Regulation of Intestinal Goblet Cells
 in situ
 , in Mucosal Explants and in the Isolated Epithelium

Neutra, Marian R.; Phillips, Teresa L.; Phillips, Thomas E.

doi:10.1002/9780470720905.ch3

Cited by 15 publications

(15 citation statements)

References 29 publications

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“…Similar findings have been reported in other goblet cell-like HT29 subclones [45]. The emptying of cytoplasmic mucins from goblet cells in Mucus Impedes Bacterial Invasion response to fluid secretion has been previously observed in cell and tissue models [4,[54][55][56] and in vivo this event may disrupt the mucous-gel layer overlying the epithelium.…”

Section: Discussionsupporting

confidence: 73%

Chloride-led Disruption of the Intestinal Mucous Layer Impedes Salmonella Invasion: Evidence for an ‘Enteric Tear’ Mechanism

Keely¹,

Feighery²,

Campion³

et al. 2011

Cell Physiol Biochem

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Background/Aims: Methods: The intestinal epithelial layer can switch from a net absorptive state to one of net secretion in the presence of luminal toxins and pathogens. This suggests an innate defence role for regulated secretion of mucus, electrolytes and water. We hypothesised that chloride-led fluid secretion across the mucus-covered intestinal epithelium alters barrier properties by influencing the overlying mucous-gel layer. Results: We demonstrated that chloride-led disruption of the epithelial-associated mucus-gel covering HT29-MTX-E12 (E12) human colonic epithelial monolayers, a goblet-cell like line derived from parental HT29 cells, resulted in reduction of associated mucus as well as a reduction in mucous-gel density and barrier properties. Changes in epithelial secretory state were accompanied by increased water transport, and the resulting loss of gel integrity reduced Salmonella typhimuriuminvasion of epithelia in both E12 monolayers and of isolated rat ileal mucosae. However, neither chloride secretion nor mucus disruption altered numbers of adhering bacteria. Conclusion: These data suggest a role for chloride led fluid secretion in the shedding of the adherent mucous-gel layer, possibly as a rate-limiting innate defence mechanism, and offer evidence for “enteric tears” in intestinal host defence.

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Section: Discussionsupporting

confidence: 73%

Chloride-led Disruption of the Intestinal Mucous Layer Impedes Salmonella Invasion: Evidence for an ‘Enteric Tear’ Mechanism

Keely¹,

Feighery²,

Campion³

et al. 2011

Cell Physiol Biochem

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“…brasiliensis [18]. Mucus production is also modulated by the enteric nervous system via innervation of mucosal mast cells [27] and goblet cells [28]. Innervation of epithelial mucus-producing cells is also important for the host mucosal response to N.…”

Section: Discussionmentioning

confidence: 99%

Delayed Goblet Cell Hyperplasia, Acetylcholine Receptor Expression, and Worm Expulsion in SMC-Specific IL-4Rα–Deficient Mice

et al. 2007

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Interleukin 4 receptor α (IL-4Rα) is essential for effective clearance of gastrointestinal nematode infections. Smooth muscle cells are considered to play a role in the type 2 immune response–driven expulsion of gastrointestinal nematodes. Previous studies have shown in vitro that signal transducer and activator of transcription 6 signaling in response to parasitic nematode infection significantly increases smooth muscle cell contractility. Inhibition of the IL-4Rα pathway inhibits this response. How this response manifests itself in vivo is unknown. In this study, smooth muscle cell IL-4Rα–deficient mice (SM-MHCCreIL-4Rα−/lox) were generated and characterized to uncover any role for IL-4/IL-13 in this non–immune cell type in response to Nippostrongylus brasiliensis infection. IL-4Rα was absent from α-actin–positive smooth muscle cells, while other cell types showed normal IL-4Rα expression, thus demonstrating efficient cell-type–specific deletion of the IL-4Rα gene. N. brasiliensis–infected SM-MHCCreIL-4Rα−/lox mice showed delayed ability to resolve infection with significantly prolonged fecal egg recovery and delayed worm expulsion. The delayed expulsion was related to a delayed intestinal goblet cell hyperplasia, reduced T helper 2 cytokine production in the mesenteric lymph node, and reduced M3 muscarinic receptor expression during infection. Together, these results demonstrate that in vivo IL-4Rα–responsive smooth muscle cells are beneficial for N. brasiliensis expulsion by coordinating T helper 2 cytokine responses, goblet hyperplasia, and acetylcholine responsiveness, which drive smooth muscle cell contractions.

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“…The precise receptor types and associated signal transduction mechanisms mediating sIgA secretion by these and possibly other enteric neurotransmitters at this mucosal immune effector site remain to be characterized. Both CCh and NE stimulate colonic mucin secretion (Smith and Butler, 1974;Neutra et al, 1984Barcelo et al, 2001; both IgA and SC bind to intestinal mucus and may function in a cooperative fashion with mucus in inhibiting bacterial adherence to the mucosal surface (Bouvet et al, 1993;Phalipon et al, 2003). The functional interrelationships between IgA and mucin secretion as well as other mucosal defense processes which are subject to enteric neuromodulation clearly warrant investigation.…”

Section: Discussionmentioning

confidence: 99%

Autonomic neurotransmitters modulate immunoglobulin A secretion in porcine colonic mucosa

Schmidt

Xie

Lyte

et al. 2007

Journal of Neuroimmunology

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Secretory immunoglobulin A (sIgA) plays a crucial role in mucosal surface defense. We tested the hypothesis that colonic sIgA secretion is under enteric neural control. Immunohistochemistry of the porcine distal colonic mucosa revealed presumptive cholinergic and adrenergic nerve fibers apposed to secretory component (SC)-positive crypt epithelial cells and neighboring IgA + plasmacytes. The cholinomimetic drug carbamylcholine elicited rapid, atropine-sensitive IgA secretion into the luminal fluid bathing mucosal explants mounted in Ussing chambers. The adrenergic receptor agonist norepinephrine also increased IgA secretion, an action inhibited by phentolamine. These effects were independent of agonist-induced anion secretion. In Western blots of luminal fluid, both agonists increased the density of protein bands co-immunoreactive for IgA and SC. Mucosal exposure to enterohemorrhagic Escherichia coli did not affect IgA secretion, and carbamylcholine treatment did not affect mucosal adherence of this enteropathogen. Acetylcholine and norepinephrine, acting respectively through muscarinic cholinergic and alpha-adrenergic receptors in the colonic mucosa, stimulate sIgA secretion and may enhance mucosal defense in vivo.

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Regulation of Intestinal Goblet Cells in situ , in Mucosal Explants and in the Isolated Epithelium

Cited by 15 publications

References 29 publications

Chloride-led Disruption of the Intestinal Mucous Layer Impedes <i>Salmonella</i> Invasion: Evidence for an ‘Enteric Tear’ Mechanism

Chloride-led Disruption of the Intestinal Mucous Layer Impedes <i>Salmonella</i> Invasion: Evidence for an ‘Enteric Tear’ Mechanism

Delayed Goblet Cell Hyperplasia, Acetylcholine Receptor Expression, and Worm Expulsion in SMC-Specific IL-4Rα–Deficient Mice

Autonomic neurotransmitters modulate immunoglobulin A secretion in porcine colonic mucosa

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