Publications by authors named "Christina L Ohland"

Background: Oat has been widely accepted as a key food for human health. It is becoming increasingly evident that individual differences in metabolism determine how different individuals benefit from diet. Both host genetics and the gut microbiota play important roles on the metabolism and function of dietary compounds.

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The intestinal microbiota is comprises a diverse community of micro-organisms that interact with many host processes. Innate immune responses to the gut microbiota are of particular importance as they influence many other downstream responses. This fascinating host-microbe crosstalk is a rapidly expanding field of study; thus, it is critical to ensure reproducibility between studies and applicability to human clinical trials through standardization of experiments.

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Intestinal epithelial Na/H exchange facilitated by the apical NHE3 (Slc9a3) is a highly regulated process inhibited by intestinal pathogens and in inflammatory bowel diseases. NHE3 mice develop spontaneous, bacterially mediated colitis, and IBD-like dysbiosis. Disruption of epithelial Na/H exchange in IBD may thus represent a host response contributing to the altered gut microbial ecology, and may play a pivotal role in modulating the severity of inflammation in a microbiome-dependent manner.

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Intestinal tuft cells are a rare, poorly understood cell type recently shown to be a critical mediator of type 2 immune response to helminth infection. Here, we present advances in segmentation algorithms and analytical tools for multiplex immunofluorescence (MxIF), a platform that enables iterative staining of over 60 antibodies on a single tissue section. These refinements have enabled a comprehensive analysis of tuft cell number, distribution, and protein expression profiles as a function of anatomical location and physiological perturbations.

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Objectives: Western-style diets high in saturated fat and refined carbohydrate have been shown to alter gut microbiota as well as being associated with altered behaviour and learning ability. The objective of this study was to determine the effects of short-term intake of a Western-style diet on intestinal cytokine expression, tryptophan metabolism, and levels of neurotransmitters in the brain.

Methods: At 7 weeks of age, 129S1/SvImJ mice were placed on a standard chow or Western-style diet (fat 33%, refined carbohydrates 49%) for 3 weeks.

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The concept that the intestinal microbiota modulates numerous physiological processes including immune development and function, nutrition and metabolism as well as pathogen exclusion is relatively well established in the scientific community. The molecular mechanisms driving these various effects and the events leading to the establishment of a "healthy" microbiome are slowly emerging. The objective of this review is to bring into focus important aspects of microbial/host interactions in the intestine and to discuss key molecular mechanisms controlling health and disease states.

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Obesity and the associated state of subchronic inflammation are risk factors for numerous pathologies, including carcinogenesis. Recently, Schulz et al. (2014) demonstrated that high-fat diet-induced intestinal dysbiosis promotes cancer development in K-ras(G12Dint) mice without inducing obesity or mucosal inflammation, positioning microbial activities as a central component of diet-induced carcinogenesis.

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Modulation of the gut microbiota with diet and probiotic bacteria can restore intestinal homeostasis in inflammatory conditions and alter behavior via the gut-brain axis. The purpose of this study was to determine whether the modulatory effects of probiotics differ depending on diet and mouse genotype. At weaning, wild type (WT) and IL-10 deficient (IL-10(-/-)) 129/SvEv mice were placed on a standard mouse chow or a Western-style diet (fat 33%, refined carbohydrate 49%)±Lactobacillus helveticus ROO52 (10(9)cfu/d) for 21 days.

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Both pathogenic and commensal strains of Escherichia coli colonize the human intestinal tract. Pathogenic strains differ only in the expression of virulence factors, many of which comprise a type III secretion system (TTSS). Little is known regarding the effect of E.

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The intestinal tract is a diverse microenvironment where more than 500 species of bacteria thrive. A single layer of epithelium is all that separates these commensal microorganisms and pathogens from the underlying immune cells, and thus epithelial barrier function is a key component in the arsenal of defense mechanisms required to prevent infection and inflammation. The epithelial barrier consists of a dense mucous layer containing secretory IgA and antimicrobial peptides as well as dynamic junctional complexes that regulate permeability between cells.

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Proteinase-activated receptor (PAR)(2) is activated by trypsin-like serine proteinases and has been implicated in intestinal inflammation. However, its role in the regulation of intestinal mucosal function remains unclear. Using the intestinal epithelial cell line, SCBN, we have studied the stimulus-secretion coupling mechanisms of PAR(2)-induced epithelial chloride transport, focusing on cyclooxygenase (COX)-1 and COX-2 activities and prostaglandin (PG) E(2) secretion.

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