Functional Muffins Exert Bifidogenic Effects along with Highly Product-Specific Effects on the Human Gut Microbiota Ex Vivo.

GoodBiome™ Foods are functional foods containing a probiotic ( HU58™) and prebiotics (mainly inulin). Their effects on the human gut microbiota were assessed using ex vivo SIFR technology, which has been validated to provide clinically predictive insights. GoodBiome™ Foods (BBM/LCM/OSM) were subjected to oral, gastric, and small intestinal digestion/absorption, after which their impact on the gut microbiome of four adults was assessed (n = 3).

Effects of combined prebiotic, probiotic, IgG and amino acid supplementation on the gut microbiome of patients with inflammatory bowel disease.

The effects of the Total Gut Restoration (TGR) system supplementation on the gut microbiome were evaluated. A mucosal simulation of the human gastrointestinal tract (M-SHIME) system was inoculated with fecal samples from patients with inflammatory bowel disease. Chambers were supplemented for 5 days with the TGR system (five probiotic strains, prebiotic mixture, immunoglobulin concentrate, amino acids and prebiotic flavonoids).

Treatment with a spore-based probiotic containing five strains of Bacillus induced changes in the metabolic activity and community composition of the gut microbiota in a SHIME® model of the human gastrointestinal system.

MegaSporeBiotic™ is an oral, spore-based probiotic comprised of five Bacillus spp. (Bacillus indicus HU36, Bacillus subtilis HU58, Bacillus coagulans SC208, Bacillus licheniformis SL307, and Bacillus clausii SC109). The effects of MegaSporeBiotic™ on gut microbiota activity and community composition were evaluated for the first time using an in vitro model of the human gastrointestinal tract, the simulator of the human intestinal microbial ecosystem (SHIME®), under healthy conditions.

An Oral Formulation of the Probiotic, HU58, Was Safe and Well Tolerated in a Pilot Study of Patients with Hepatic Encephalopathy.

Background: Hepatic encephalopathy often results in high blood ammonia levels because of inefficient ammonia processing by the liver. Lactulose treatment promotes the growth of urease-producing gut bacteria and a reduced colon pH, thus reducing blood ammonia absorption. It is thought that probiotics as an add-on therapy may be beneficial.

HU58 and SC208 Probiotics Reduced the Effects of Antibiotic-Induced Gut Microbiome Dysbiosis in An M-SHIME Model.

Benefits associated with probiotic use have been reported; however, the mechanisms behind these benefits are poorly understood. The effects of a probiotic formulation (MegaDuo™) containing SC208 and HU58 on intestinal permeability and immune markers was assessed using a combination of the in vitro gut model, the mucosal simulator of the human intestinal microbial ecosystem (M-SHIME), and an in vitro inflammatory bowel disease-like Caco-2/THP1 co-culture model in both healthy and antibiotic-induced dysbiosis conditions. Established M-SHIME proximal colon vessels were treated with/without clindamycin (1 week) and then with/without daily MegaDuo™ treatment (2 weeks).

Correction: Generation and Improvement of Effector Function of a Novel Broadly Reactive and Protective Monoclonal Antibody against Pneumococcal Surface Protein A of Streptococcus pneumoniae.

[This corrects the article DOI: 10.1371/journal.pone.

Generation and Improvement of Effector Function of a Novel Broadly Reactive and Protective Monoclonal Antibody against Pneumococcal Surface Protein A of Streptococcus pneumoniae.

A proof-of-concept study evaluating the potential of Streptococcus pneumoniae Pneumococcal Surface Protein A (PspA) as a passive immunization target was conducted. We describe the generation and isolation of several broadly reactive mouse anti-PspA monoclonal antibodies (mAbs). MAb 140H1 displayed (i) 98% strain coverage, (ii) activity in complement deposition and opsonophagocytic killing (OPK) assays, which are thought to predict the in vivo efficacy of anti-pneumococcal mAbs, (iii) efficacy in mouse sepsis models both alone and in combination with standard-of-care antibiotics, and (iv) therapeutic activity in a mouse pneumonia model.

The transcriptional regulator Nrg1p controls Candida albicans biofilm formation and dispersion.

The ability of Candida albicans to reversibly switch morphologies is important for biofilm formation and dispersion. In this pathogen, Nrg1p functions as a key negative regulator of the yeast-to-hypha morphogenetic transition. We have previously described a genetically engineered C.

YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia.

Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.

Results: Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection.

Yersinia pestis CO92 delta yopH is a potent live, attenuated plague vaccine.

An in-frame deletion of the yopH gene in Yersinia pestis CO92 attenuates virulence in both bubonic and pneumonic plague models. When it is used as a live, attenuated vaccine, CO92 delta yopH provides a high degree of protection from parental and respiratory challenge with Y. pestis CO92.

Delayed inflammatory response to primary pneumonic plague occurs in both outbred and inbred mice.

Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses the innate immune response to infection.