Vasoactive intestinal peptide induces IL-8 production in human colonic epithelial cells via MAP kinase-dependent and PKA-independent pathways

Toumi, Férial; Neunlist, Michel; Denis, Marc G.; Oreshkova, Tsvetelina; Laboisse, Christian L.; Galmiche, Jean–Paul; Jarry, Anne

doi:10.1016/j.bbrc.2004.03.033

Cited by 31 publications

(28 citation statements)

References 19 publications

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“…Moreover, two coculture models, consisting of human submucosa containing the submucosal neuronal network and human fully differentiated, mucus-secreting HT29-Cl.16E or enterocyte-like Caco-2 monolayers, have been described. These models have been used to investigate the effects of submucosal neuron activation by electrical field stimulation on cell proliferation (239) and on the VIPergic neuronal pathway controlling the paracellular permeability and structural organization of TJs (70) and the PKA-independent and MAPK-dependent IL-8 production (240). In addition, an interesting in vitro three-dimensional organoid culture using intestinal stem cells has also been developed (873,874).…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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Section: Discussionmentioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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“…Asterisks indicate blood vessel walls regulation of the proliferation of intestinal epithelial cells [32]. VIP has also been reported to play an immunomodulatory role in intestinal epithelial cells via the regulation of IL-8 secretion [33].…”

Section: Discussionmentioning

confidence: 99%

Epithelial Expression of Vasoactive Intestinal Peptide in Ulcerative Colitis: Down-Regulation in Markedly Inflamed Colon

2011

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The findings suggest that there is a local production of VIP in the epithelial cells in normal and slightly/moderately inflamed mucosa but not in severely inflamed mucosa. Furthermore, a marked downregulation in VPAC1 receptor expressions occurs in the epithelium in severe UC. Based on the knowledge that VIP can have trophic, healing and anti-inflammatory effects, it is likely that the decrease in VIP mRNA and VPAC1 receptor reactions seen in severely affected mucosa in UC may be associated with adverse effects on intestinal function.

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“…The figure shows transmission electron micrographs of ultrastructural characteristics of mucosal mast cells: a resting mast cell in health (H ), with granules filled (white arrows) and no signs of degranulation; piecemeal degranulation in a mast cell from a patient with irritable bowel syndrome (IBS), identified by partial or total emptiness of granules content (black arrows) and intact granules (white arrow); and anaphylactic degranulation in a mast cell from a food allergy patient (FA), identified by fusion of granule membranes devoid of content (black arrow). Barr indicates 2 μm [166,167]. Psychological stress increases vasoactive intestinal peptide levels in the small intestine of mice [168] and vasoactive intestinal peptide has been implicated in the regulation of the intestinal barrier function, through its direct effect on tight junction-associated protein, ZO-1, in epithelial cells [169].…”

Section: Stress Hormones and Neurotransmittersmentioning

confidence: 99%

Intestinal Barrier Function and the Brain-Gut Axis

Alonso

Vicario

Pigrau

et al. 2014

Advances in Experimental Medicine and Biology

105

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The luminal-mucosal interface of the intestinal tract is the first relevant location where microorganism-derived antigens and all other potentially immunogenic particles face the scrutiny of the powerful mammalian immune system. Upon regular functioning conditions, the intestinal barrier is able to effectively prevent most environmental and external antigens to interact openly with the numerous and versatile elements that compose the mucosal-associated immune system. This evolutionary super system is capable of processing an astonishing amount of antigens and non-immunogenic particles, approximately 100 tons in one individual lifetime, only considering food-derived components. Most important, to develop oral tolerance and proper active immune responses needed to prevent disease and inflammation, this giant immunogenic load has to be managed in a way that physiological inflammatory balance is constantly preserved. Adequate functioning of the intestinal barrier involves local and distant regulatory networks integrating the so-called brain-gut axis. Along this complex axis both brain and gut structures participate in the processing and execution of response signals to external and internal changes coming from the digestive tract, using multidirectional pathways to communicate. Dysfunction of brain-gut axis facilitates malfunctioning of the intestinal barrier, and vice versa, increasing the risk of uncontrolled immunological reactions that may trigger mucosal and brain low-grade inflammation, a putative first step to the initiation of more permanent gut disorders. In this chapter, we describe the structure, function and interactions of intestinal barrier, microbiota and brain-gut axis in both healthy and pathological conditions.

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Vasoactive intestinal peptide induces IL-8 production in human colonic epithelial cells via MAP kinase-dependent and PKA-independent pathways

Cited by 31 publications

References 19 publications

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Epithelial Expression of Vasoactive Intestinal Peptide in Ulcerative Colitis: Down-Regulation in Markedly Inflamed Colon

Intestinal Barrier Function and the Brain-Gut Axis

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