Butyrate-producing human gut symbiont, Clostridium butyricum, and its role in health and disease.

Clostridium butyricum is a butyrate-producing human gut symbiont that has been safely used as a probiotic for decades. C. butyricum strains have been investigated for potential protective or ameliorative effects in a wide range of human diseases, including gut-acquired infection, intestinal injury, irritable bowel syndrome, inflammatory bowel disease, neurodegenerative disease, metabolic disease, and colorectal cancer. In this review we summarize the studies on C. butyricum supplementation with special attention to proposed mechanisms for the associated health benefits and the supporting experimental evidence. These mechanisms center on molecular signals (especially butyrate) as well as immunological signals in the digestive system that cascade well beyond the gut to the liver, adipose tissue, brain, and more. The safety of probiotic C. butyricum strains appears well-established. We identify areas where additional human randomized controlled trials would provide valuable further data related to the strains' utility as an intervention.

A randomized trial of the bactericidal effects of chlorhexidine vs povidone-iodine vaginal preparation.

BACKGROUND: Precesarean vaginal preparation significantly reduces postpartum infections. Although povidone-iodine is the most commonly used vaginal antiseptic, evidence suggests that chlorhexidine gluconate may be more effective. OBJECTIVE: We aimed to compare the bactericidal effect of chlorhexidine gluconate and povidone-iodine on vaginal bacterial colony counts in pregnancy. MATERIALS AND METHODS: We conducted a prospective randomized controlled trial of vaginal preparation with 0.5% chlorhexidine gluconate vs 10% povidone-iodine vs saline in women undergoing cesarean delivery at ≥34 weeks' gestation. Women in labor or those with ruptured membranes, chorioamnionitis, abnormal placentation, or allergy to study agents were excluded. Vaginal specimens were collected aseptically in the operating room immediately before and 5-10 minutes after vaginal cleansing with 3 sterile sponge sticks. Our primary outcome was postintervention aerobic and anaerobic bacterial colony counts, assessed by blinded investigators. Two-way analysis of variance with simple-effects analysis and Tukey post hoc test were used for multiple group comparisons. Secondary outcomes included baseline colony counts, change in colony counts, adverse events, and maternal infections. RESULTS: A total of 29 women consented and underwent vaginal preparation with chlorhexidine gluconate (n=10), povidone-iodine (n=9), or saline (n=10). Groups were similar with respect to maternal age, body mass index, race, ethnicity, parity, group B streptococcus status, and gestational age. There were no differences in baseline colony counts. Vaginal preparation with povidone-iodine resulted in lower aerobic and anaerobic colony counts compared with chlorhexidine gluconate and saline (P≤.01 and P≤.0001, respectively). Povidone-iodine eliminated more than 99.9% of bacteria, whereas chlorhexidine gluconate and saline eliminated more than 99% and 95% of bacteria, respectively. Although all agents decreased aerobic and anaerobic bacterial counts, 0.5% chlorhexidine gluconate was no more effective than saline in reducing anaerobic bacteria. There were no reported adverse effects or postpartum infections. CONCLUSION: Compared with 0.5% chlorhexidine gluconate, 10% povidone-iodine was more effective in reducing vaginal bacterial colony counts before cesarean delivery.

Omega-3 fatty acids suppress Fusobacterium nucleatum-induced placental inflammation originating from maternal endothelial cells.

Fusobacterium nucleatum is an oral anaerobe prevalent in intrauterine infection associated with a wide spectrum of adverse pregnancy outcomes. We demonstrate here that F. nucleatum triggers placental inflammation through maternal, rather than paternal, TLR4-mediated signaling. Elimination of TLR4 from maternal endothelial cells alleviated placental inflammation and reduced fetal and neonatal death, while elimination of TLR4 in the hematopoietic cells had no effect. The placental inflammatory response followed a spatiotemporal pattern, with NF-κB activation observed first in the maternal endothelial cells and then in the decidual cells surrounding the endothelium, followed by induction of inflammatory cytokines and chemokines. Supplementation of pregnant mice with fish oil as a source of omega-3 fatty acids suppressed placental inflammation, reduced F. nucleatum proliferation in the placenta, and increased fetal and neonatal survival. In vitro analysis illustrates that omega-3 fatty acids inhibit bacterial-induced inflammatory responses from human umbilical cord endothelial cells. Our study therefore reveals a mechanism by which microbial infections affect pregnancy and identifies a prophylactic therapy to protect against intrauterine infections.