Tales from the crypts: regulatory peptides and cytokines in gastrointestinal homeostasis and disease

Merchant, Juanita L.

doi:10.1172/jci30974

Cited by 12 publications

(7 citation statements)

References 78 publications

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“…Merchant, 2007). Some observations would suggest that the afferents might monitor and perhaps contribute to the regulation of secretory activity of the crypts (i.e., intestinal glands).…”

Section: Discussionmentioning

confidence: 99%

Vagal afferent innervation of the proximal gastrointestinal tract mucosa: Chemoreceptor and mechanoreceptor architecture

Powley

Spaulding

Haglof

2011

J of Comparative Neurology

127

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The vagus nerve supplies low-threshold chemo- and mechanosensitive afferents to the mucosa of the proximal gastrointestinal (GI) tract. The absence of a full characterization of the morphology and distributions of these projections has hampered comprehensive functional analyses. In the present experiment, dextran (10K) conjugated with tetramethylrhodamine and biotin was injected into the nodose ganglion and used to label the terminal arbors of individual vagal afferents of both rats and mice. Series of serial 100-µm thick sections of the initial segment of the duodenum as well as the pyloric antrum were collected and processed with diaminobenzidine for permanent tracer labeling. Examination of over 400 isolated afferent fibers, more than 200 from each species, indicated that three vagal afferent specializations, each distinct in morphology and in targets, innervate the mucosa of the proximal GI tract. One population of fibers, the villus afferents, supplies plates of varicose endings to the apical tips of intestinal villi, immediately subjacent to the epithelial wall. A second type of afferent, the crypt afferent, forms subepithelial rings of varicose processes encircling the intestinal glands or crypts, immediately below the cryptvillus junction. Statistical assessment of the isolated fibers indicated that the villus arbors and the crypt endings are independent, issued by different vagal afferents. A third vagal afferent specialization, the antral gland afferent, arborizes along the gastric antral glands and forms terminal concentrations immediately below the luminal epithelial wall. The terminal locations, morphological features, and regional distributions of these three specializations provide inferences about the sensitivities of the afferents.

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“…Merchant, 2007). Some observations would suggest that the afferents might monitor and perhaps contribute to the regulation of secretory activity of the crypts (i.e., intestinal glands).…”

Section: Discussionmentioning

confidence: 99%

Vagal afferent innervation of the proximal gastrointestinal tract mucosa: Chemoreceptor and mechanoreceptor architecture

Powley

Spaulding

Haglof

2011

J of Comparative Neurology

127

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“…The intestine is rich in enteroendocrine cells that elaborate various hormones. 33,34,39 Examples include the incretin peptides (glucose-dependent insulinotropic peptide, glucagon-like peptide-1), glucagon-like peptide-2, oxyntomodulin, cholecystokinin, gastrin, and other factors. 33,34,39 In addition, intestinal absorptive cells produce factors such as apolipoprotein A IV that modulate satiety.…”

Section: Evidence For An Enteric-renal Phosphate-transport Regulatingmentioning

confidence: 99%

“…33,34,39 Examples include the incretin peptides (glucose-dependent insulinotropic peptide, glucagon-like peptide-1), glucagon-like peptide-2, oxyntomodulin, cholecystokinin, gastrin, and other factors. 33,34,39 In addition, intestinal absorptive cells produce factors such as apolipoprotein A IV that modulate satiety. 33,34,39 The source of the phosphaturic substance may be any one of these cells or some other cell type found in the intestinal wall.…”

Section: Evidence For An Enteric-renal Phosphate-transport Regulatingmentioning

confidence: 99%

“…33,34,39 In addition, intestinal absorptive cells produce factors such as apolipoprotein A IV that modulate satiety. 33,34,39 The source of the phosphaturic substance may be any one of these cells or some other cell type found in the intestinal wall. Efforts to identify the chemical identity of this factor are under way.…”

Section: Evidence For An Enteric-renal Phosphate-transport Regulatingmentioning

confidence: 99%

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Control of Renal Solute Excretion by Enteric Signals and Mediators

