Infection-induced viscerosensory signals from the gut enhance anxiety: Implications for psychoneuroimmunology

Goehler, Lisa E.; Lyte, Mark; Gaykema, Ronald P.

doi:10.1016/j.bbi.2007.02.005

Cited by 119 publications

(89 citation statements)

References 32 publications

(40 reference statements)

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“…By directly recognizing a characteristic microbial component and not only a generic inflammatory event, DRGs sensory neurons could be the first element in a labeled neural pathway, conveying to the CNS early and specific information on the nature and localization of microorganisms detected in the intestinal wall. Involvement of sensory pathways in conveying non-circulating microorganism-related signals has already been shown for the vagus nerve (Goehler et al 2005,2007), and because its sensory ganglion expresses TLR4 (Hosoi et al 2005), a direct activation by pathogens has been hypothesized (Goehler et al 2007). It has also been shown that electrophysiological responses of DRGs sensory neurons projecting to the intestine can be modulated by oral inoculation of probiotics (Kamiya et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Toll-like Receptors 3, 4, and 7 Are Expressed in the Enteric Nervous System and Dorsal Root Ganglia

Barajon¹,

Serrao

Arnaboldi

et al. 2009

J Histochem Cytochem.

246

199

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S U M M A R Y The aim of the present study was to evaluate the expression of innate immunity receptors belonging to the Toll-like family in the neural plexuses of the different tracts of murine intestine, of the human ileum, and in lower dorsal root ganglia (DRGs) from where extrinsic afferents to these plexuses originate. Results obtained by immunohistochemistry and immunofluorescence on paraffin-embedded tissue and whole-mount preparations show that Toll-like receptors (TLRs) -3 and -7, recognizing viral RNA, and TLR4, recognizing lipopolysaccharide (membrane component of Gram-negative bacteria), are expressed in the myenteric and submucous plexuses of murine intestine and human ileum, and in DRGs primary sensory neurons. They also show that TLR4 immunostaining is stronger in murine distal large bowel. In murine tissue, expression of TLRs was present in both neurons and glial cells. These observations indicate that the enteric neural network might be directly activated by bacterial and viral components and is therefore more in the forefront than previously envisaged in defense responses of the intestinal wall and in the cross-talk with intestinal microbiota. They also highlight the presence of a peripheral neural network that by way of hardwired neurotransmission could potentially convey to the central nervous system specific information on our microbial counterpart and invading or potentially invading pathogens. (J Histochem Cytochem

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Section: Discussionmentioning

confidence: 99%

Toll-like Receptors 3, 4, and 7 Are Expressed in the Enteric Nervous System and Dorsal Root Ganglia

Barajon¹,

Serrao

Arnaboldi

et al. 2009

J Histochem Cytochem.

246

199

View full text Add to dashboard Cite

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“…For example, production of the SCFA butyrate by bacteria affects gene expression and the phenotype of enteric neurons in a similar manner to that observed in the colons of patients treated with prokinetic agents (166,169). Gastrointestinal microbiota may also contribute to the affective symptoms associated with GI disorders by impacting the CNS via immune, hormonal, and neural mechanisms (17,69,155). Preliminary studies have demonstrated that alterations in the GI microbiota can lead to long-term increased anxiety (69,115,116) and altered exploratory behavior in mice (18,19).…”

Section: The Intestinal Microbiota and Brain-gut Axismentioning

confidence: 99%

“…Gastrointestinal microbiota may also contribute to the affective symptoms associated with GI disorders by impacting the CNS via immune, hormonal, and neural mechanisms (17,69,155). Preliminary studies have demonstrated that alterations in the GI microbiota can lead to long-term increased anxiety (69,115,116) and altered exploratory behavior in mice (18,19). Similarly, psychosocial stressors can change the composition of the intestinal microbiota and affect the brain-gut axis function (6,7,119).…”

