Vagal nerve stimulation protects against burn-induced intestinal injury through activation of enteric glia cells

Costantini, Todd W.; Bansal, Vishal; Krzyżaniak, Michael; Putnam, James G.; Peterson, Carrie Y.; Loomis, William; Wolf, Paul L.; Baird, Andrew; Eliceiri, Brian P.; Coimbra, Raúl

doi:10.1152/ajpgi.00156.2010

Cited by 139 publications

(153 citation statements)

References 25 publications

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“…T/HS has been shown to alter splenic DC maturation at 2 h following resuscitation, supporting the potential for injury to cause rapid changes in tissue DCs (7). Studies evaluating mobilization of intestinal CD103…”

Section: Discussionmentioning

confidence: 94%

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Neuroenteric axis modulates the balance of regulatory T cells and T-helper 17 cells in the mesenteric lymph node following trauma/hemorrhagic shock

Coimbra

Langness

Eliceiri

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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Morishita K, Coimbra R, Langness S, Eliceiri BP, Costantini TW. Neuroenteric axis modulates the balance of regulatory T cells and T-helper 17 cells in the mesenteric lymph node following trauma/hemorrhagic shock. Am J Physiol Gastrointest Liver Physiol 309: G202-G208, 2015. First published June 4, 2015 doi:10.1152 doi:10. /ajpgi.00097.2015 ϩ dendritic cells (DCs) continuously migrate from the intestine to the mesenteric lymph nodes (MLNs) and maintain tolerance by driving the development of regulatory T cells (Treg) in the gut. The relative expression of Treg and T-helper 17 (Th17) cells determines the balance between tolerance and immunity in the gut. We hypothesized that trauma/hemorrhagic shock (T/HS) would decrease the CD103 ϩ DC population in the mesenteric lymph and alter the Treg-to-Th17 ratio in the MLN. We further hypothesized that vagus nerve stimulation (VNS) would promote tolerance to inflammation by increasing the Treg-to-Th17 ratio in the MLN after injury. Male rats were assigned to sham shock (SS), trauma/sham shock (T/SS), or T/HS. T/HS was induced by laparotomy and 60 min of HS (blood pressure 35 mmHg) followed by fluid resuscitation. A separate cohort of animals underwent cervical VNS after the HS phase. MLN samples were collected 24 h after resuscitation. The CD103 ϩ DC population and Treg-to-Th17 cell ratio in the MLN were decreased after T/HS compared with SS and T/SS, suggesting a shift to an inflammatory response. VNS prevented the T/HS-induced decrease in the CD103 ϩ DC population and increased the Treg-to-Th17 ratio compared with T/HS alone. VNS alters the gut inflammatory response to injury by modulating the Treg-Th17 cell balance in the MLN. VNS promotes tolerance to inflammation in the gut, further supporting its ability to modulate the inflammatory set point and alter the response to injury. vagus nerve; gut inflammation; mesenteric lymph; systemic inflammatory response

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Section: Discussionmentioning

confidence: 94%

“…Vagus nerve stimulation (VNS) modulates the inflammatory set point by altering the gut inflammatory response to acute injury, independent of splenic TNF-␣ production (7,29,47). Our previous studies demonstrated that VNS prevents injuryinduced gut barrier failure and alters the DC profile in the ML after trauma/hemorrhagic shock (T/HS) (36).…”

mentioning

confidence: 99%

Neuroenteric axis modulates the balance of regulatory T cells and T-helper 17 cells in the mesenteric lymph node following trauma/hemorrhagic shock

Coimbra

Langness

Eliceiri

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The Tracey laboratories, for example, established that efferent signaling of the vagus nerve acts exclusively via α7nAChR activation in the spleen to regulate systemic cytokine responses to infection in mice (15)(16)(17)(18)(19)(20). Similarly, Costantini and colleagues demonstrated the existence of a similar α7nAChR-dependent regulation of the local inflammatory response in tissues (21)(22)(23)(24)(25)(26)(27). With α7nAChR activation clearly essential to inflammation, not to mention vagus nerve responsiveness and leukocyte function (28,29), we reasoned that it was therefore critical to understand how a human-specific α7nAChR in human leukocytes might influence human leukocyte function, the regulation of its expression and the biological consequences of its expression.…”

Section: Introductionmentioning

confidence: 99%

A Human-Specific α7-Nicotinic Acetylcholine Receptor Gene in Human Leukocytes: Identification, Regulation and the Consequences of CHRFAM7A Expression