Thomas

Kumar

2008

Journal of the American Society of Nephrology

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The renal response to ingested solutes and the regulation of nutrient and solute balance are vital for the well-being of an organism. Foods that contain protein, carbohydrate, and fat are processed to amino acids, monosaccharides, and fatty acids and triglycerides. These substances and electrolytes and minerals are absorbed with varying degrees of efficiency in the intestine, often in response to the perceived needs of the organism. In some instances, the amount of the nutrient absorbed in the intestine depends on the amount present in the diet, and with large influxes of nutrient materials into the extracellular fluid, it falls to the kidney to remove the excessive amounts absorbed by the intestine from the serum and extracellular fluid, either by increasing the amount excreted by tubular processes or by reducing the amount reabsorbed in the tubule after glomerular filtration.It is widely believed that the renal response to ingested solutes is regulated by hormones such as aldosterone, in the case of sodium and potassium, and parathyroid hormone and the vitamin D endocrine system, in the case of calcium and phosphate. New (and old) information also suggests that factors produced in the gastrointestinal tract are released after changes in intestinal luminal solute concentrations and mediate changes in renal solute transport. This "enteric-renal solute-transporting regulating axis" represents an underappreciated mechanism by which renal solute transport is regulated. ENTERIC MODULATION OF RENAL SODIUM AND POTASSIUMDietary sodium induces a more marked natriuresis than intravenous sodium. The regulation of renal excretory or reabsorptive processes exclusively depends on the activity of various hormones or local renal factors, the synthesis or release of which depends on alterations in the serum or extracellular fluid concentrations of the various ions. Decreases in renal sodium excretion in response to a low-salt diet depend on changes in aldosterone synthesis. 1 Indeed, a lack of aldosterone synthesis is responsible for many of the manifestations of Addison's disease. The role of aldosterone (and inhibition of its synthesis) in increasing salt excretion is less clearly defined when a high-salt diet is ingested. Data suggest that other factors play a role in this process and that the role of aldosterone is minimal in the adaptation to high-sodium meals. Carey and others 2-4 have demonstrated that salt-depleted individuals who were given oral sodium chloride excreted much more sodium in their urine than did individuals who were given the same amount of sodium chloride intravenously. Plasma aldosterone ABSTRACTRenal solute excretion is important for the homeostasis of various ions. It is widely believed that hormones such as aldosterone, parathyroid hormone, the vitamin D endocrine system, and growth factors are responsible for alterations in renal ion transport in response to increased absorption of enteric solutes. In the cases of sodium, potassium, and phosphorus, moieties produced in the gastrointestinal tract a...

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“…In the GI tract, many subtypes of EECs produce a variety of neuropeptides in response to luminal and GI cues (Gribble and Reimann, 2016; Gunawardene et al, 2011). Intriguingly, enteric neurons can have similar neurochemical profiles to EECs, and are also responsive to the neuropeptides that EECs produce (Fantaguzzi et al, 2009; Merchant, 2007). As such, the molecules glucagon like peptide 1 (GLP-1) (Amato et al, 2010) and cholecystokinin (CCK) (Ngu, 1985) are known effector molecules of EECs, but also modulate ENS activity.…”

Section: Introductionmentioning

confidence: 99%

The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut

2017

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SUMMARY Interactions between the nervous and immune systems enable the gut to respond to the variety of dietary products that it absorbs, the broad spectrum of pathogens that it encounters, and the diverse microbiome that it harbors. The enteric nervous system (ENS) senses and reacts to the dynamic ecosystem of the gastrointestinal (GI) tract by translating chemical cues from the environment into neuronal impulses that propagate throughout the gut, and into other organs in the body including the central nervous system (CNS). This review will describe the current understanding of the anatomy and physiology of the GI tract, focusing on the ENS and the mucosal immune system. We highlight emerging literature that the ENS is essential for important aspects of microbe-induced immune responses in the gut. While most basic and applied research in neuroscience has focused on the brain, the proximity of the ENS to the immune system and its interface with the external environment suggest that novel paradigms for nervous system function await discovery.

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Tales from the crypts: regulatory peptides and cytokines in gastrointestinal homeostasis and disease

Cited by 12 publications

References 78 publications

Vagal afferent innervation of the proximal gastrointestinal tract mucosa: Chemoreceptor and mechanoreceptor architecture

Vagal afferent innervation of the proximal gastrointestinal tract mucosa: Chemoreceptor and mechanoreceptor architecture

Control of Renal Solute Excretion by Enteric Signals and Mediators

The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut

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