Reduced expression of basal and probiotic-inducible G-CSF in intestinal mononuclear cells is associated with inflammatory bowel disease

Martins, Andrew J.; Colquhoun, Patrick; Reid, Gregor; Kim, Sung Ouk

doi:10.1002/ibd.20808

Cited by 19 publications

(19 citation statements)

References 60 publications

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“…High levels of G-CSF are constitutively expressed in normal mouse or human intestine, and an exogenous commensal probiotic, Lactobacillus rhamnosus , was able to further enhance the expression [53]. In the absence of tributyrin, we found that ethanol-exposed mice had lower expression of G-CSF in the proximal colon.…”

Section: Discussionmentioning

confidence: 92%

Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Glueck

Han

Cresci

2018

Journal of Immunology Research

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Excessive ethanol consumption causes adverse effects and contributes to organ dysfunction. Ethanol metabolism triggers oxidative stress, altered immune function, and gut dysbiosis. The gut microbiome is known to contribute to the maintenance of intestinal homeostasis, and disturbances are associated with pathology. A consequence of gut dysbiosis is also alterations in its metabolic and fermentation byproducts. The gut microbiota ferments undigested dietary polysaccharides to yield short-chain fatty acids, predominantly acetate, propionate, and butyrate. Butyrate has many biological mechanisms of action including anti-inflammatory and immunoprotective effects, and its depletion is associated with intestinal injury. We previously showed that butyrate protects gut-liver injury during ethanol exposure. While the intestine is the largest immune organ in the body, little is known regarding the effects of ethanol on intestinal immune function. This work is aimed at investigating the effects of butyrate supplementation, in the form of the structured triglyceride tributyrin, on intestinal innate immune responses and oxidative stress following chronic-binge ethanol exposure in mice. Our work suggests that tributyrin supplementation preserved immune responses and reduced oxidative stress in the proximal colon during chronic-binge ethanol exposure. Our results also indicate a possible involvement of tributyrin in maintaining the integrity of intestinal villi vasculature disrupted by chronic-binge ethanol exposure.

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Section: Discussionmentioning

confidence: 92%

Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Glueck

Han

Cresci

2018

Journal of Immunology Research

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“…However, it remains unclear how oral VSL#3 treatment leads to changes in systemic immunity and circulating TNF-␣ levels. Probiotic administration has been reported previously to induce increased intestinal production of the cytokine G-CSF (Martins et al, 2009). In our current study, consistent with this previous report, we found a striking increase in plasma G-CSF levels in VSL#3-treated BDL mice compared with placebo-treated BDL and sham mice.…”

Section: Discussionmentioning

confidence: 97%

Probiotics Improve Inflammation-Associated Sickness Behavior by Altering Communication between the Peripheral Immune System and the Brain

D’Mello

Ronaghan

Zaheer

et al. 2015

Journal of Neuroscience

159

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Patients with systemic inflammatory diseases (e.g., rheumatoid arthritis, inflammatory bowel disease, chronic liver disease) commonly develop debilitating symptoms (i.e., sickness behaviors) that arise from changes in brain function. The microbiota-gut-brain axis alters brain function and probiotic ingestion can influence behavior. However, how probiotics do this remains unclear. We have previously described a novel periphery-to-brain communication pathway in the setting of peripheral organ inflammation whereby monocytes are recruited to the brain in response to systemic TNF-␣ signaling, leading to microglial activation and subsequently driving sickness behavior development. Therefore, we investigated whether probiotic ingestion (i.e., probiotic mixture VSL#3) alters this periphery-tobrain communication pathway, thereby reducing subsequent sickness behavior development. Using a well characterized mouse model of liver inflammation, we now show that probiotic (VSL#3) treatment attenuates sickness behavior development in mice with liver inflammation without affecting disease severity, gut microbiota composition, or gut permeability. Attenuation of sickness behavior development was associated with reductions in microglial activation and cerebral monocyte infiltration. These events were paralleled by changes in markers of systemic immune activation, including decreased circulating TNF-␣ levels. Our observations highlight a novel pathway through which probiotics mediate cerebral changes and alter behavior. These findings allow for the potential development of novel therapeutic interventions targeted at the gut microbiome to treat inflammation-associated sickness behaviors in patients with systemic inflammatory diseases.

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“…Conversely, LP macrophages from IBD patients produce less of the cytokine G-CSF, which is protective in experimental models of colitis, in response to the probiotic Lactobacillus rhamnosus GR-1 compared to those from healthy controls. 134 …”

Section: Macrophages and Dcs In Ibd Pathogenesismentioning

confidence: 99%

The Role of Macrophages and Dendritic Cells in the Initiation of Inflammation in IBD

Steinbach

Plevy

2014

Inflammatory Bowel Diseases

208

165

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In the healthy gastrointestinal tract, homeostasis is an active process that requires a careful balance of host responses to the enteric luminal contents. Intestinal macrophages and dendritic cells comprise a unique group of tissue immune cells that are ideally situated at the interface of the host and the enteric luminal environment to appropriately respond to microbes and ingested stimuli. However, intrinsic defects in macrophage and dendritic cell function contribute to the pathogenesis of inflammatory bowel diseases (IBD), as highlighted by recent genome-wide association studies. Gastrointestinal macrophages and dendritic cells participate in IBD development through inappropriate responses to enteric microbial stimuli, inefficient clearance of microbes from host tissues, and impaired transition from appropriate pro-inflammatory responses to anti-inflammatory responses that promote resolution. By understanding how intestinal macrophages and dendritic cells initiate chronic inflammation, new pathogenesis-based therapeutic strategies to treat human IBD will be elucidated.

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Reduced expression of basal and probiotic-inducible G-CSF in intestinal mononuclear cells is associated with inflammatory bowel disease

Abstract: These results suggest that high G-CSF production induced by commensals such as L. rhamnosus is important in maintaining normal immunological homeostasis in the intestine and defects in the production of G-CSF are associated with IBD.

Cited by 19 publications

References 60 publications

Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Probiotics Improve Inflammation-Associated Sickness Behavior by Altering Communication between the Peripheral Immune System and the Brain

The Role of Macrophages and Dendritic Cells in the Initiation of Inflammation in IBD

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