Costantini

Dang

Yurchyshyna

et al. 2015

Mol Med

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The human genome contains a variant form of the α7-nicotinic acetylcholine receptor (α7nAChR) gene that is uniquely human. This CHRFAM7A gene arose during human speciation and recent data suggests that its expression alters ligand tropism of the normally homopentameric human α7-AChR ligand-gated cell surface ion channel that is found on the surface of many different cell types. To understand its possible significance in regulating inflammation in humans, we investigated its expression in normal human leukocytes and leukocyte cell lines, compared CHRFAM7A expression to that of the CHRNA7 gene, mapped its promoter and characterized the effects of stable CHRFAM7A overexpression. We report here that CHRFAM7A is highly expressed in human leukocytes but that the levels of both CHRFAM7A and CHRNA7 mRNAs were independent and varied widely. To this end, mapping of the CHRFAM7A promoter in its 5′-untranslated region (UTR) identified a unique 1-kb sequence that independently regulates CHRFAM7A gene expression. Because overexpression of CHRFAM7A in THP1 cells altered the cell phenotype and modified the expression of genes associated with focal adhesion (for example, FAK, P13K, Akt, rho, GEF, Elk1, CycD), leukocyte transepithelial migration (Nox, ITG, MMPs, PKC) and cancer (kit, kitL, ras, cFos cyclinD1, Frizzled and GPCR), we conclude that CHRFAM7A is biologically active. Most surprisingly however, stable CHRFAM7A overexpression in THP1 cells upregulated CHRNA7, which, in turn, led to increased binding of the specific α7nAChR ligand, bungarotoxin, on the THP1 cell surface. Taken together, these data confirm the close association between CHRFAM7A and CHRNA7 expression, establish a biological consequence to CHRFAM7A expression in human leukocytes and support the possibility that this human-specific gene might contribute to, and/or gauge, a human-specific response to inflammation.

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“…In the enteric nervous system, increases in the expression of glial fibrillary acidic protein (GFAP) and proliferation of glial cells have also been reported in bowel inflammation such as ulcerative colitis [9][10][11][12]. As to the 'neuroendocrine' islet, it remains unclear whether similar reactive cellular responses occur in islet injuries, such as insulitis, in the progression of type 1 diabetes.…”

Section: Introductionmentioning

confidence: 99%

Plasticity of Schwann cells and pericytes in response to islet injury in mice

et al. 2013

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Aims/hypothesis Islet Schwann (glial) cells and pericytes are the microorgan's accessory cells positioned at the external and internal boundaries facing the exocrine pancreas and endothelium, respectively, adjacent to the endocrine cells. Plasticity of glial cells and pericytes is shown in the glial scar formation after injury to the central nervous system. It remains unclear whether similar reactive cellular responses occur in insulitis. We applied three-dimensional (3D) histology to perform qualitative and quantitative analyses of the islet Schwann cell network and pericytes in normal, streptozotocin-injected (positive control of gliosis) and NOD mouse models. Methods Vessel painting paired with immunostaining of mouse pancreatic tissue was used to reveal the islet Schwann cells and pericytes and their association with vasculature. Transparent islet specimens were prepared by optical clearing to facilitate 3D confocal microscopy for panoramic visualisation of the tissue networks.Results In-depth microscopy showed that the islet Schwann cell network extends from the peri-islet domain into the core. One week after streptozotocin injection, we observed intraislet perivascular gliosis and an increase in pericyte density. In early/moderate insulitis in the NOD mice, perilesional gliosis occurred at the front of the lymphocytic infiltration with atypical islet Schwann cell morphologies, including excessive branching and perivascular gliosis. Meanwhile, pericytes aggregated on the walls of the feeding arteriole at the peri-and intralesional domains with a marked increase in surface marker density. Conclusions/interpretationThe reactive cellular responses demonstrate plasticity and suggest a stop-gap mechanism consisting of the Schwann cells and pericytes in association with the islet lesion and vasculature when injury occurs.

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Vagal nerve stimulation protects against burn-induced intestinal injury through activation of enteric glia cells

Abstract: nerve stimulation protects against burn-induced intestinal injury through activation of enteric glia cells.

Cited by 139 publications

References 25 publications

Neuroenteric axis modulates the balance of regulatory T cells and T-helper 17 cells in the mesenteric lymph node following trauma/hemorrhagic shock

Neuroenteric axis modulates the balance of regulatory T cells and T-helper 17 cells in the mesenteric lymph node following trauma/hemorrhagic shock

A Human-Specific α7-Nicotinic Acetylcholine Receptor Gene in Human Leukocytes: Identification, Regulation and the Consequences of CHRFAM7A Expression

Plasticity of Schwann cells and pericytes in response to islet injury in mice

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