Abstract: The inventions described herein relate generally to the use of compositions to increase output of acetate and lactate while reducing pH and the levels of pathogenic bacteria and inflammation in the gut of a nursing infant mammal including humans. These compositions generally comprise one or more bacterial strains selected for their growth on mammalian milk oligosaccharides, a source of mammalian milk oligosaccharides, and, optionally, nutritive components required for the growth of that infant mammal.

Abstract: The inventions described herein relate generally to compositions comprising bioactive proteins including, but not limited to, enzymes and antimicrobial proteins. Such bioactive protein compositions may be present alone or in a mammalian milk or soy-based nutritional product to increase colonization of desired commensal organisms, reduce potential pathogens, restore microbiome function, and/or otherwise improve health in a mammal consuming same.

Abstract: The inventions described herein relate generally to the use of compositions to increase output of acetate and lactate while reducing pH and the levels of pathogenic bacteria and inflammation in the gut of a nursing infant mammal including humans. These compositions generally comprise one or more bacterial strains selected for their growth on mammalian milk oligosaccharides, a source of mammalian milk oligosaccharides, and, optionally, nutritive components required for the growth of that infant mammal.

Abstract: Methods of reducing milk glycans, and thus enteric pathogens that use such glycans as carbon sources, in the gut of nursing mammals.

Abstract: This invention provides a method of determining risk of necrotizing enterocolitis (NEC) in an infant, comprising the steps of: (a) obtaining a fecal sample of the infant's relevant microbiome; (b) sequencing genetic material in the sample to obtain sequence data for the relevant microbiome; (c) analyzing sequence data for the relevant microbiome to identify biomarkers in the infant's microbiome; and (d) categorizing the NEC risk of the infant using the biomarkers identified in the microbiome of the infant.

Abstract: Bifidobacterium longum subsp. infantis comprising a functional H5 cluster, including the Bifidobacterium longum subsp. infantis EVC001 deposited under ATCC Accession No. PTA-125180 may be used in compositions for improving gut health in infants and adults.

Abstract: Compositions comprising vitamin A, vitamin D, threonine, mammalian milk oligosaccharides, and Bifidobacterium, B. infantis cell wall components and their uses to treat or prevent diseases, support therapies including metabolic and autoimmune diseases.

Abstract: Mare's milk plays a major role in the health of neonatal foals and may be used for human or other mammalian health. Oligosaccharides (OS) possess various bioactivities in many mammalian milks, and Mare's milk may be a source of novel oligosaccharides. The invention relates to the identification of novel structures in mare's milk that may be synthesized or otherwise purified for use in a variety of animal and human applications related to the gut microbiome and mammalian health.

Abstract: The inventions described herein relate generally to the use of compositions to increase output of particular metabolites in the gut of a nursing infant mammal including humans. These compositions generally comprise one or more bacterial strains selected for their growth on mammalian milk oligosaccharides, a source of mammalian milk oligosaccharides, and, optionally, nutritive components required for the growth of that infant mammal.

Abstract: Methods of reducing milk glycans, and thus enteric pathogens that use such glycans as carbon sources, in the gut of nursing mammals.

Abstract: The inventions described herein relate generally to the methods for monitoring the health of the mammalian gut by checking for whether dysbiotic parameters exceed a threshold level or not. In particular, this invention is directed to the use of parameters which correlate with the level of bifidobacteria, especially Bifidobacterium longum subsp. infantis in the mammalian colon.

Abstract: This invention relates generally to methods and compositions to achieve and maintain a desirable in vivo phenotype during fermentation and processing of food products for human or animal consumption. The methods and compositions of this invention require an activator that acts as a metabolic trigger for Mammalian Milk Oligosaccharide (MMO) consumption phenotype without necessarily requiring oligosaccharides (i.e a sugar polymer of 3 or more monosaccharides) within the fermentation medium. Compositions containing a non-oligosaccharide activator (e.g. monomers and dimers, and combinations thereof) may be used in fermentation processes of this invention. Turning on MMO-related genes without the use of oligosaccharides is one method of preparing activated commensal bacteria.

Abstract: Methods of reducing milk glycans, and thus enteric pathogens that use such glycans as carbon sources, in the gut of nursing mammals.

Abstract: This invention provides compositions of oligosaccharides, their preparation, and their use to facilitate the growth of certain beneficial gut bacteria over other gut bacteria in a mammal in order to prevent gastrointestinal distress associated with a major change in gut microflora, such as that which occurs when an infant is weaned from its mother's milk to alternative food sources, or during the recovery of the gut microbiome after a course of oral antibiotics, hospitalization, therapy such as chemotherapy or radiation treatments, or conditions where a deficiency in dietary fiber is observed. Novel compositions of oligosaccharides, oligosaccharides and bacteria, foods comprising those compositions, and methods of preparation and use of those compositions are described.

Abstract: Compositions comprising at least two non-pathogenic microbes are described herein. The non-pathogenic microbes may be from a first species capable of internalizing and/or metabolizing dietary glycans and/or from a second species capable of consuming and metabolizing free sugar monomers. Methods of making and use in treating and/or preventing the overgrowth of pathogenic bacteria in mammals are also described herein.

Abstract: The inventions described herein relate generally to administering compounds to promote mucosal healing in mammals in need thereof including, but not limited to humans. The compounds may include bifidobacteria and mammalian milk oligosaccharides.

Abstract: Methods of reducing milk glycans, and thus enteric pathogens that use such glycans as carbon sources, in the gut of nursing mammals.

Abstract: The inventions described herein relate generally to the use of compositions to increase output of acetate and lactate while reducing pH and the levels of pathogenic bacteria and inflammation in the gut of a nursing infant mammal including humans. These compositions generally comprise one or more bacterial strains selected for their growth on mammalian milk oligosaccharides, a source of mammalian milk oligosaccharides, and, optionally, nutritive components required for the growth of that infant mammal.

Abstract: Methods of reducing milk glycans, and thus enteric pathogens that use such glycans as carbon sources, in the gut of nursing mammals.

Abstract: The inventions described herein relate generally to digestive healthcare, and more particularly, to the feeding of mammals, particularly human infants, who are making a transition from a microbiome with lower diversity to a microbiome with higher diversity. These inventions relate to certain foods comprising a fermentable nutritional component and a probiotic component, where the probiotic component is selected, based on genetic and/or metabolic criteria, to specifically metabolize any Free Sugar Monomers (FSMs) and Free Amino Acids (FAAs) or peptides that accumulate as a result of the fermentable nutritional component in the lower intestine, where they otherwise might be left in the environment to be fermented and metabolized by less adapted/opportunistic bacteria, creating blooms of deleterious intestinal bacteria and shifting the microbiome to a potentially dysbiotic state.