Section: The Intestinal Microbiota and Brain-gut Axismentioning

confidence: 99%

Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome

Ringel

Maharshak

2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ringel Y, Maharshak N.Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol 305: G529-G541, 2013. First published July 25, 2013; doi:10.1152/ajpgi.00207.2012.-The pathophysiology of irritable bowel syndrome (IBS) is believed to involve alterations in the brain-gut axis; however, the etiological triggers and mechanisms by which these changes lead to symptoms of IBS remain poorly understood. Although IBS is often considered a condition without an identified "organic" etiology, emerging evidence suggests that alterations in the gastrointestinal microbiota and altered immune function may play a role in the pathogenesis of the disorder. These recent data suggest a plausible model in which changes in the intestinal microbiota and activation of the enteric immune system may impinge upon the brain-gut axis, causing the alterations in gastrointestinal function and the clinical symptoms observed in patients with IBS. This review summarizes the current evidence for altered intestinal microbiota and immune function in IBS. It discusses the potential etiological role of these factors, suggests an updated conceptual model for the pathogenesis of the disorder, and identifies areas for future research.inflammation; gastrointestinal; microbiota IRRITABLE BOWEL SYNDROME (IBS) is the most common and best studied condition of a larger group of functional gastrointestinal (GI) disorders. Functional GI disorders refer to the presence of a variable combination of chronic or recurrent GI symptoms not explained by structural or biochemical abnormalities (130,159). IBS is characterized by chronic or recurring abdominal pain or discomfort that is associated with altered bowel habits (53, 99). The condition is often associated with other GI symptoms (e.g., bloating, distention, and gas), other functional GI disorders (e.g., functional dyspepsia), other non-GI disorders (e.g., fibromyalgia, interstitial cystitis, migraine headache), and psychological disorders (e.g., depression, anxiety, somatization) (96,146,167). Traditionally, IBS has been subtyped on the basis of the patient's predominant symptom/stool pattern (99). These subtypes include diarrhea predominant (IBS-D), constipation predominant (IBS-C), and mixed type (IBS-M), in which patients experience alternating periods of diarrhea and constipation. Unlike other conditions that can be associated with abdominal pain and abnormal bowel patterns such as inflammatory bowel diseases (IBD), IBS is not associated with any overt histopathology, structural, or biochemical abnormalities. IBS has been generally considered to be caused by alterations in the brain-gut axis (the bidirectional communication network involving the enteric nervous system, the autonomic nervous system, and the central nervous system) (60,108,125), and the pathophysiological mechanisms behind this condition remain unclear. Traditionally, IBS is considered to be a multifactorial condition in which multiple environmental, genetic, physiological, ...

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“…18 reFerences "Our paper supports a second therapeutic strategy for treating IBD-highly selective nicotinic receptor agonists. "…”

Section: Model Behaviormentioning

confidence: 99%

Getting nervous about IBD

Fulmer¹

2008

Science-Business eXchange

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A paper published in The Journal of Clinical Investigation suggests that antidepressants used to treat psychological disorders often associated with gastrointestinal diseases may have the added therapeutic effect of reducing bowel inflammation. Harnessing this double effect to treat conditions such as ulcerative colitis and Crohn's disease will require determining which drugs are most efficient at achieving both therapeutic endpoints and whether such candidates would be used in place of, or on top of, existing treatments.Common strategies for treating inflammatory bowel disease (IBD) involve suppressing the immune response with small molecules or antibodies that target proinflammatory cytokines. 1 The major forms of IBD-ulcerative colitis (UC) and Crohn's disease-are characterized by inflammation of the large and small intestine. UC is usually restricted to the colon and rectum, and Crohn's disease can affect any part of the GI tract. 2 IBD patients often suffer from psychological disorders such as stress and depression that may have a negative impact on their response to IBD therapy. 3 However, it isn't known whether IBD patients suffer from depression prior to getting IBD or as a result of having IBD. Some researchers contacted by SciBX believe there is probably a bidirectional relationship between psychiatric disorders and inflammation.Stephen Collins, a professor of medicine at McMaster University, and his coauthors on the JCI study believe their data suggest strategies for treating inflammation by modulation of the nervous system. This includes antidepressants that act on the brain or nicotinic receptor agonists that act on the vagus nerve. Both types of compounds, according to the team's data, could potentially alleviate psychiatric symptoms while also reducing inflammation in regions of the gut.The researchers found that treating chemically induced colitis in mouse models of depression with a tricyclic antidepressant not only alleviated depressed behavior but also significantly reduced inflammation compared with what was seen in control mice (p<0.05). 4 Previous mouse data from Collins' lab had linked antidepressant therapy to reduced susceptibility to colitis 5 and implicated the vagus nerve in protecting the colon from the disease. 6 In the current paper, the researchers tested the hypothesis that antidepressants reduce colitis in depressed mice by restoring proper function of the vagus nerve in the gut. The vagus is a cranial nerve that innervates the pharynx, larynx, esophagus, heart and most GI organs.The researchers found that the generic tricyclic antidepressant desmethylimipramine (also known as desipramine) reduced multiple parameters of colon inflammation in depressed mice without directly acting on the colon. Furthermore, vagotomy-severing the vagus nerve-abolished the anti-inflammatory activity of the compound in the same mice. Thus, the antidepressant effect of desipramine "is due to restoration of vagal parasympathetic function," the authors concluded. Targeting IBD in the brainResearchers c...

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Infection-induced viscerosensory signals from the gut enhance anxiety: Implications for psychoneuroimmunology

Cited by 119 publications

References 32 publications

Toll-like Receptors 3, 4, and 7 Are Expressed in the Enteric Nervous System and Dorsal Root Ganglia

Toll-like Receptors 3, 4, and 7 Are Expressed in the Enteric Nervous System and Dorsal Root Ganglia

Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome

Getting nervous about IBD

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