to Japanese medaka embryos, and later effects on population growth rate.

Fish embryo toxicology is important because embryos are more susceptible than adults to toxicants. In addition, the aquatic toxicity of chemicals depends on water quality. We examined the toxicities to medaka embryos of three types of silver-AgNO, silver nanocolloids (SNCs), and silver ions from silver nanoparticle plates (SNPPs)-under three pH conditions (4.