Carbamylcholine- and catecholamine-induced intracellular calcium dynamics of epithelial cells in mouse ileal crypts

Satoh, Yuichi; Habara, Yoshiaki; Ono, Kazuyuki; Kanno, Tomio

doi:10.1016/0016-5085(95)90681-9

Cited by 85 publications

(64 citation statements)

References 42 publications

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“…To assess the specificity of MDP for the induction of bacteria killing in this assay, we used inactive MDP chiral isomers. As a positive control, we used a muscarinic receptor agonist, carbamylcholine (CCH), that selectively modulates intracellular Ca 2ϩ concentrations and induces secretion of antimicrobials from Paneth cells (26). Although both CCH and MDP could induce bacteria killing, the inactive chiral isomer MDP DD could not (Fig.…”

Section: The Nod2 Ligand Induces Bacteria-killing Activity In Intestimentioning

confidence: 99%

Nod2 is required for the regulation of commensal microbiota in the intestine

Petnicki‐Ocwieja

Hrncírová

Liu

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

503

450

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Mutations in the Nod2 gene are among the strongest genetic risk factors in the pathogenesis of ileal Crohn's disease, but the exact contributions of Nod2 to intestinal mucosal homeostasis are not understood. Here we show that Nod2 plays an essential role in controlling commensal bacterial flora in the intestine. Analysis of intestinal bacteria from the terminal ilea of Nod2-deficient mice showed that they harbor an increased load of commensal resident bacteria. Furthermore, Nod2-deficient mice had a diminished ability to prevent intestinal colonization of pathogenic bacteria. In vitro, intestinal crypts isolated from terminal ilea of Nod2-deficient mice were unable to kill bacteria effectively, suggesting an important role of Nod2 signaling in crypt function. Interestingly, the expression of Nod2 is dependent on the presence of commensal bacteria, because mice re-derived into germ-free conditions expressed significantly less Nod2 in their terminal ilea, and complementation of commensal bacteria into germ-free mice induced Nod2 expression. Therefore, Nod2 and intestinal commensal bacterial flora maintain a balance by regulating each other through a feedback mechanism. Dysfunction of Nod2 results in a break-down of this homeostasis.commensal bacteria ͉ Crohn's disease ͉ mouse ͉ NLR

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Section: The Nod2 Ligand Induces Bacteria-killing Activity In Intestimentioning

confidence: 99%

Nod2 is required for the regulation of commensal microbiota in the intestine

Petnicki‐Ocwieja

Hrncírová

Liu

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

503

450

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“…Paneth cells secrete granules in a dose-dependent manner following interaction with bacterial antigens and in response to pharmacologic stimulation (2,(49)(50)(51). Live gram-negative and gram-positive bacteria and also commercially available preparations of lipopolysaccharide (LPS), lipoteichoic acid (LTA), lipid A, and muramyl dipeptide all induced rapid secretion by mouse Paneth cells.…”

mentioning

confidence: 99%

Mouse Paneth Cell Secretory Responses to Cell Surface Glycolipids of Virulent and Attenuated Pathogenic Bacteria

Tanabe¹,

Ayabe²,

Bainbridge³

et al. 2005

Infect Immun

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The ␣-defensins are 3-to 4-kDa microbicidal peptides expressed by cells of myeloid origin and by epithelial lineages in mammals (30, 58). These cationic, ␤-sheet-containing peptides contain a defining tridisulfide array and amphipathicity that contributes to peptide bactericidal activity by inducing target cell membrane disruption (23,47,53). In cells of myeloid origin, fully processed ␣-defensins accumulate in azurophilic granules of phagocytic leukocytes, from which they function in microbial cell killing by nonoxidative mechanisms following phagolysosomal fusion (17). Epithelial cells on mucosal surfaces also express ␣-or ␤-defensins that may be secreted by apparent constitutive means or as granule constituents of regulated secretory pathways (39,40,44,52). In mouse small intestinal epithelium, exocytotic Paneth cells located at the base of the crypts of Lieberkühn release activated ␣-defensins, termed cryptdins, in response to cholinergic and bacterial stimuli (2, 3, 48, 51).Paneth cells secrete granules in a dose-dependent manner following interaction with bacterial antigens and in response to pharmacologic stimulation (2, 49-51). Live gram-negative and gram-positive bacteria and also commercially available preparations of lipopolysaccharide (LPS), lipoteichoic acid (LTA), lipid A, and muramyl dipeptide all induced rapid secretion by mouse Paneth cells. In contrast, mouse Paneth cells are unresponsive to Candida albicans, Cryptococcus neoformans, and trophozoites of Giardia lamblia (2). Both carbamyl choline and bacterial antigens stimulate Paneth cells in isolated mouse small intestinal crypts to secrete by inducing an increase in cytosolic [Ca 2ϩ ] by the sequential mobilization of intracellular and extracellular Ca 2ϩ stores (3, 49). The inhibition of Paneth cell secretion by highly selective blockers of mIKCa1, a Ca 2ϩ -activated K ϩ channel (3), provided evidence that bacterial antigens also induce secretion by modulating cytosolic Ca 2ϩ dynamics.Bacteria regulate and modify lipid A, the glycolipid anchor of their cell surface LPS, in response to the host microenvironment. For example, growth under Mg 2ϩ limitation results in a modification of lipid A acylation in several bacterial species (13,(19)(20)(21), and the extent of lipid A acylation modulates LPS-mediated bacterial recognition when human host cells are exposed to viable bacteria. pagP, a gene activated by the phoPphoQ regulon of salmonellae, increases lipid A acylation (22,59), and pagP mutants show increased outer membrane permeability to ␣-helical peptides (22), suggesting that lipid A modification may influence sensitivity to endogenous cationic antimicrobial peptides, including ␣-defensins. Also, the prevailing lipid A synthesized by wild-type PAK and PAO-1 strains of Pseudomonas aeruginosa grown in high concentrations of Mg 2ϩ is a penta-acylated form, and growth of P. aeruginosa strains in low concentrations of Mg 2ϩ results in lipid A modification to contain aminoarabinose (4-amino-4-deoxy-L-arabinose) on the 1Ј and/or 4Ј phosphates ...

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“…Interestingly, recent studies have identified that Paneth cells could express nucleotide oligomerization domain (NOD)2 (a critical intracellular pattern recognition receptor for muramyl dipeptide), whose precise functions in Paneth cells are yet to be clearly determined (Lala et al, 2003;Rumio et al, 2004;Kobayashi et al, 2005). Cholinergic agonists can also stimulate -defensins secretion by a mechanism that appears to involve both increased cytosolic Ca 2+ and mIKCa1 potassium channels (Satoh et al, 1995;Ayabe et al, 2002). Proteolytic processing is an important step in regulating expression of active Paneth cellderived defensins.…”

Section: Posttranslational Activation Of α-Defensinsmentioning

confidence: 99%