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A microfluidic chip approach utilising integrated electrically connected stationary SERS targets based on inkjet-printed silver nanoparticles is presented. It enables multiple interference-free consecutive surface-enhanced Raman measurements inside chip channels by electrically assisted regeneration of the stationary SERS substrate. Thereby it circumvents common adsorption and memory effect problems associated with stationary SERS targets allowing multiple consecutive measurements in a continuous-flow system. [ABSTRACT FROM AUTHOR]

The intestinal mucosa contains the largest population of antibody-secreting plasma cells in the body, and in humans several grams of secretory immunoglobulin A (SIgA) are released into the intestine each day. In the gut lumen, SIgA serves as a first-line barrier that protects the epithelium from pathogens and toxins. Recently, next-generation sequencing has revolutionized our understanding of the nature of the intestinal microbiota and has also shed new light on the important roles of SIgA in the regulation of host-commensal homeostasis. Here, I discuss pathways of IgA induction in the context of SIgA specificity and function. [ABSTRACT FROM AUTHOR]

Background Enterochromaffin cells and enteric neurons synthesize and release serotonin (5-HT). Reuptake, mediated by a plasmalemmal transporter (SERT) terminates the action of released 5-HT. Serotonin secretion and serotonin reuptake transporter (SERT) expression have been reported to be decreased in TNBS-induced experimental colitis and in patients with ulcerative colitis. The present study was designed to utilize the transgenic deletion of SERT as a gain-of-function model to test the hypothesis that 5-HT is a pro-inflammatory mediator in experimental colitis. Methods Colitis was compared in animals with IL10+/+SERT+/+ (wild-type), IL10−/−SERT+/+, IL10−/−SERT+/−, and IL10−/−/SERT−/− (double knockout) genotypes. Macroscopic and histological damage scores were evaluated after a time period of up to 15 weeks. Key Results Serotonin reuptake transporter expression was significantly increased in the inflamed colons of IL-10−/− mice, which displayed intestinal damage and a minor decrement in general health. General health was significantly worse and intestinal inflammation was more severe in IL-10−/−SERT+/−, and IL-10−/−SERT−/− mice than in IL-10−/−SERT+/+ or wild-type animals. Regardless of the associated SERT genotype, the number of 5-HT-immunoreactive cells was decreased by ∼55–65% in all mice lacking IL-10. Conclusions & Inferences Our observations indicate that colitis associated with IL-10 deficient mice is enhanced when the IL-10 deficiency is combined with a SERT deficiency. The data support the concept that 5-HT is a pro-inflammatory mediator in the gut. [ABSTRACT FROM AUTHOR]

NKX2 genes in vertebrates encode a sub- family of homeodomain-containing transcription factors which regulate morphogenetic events and cell differentiation during embryogenesis. In mouse embryos several NKX2 genes are expressed in the ventral midline domains of the neuroectoderm, while other NKX2 genes are primarily expressed in the mesendoderm and mesendodermally derived organs, such as heart and gut. Within several patterning centers for tissue organization sonic hedgehog (Shh) is an important signal in the formation of ventral midline structures in vertebrate embryos. Here, we investigated the role of Shh in the embryonic expression of six different but closely related NKX2 genes in Shh null mutant mice. We found that expression of NKX2.1, NKX2.2, and NKX2.9 in neural domains requires Shh signaling, whereas NKX2.3, NKX2.5 and NKX2.6 expression in endoderm and mesoderm is independent of Shh. [ABSTRACT FROM AUTHOR]