Gut‐derived cholecystokinin contributes to visceral hypersensitivity via nerve growth factor‐dependent neurite outgrowth

Hsu, Luo-Ting; Hung, Kuan-Yang; Wu, Hsiu-Wei; Liu, Weiwen; She, Meng-Ping; Lee, Tsung-Chun; Sun, Chin-Hung; Yu, Winston; Buret, André G.; Yu, Linda Chia‐Hui

doi:10.1111/jgh.13296

Cited by 9 publications

(8 citation statements)

References 56 publications

(125 reference statements)

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“…Moreover, depletion of CCK 1 in mice reduces firing in NTS neurons, indicating that the activation of the vagal afferent neurons was inhibited [289]. However, germ-free mice have reduced concentrations of gut CCK and delayed intestinal transit [125,126], whereas infection of germ-free rodents with Giardia increased colonic expression of CCK [283], corroborating previous studies showing that intestinal infection could facilitate CCK stimulation of vagal afferent neurons [290,291].…”

Section: Gut Microbiota and Cck: Relevance To Anxiety And Depressionsupporting

confidence: 85%

“…Gut CCK has also been implicated in the pathophysiology of both IBS and IBD. The densities of CCK cells are reduced in IBD, which may lower the levels of gastric secretion, such as bicarbonate, pancreatic enzymes, and bile salts, resulting in the development of IBS [283,284]. Interestingly, a potential role for CCK in regulating the immune system has also been suggested in mice.…”

Section: Gut Microbiota and Cck: Relevance To Anxiety And Depressionmentioning

confidence: 99%

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Anxiety, Depression, and the Microbiome: A Role for Gut Peptides

et al. 2018

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The complex bidirectional communication between the gut and the brain is finely orchestrated by different systems, including the endocrine, immune, autonomic, and enteric nervous systems. Moreover, increasing evidence supports the role of the microbiome and microbiota-derived molecules in regulating such interactions; however, the mechanisms underpinning such effects are only beginning to be resolved. Microbiota-gut peptide interactions are poised to be of great significance in the regulation of gut-brain signaling. Given the emerging role of the gut-brain axis in a variety of brain disorders, such as anxiety and depression, it is important to understand the contribution of bidirectional interactions between peptide hormones released from the gut and intestinal bacteria in the context of this axis. Indeed, the gastrointestinal tract is the largest endocrine organ in mammals, secreting dozens of different signaling molecules, including peptides. Gut peptides in the systemic circulation can bind cognate receptors on immune cells and vagus nerve terminals thereby enabling indirect gut-brain communication. Gut peptide concentrations are not only modulated by enteric microbiota signals, but also vary according to the composition of the intestinal microbiota. In this review, we will discuss the gut microbiota as a regulator of anxiety and depression, and explore the role of gut-derived peptides as signaling molecules in microbiome-gut-brain communication. Here, we summarize the potential interactions of the microbiota with gut hormones and endocrine peptides, including neuropeptide Y, peptide YY, pancreatic polypeptide, cholecystokinin, glucagon-like peptide, corticotropin-releasing factor, oxytocin, and ghrelin in microbiome-to-brain signaling. Together, gut peptides are important regulators of microbiota-gut-brain signaling in health and stress-related psychiatric illnesses.

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Section: Gut Microbiota and Cck: Relevance To Anxiety And Depressionsupporting

confidence: 85%

Section: Gut Microbiota and Cck: Relevance To Anxiety And Depressionmentioning

confidence: 99%

Anxiety, Depression, and the Microbiome: A Role for Gut Peptides

et al. 2018

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“…Enhanced muscle contractility in conjunction with NOS1-mediated muscle relaxation leads to the promotion of intestinal propulsion and hypermotility [99]. Hsu et al ., [100] also describe an increase in CCK levels in the colon of Giardia infected mice, although blockade of CCK receptors did not ameliorate the visceral hypersensitivity induced by infection [101]. In human Giardia infections, CCK was found to be elevated among a small number of patients with symptomatic giardiasis [102].…”

Section: Immunopathologymentioning

confidence: 99%

The Intersection of Immune Responses, Microbiota, and Pathogenesis in Giardiasis

Fink

Singer

2017

Trends in Parasitology

104

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Giardia lamblia is one of the most common infectious protozoans in the world. Giardia rarely causes severe life-threatening diarrhea, and may even have a slight protective effect in this regard, but it is a major contributor to malnutrition and growth faltering in children in the developing world. Giardia infection also appears to be a significant risk factor for post-infectious irritable bowel and chronic fatigue syndromes. In this review we highlight recent work focused on the impact of giardiasis and the mechanisms that contribute to the various outcomes of this infection, including changes in the composition of the microbiota, activation of immune responses, and immunopathology.

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“…A combination of immunological stress using infection with Giardia lamblia and psychological stress using the water avoidance model increases CCK levels in the colonic mucosa of mice (139). The stress-induced visceral hypersensitivity could be blocked using the CCK A antagonist, L-364718, and the CCK B antagonist, L-365260 following psychological but not immunological stress (139) giving rise to a role of CCK in visceral sensitivity under selective stress conditions.…”

Section: Modulation Of Gut-brain Signaling Under Conditions Of Stressmentioning

confidence: 99%

“…The stress-induced visceral hypersensitivity could be blocked using the CCK A antagonist, L-364718, and the CCK B antagonist, L-365260 following psychological but not immunological stress (139) giving rise to a role of CCK in visceral sensitivity under selective stress conditions. By contrast, acute or chronic intraperitoneal injection of CCK exerts a protective effect on the impairment of memory functions under conditions of chronic restraint stress (140, 141).…”

Section: Modulation Of Gut-brain Signaling Under Conditions Of Stressmentioning

confidence: 99%

Gut-Brain Neuroendocrine Signaling Under Conditions of Stress—Focus on Food Intake-Regulatory Mediators

Stengel

Taché

2018

Front. Endocrinol.

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The gut-brain axis represents a bidirectional communication route between the gut and the central nervous system comprised of neuronal as well as humoral signaling. This system plays an important role in the regulation of gastrointestinal as well as homeostatic functions such as hunger and satiety. Recent years also witnessed an increased knowledge on the modulation of this axis under conditions of exogenous or endogenous stressors. The present review will discuss the alterations of neuroendocrine gut-brain signaling under conditions of stress and the respective implications for the regulation of food intake.

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Gut‐derived cholecystokinin contributes to visceral hypersensitivity via nerve growth factor‐dependent neurite outgrowth

Abstract: This new model successfully recapitulates intestinal hypernociception induced by stress or Giardia. Colonic CCK contributes to visceral hypersensitivity caused by stress, but not by Giardia, partly via NGF-dependent neurite outgrowth.

Cited by 9 publications

References 56 publications

Anxiety, Depression, and the Microbiome: A Role for Gut Peptides

Anxiety, Depression, and the Microbiome: A Role for Gut Peptides

The Intersection of Immune Responses, Microbiota, and Pathogenesis in Giardiasis

Gut-Brain Neuroendocrine Signaling Under Conditions of Stress—Focus on Food Intake-Regulatory Mediators

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