![]() (A) Recombinant SPRR2A was expressed in a baculovirus expression system and purified by size exclusion chromatography. Values were normalized to Gapdh expression. PBS was administered as a vehicle control. ( I) qPCR analysis of Sprr2a expression in the small intestines of germ-free Swiss-Webster mice treated with lipopolysaccharide (LPS). ![]() ![]() Epithelial cells were harvested by laser capture microdissection. ( H) qPCR analysis of epithelial cell Sprr2a expression in germ-free (GF) wild-type (WT) and Myd88-deficient ( Myd88 −/−) C57BL/6 mice with or without conventionalization (CV). (G) Immunoblot detection of SPRR2A protein in mouse colon, the colon mucus layer, and stool samples. ![]() (F) Immunofluorescence detection of SPRR2A (red) in OCT-embedded frozen sections of mouse small-intestinal organoids. Sections from Sprr2a −/− mice (generated as shown in fig. Nuclei were detected with 4’,6-diamidino-2-phenylindole (DAPI). Ulex europaeus agglutinin-I (UEA-I) (D) and anti-lysozyme antibody (E) were used to identify goblet cells (UEA-I) and Paneth cells (UEA-I and anti-lysozyme). ( D and E) Immunofluorescence detection of SPRR2A (red) in sections of paraffin-embedded mouse small intestine. Examples of positive signals are indicated by yellow arrowheads. (C) In situ hybridization of small intestine sections with anti-sense and sense Sprr2a RNA probes. Values were normalized to 18 S rRNA expression. (B) qPCR analysis of Sprr2a expression in mouse small intestine (SI), small intestinal epithelial cells (IEC) acquired by laser capture microdissection, lamina propria lymphocytes (LPL), and intraepithelial lymphocytes (IEL). Future studies will focus on understanding the mechanisms underlying the microbiota-gut-brain axis and attempt to elucidate microbial-based intervention and therapeutic strategies for neuropsychiatric disorders.īrain-gut microbiome neurogastroenterology second brain stress.(A) Quantitative PCR (qPCR) analysis of Sprr2a expression in various organs of wild-type C57BL/6 mice. Moreover, translational human studies are ongoing and will greatly enhance the field. Animal models have been paramount in linking the regulation of fundamental neural processes, such as neurogenesis and myelination, to microbiome activation of microglia. Much recent work has implicated the gut microbiota in many conditions including autism, anxiety, obesity, schizophrenia, Parkinson's disease, and Alzheimer's disease. Stress, in particular, can significantly impact the microbiota-gut-brain axis at all stages of life. At the other extreme of life, microbial diversity diminishes with aging. Many factors can influence microbiota composition in early life, including infection, mode of birth delivery, use of antibiotic medications, the nature of nutritional provision, environmental stressors, and host genetics. The microbiota and the brain communicate with each other via various routes including the immune system, tryptophan metabolism, the vagus nerve and the enteric nervous system, involving microbial metabolites such as short-chain fatty acids, branched chain amino acids, and peptidoglycans. This axis is gaining ever more traction in fields investigating the biological and physiological basis of psychiatric, neurodevelopmental, age-related, and neurodegenerative disorders. However, the past 15 yr have seen the emergence of the microbiota (the trillions of microorganisms within and on our bodies) as one of the key regulators of gut-brain function and has led to the appreciation of the importance of a distinct microbiota-gut-brain axis. The importance of the gut-brain axis in maintaining homeostasis has long been appreciated.
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