New aspects concerning ulcerative colitis and colonic carcinoma: Analysis of levels of neuropeptides, neurotrophins, and TNFalpha/TNFreceptor in plasma and mucosa in parallel with histological evaluation of the intestine

Johansson, Malin; Jönsson, Maria; Norrgård, Örjan; Forsgren, Sture

doi:10.1002/ibd.20487

Cited by 29 publications

(22 citation statements)

References 51 publications

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“…Septic shock or endotoxemia is also linked to murine CMV and HCMV reactivation in mice (13,14) and humans (26,43,80), respectively. VIP levels are also elevated in persons suffering from inflammatory bowel disease (16,32), another medical condition in which HCMV reactivates with greater frequency (33,51), even in the absence of immunosuppressive therapy (40). Lastly, VIP's presence in the secretome of HCMV Ad169-infected HFF (17) is consistent with the idea that VIP may promote the active phase of viral infection.…”

Section: Discussionmentioning

confidence: 57%

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Breaking Human Cytomegalovirus Major Immediate-Early Gene Silence by Vasoactive Intestinal Peptide Stimulation of the Protein Kinase A-CREB-TORC2 Signaling Cascade in Human Pluripotent Embryonal NTera2 Cells

Yuan

Liu

et al. 2009

J Virol

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. We speculate that neurohormonal stimulation via this signaling cascade is a possible means for reversing HCMV silence in vivo.Persons with impaired cellular immunity risk tissue-invasive disease from reactivation of latent human cytomegalovirus (HCMV). HCMV reactivation in tissues or blood of immunocompetent patients suffering illness from another cause also occurs but usually goes unnoticed and is self-limiting. For instance, nearly one-third of patients who are critically ill or in septic shock have detectable findings of HCMV reactivation in their bloodstream (12,26,43,45,80). HCMV reactivation infection in intestinal tissues with preexisting inflammatory disease (e.g., inflammatory bowel disease) is also well described for immunocompetent patients (28,39,40,51). The precise triggering mechanisms that underlie HCMV reactivation are unknown.So far, only cells of myeloid lineage have been determined to fulfill criteria for cellular sites of HCMV latency in vivo. In healthy HCMV-seropositive persons, precursors of macrophages and dendritic cells, including CD34ϩ hematopoietic progenitor cells, carry latent HCMV genomes at a low frequency (75). The terminal differentiation of these cells into a macrophage-or dendritic cell-like phenotype is a prerequisite for HCMV reactivation ex vivo (67, 76). However, this reactivation appears to be a rare event, suggesting that other, as yet unidentified factors may promote HCMV reactivation. Stimulation with tumor necrosis factor alpha (TNF-␣) or gamma interferon may promote HCMV reactivation from differentiated counterparts of monocytic-dendritic cell precursors that had been infected latently in vitro or in vivo (25,66,67,76).For both HCMV and murine CMV, viral major immediateearly (MIE) gene expression is greatly restricted or shut off during viral latency, and the productive viral life cycle cannot advance without this expression (57,74,75,78). The MIE enhancer/promoter controlling expression is regulated by the coordinated actions of multiple types of cis-acting elements (57). These elements are bound by cellular transcription factors whose functions are modulated by input supplied by the cell, the virus, and the external surrounding (57). Higher-order chromatin structure contributes to this regulation. Heterochromatin components amass on the inactive MIE enhancer/promoter in viral latency, whereas the chromatin signatures of transcriptional activity predominate at the active MIE enhancer/ promoter in acute and reactivation infections (47,67). MIE enhancer/promoter silencing is also favored by innate antiviral mechanisms that partly involve the repressive actions of nuclear ND10 domain components (e.g., hDAXX, PML, ATRX, and histone deacetylase [HDAC]) (52) but does not involve CpG methylation of the MIE enhancer/promoter (29).Quiescent HCMV infection of human NTera2/D1 cells (NT2 cells) is a tractable model system for studying the regulation of HCMV MIE enhancer/promoter reactivation (37, 54). NT2 cells share many phenotypic features with pluripotent

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Section: Discussionmentioning

confidence: 57%

“…The mean and SD were calculated for the percentage of MIE-positive cells among DAPI-positive cells. (4,16,32) in which HCMV also reactivates with greater frequency (26,33,40,43,51,80). VIP receptors are expressed on progenitors of neuronal, hepatic, retinal pigment epithelial, and hematopoietic cells (6,7,35,82).…”

Section: Cells and Virusesmentioning

confidence: 99%

Breaking Human Cytomegalovirus Major Immediate-Early Gene Silence by Vasoactive Intestinal Peptide Stimulation of the Protein Kinase A-CREB-TORC2 Signaling Cascade in Human Pluripotent Embryonal NTera2 Cells

Yuan

Liu

et al. 2009

J Virol

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“…Similarly, hypercontractility of airway smooth muscle is also a hallmark of lung inflammation and BDNF upregulation during airway inflammation has been shown to mediate this hypercontractility (1,28,40,49,57). In the same manner, the increase in BDNF expression induced by cytokines during gut inflammation (30,60) may, in part, explain the hypercontractility and altered motor function associated with gut inflammation.…”

Section: Discussionmentioning

confidence: 96%

Brain-derived neurotrophic factor enhances cholinergic contraction of longitudinal muscle of rabbit intestine via activation of phospholipase C

Qudah

Anderson

Mahavadi

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Al-Qudah M, Anderson CD, Mahavadi S, Bradley ZL, Akbarali HI, Murthy KS, Grider JR. Brain-derived neurotrophic factor enhances cholinergic contraction of longitudinal muscle of rabbit intestine via activation of phospholipase C. Am J Physiol Gastrointest Liver Physiol 306: G328 -G337, 2014. First published December 19, 2013 doi:10.1152/ajpgi.00203.2013.-Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family of proteins best known for its role in neuronal survival, differentiation, migration, and synaptic plasticity in central and peripheral neurons. BDNF is also widely expressed in nonneuronal tissues including the gastrointestinal tract. The role of BDNF in intestinal smooth muscle contractility is not well defined. The aim of this study was to identify the role of BDNF in carbachol (CCh)-and substance P (SP)-induced contraction of intestinal longitudinal smooth muscle. BDNF, selective tropomyosin-related kinase B (TrkB) receptor agonists, and pharmacological inhibitors of signaling pathways were examined for their effects on contraction of rabbit intestinal longitudinal muscle strips induced by CCh and SP. BDNF activation of intracellular signaling pathways was examined by Western blot in homogenates of muscle strips and isolated muscle cells. One-hour preincubation with BDNF enhanced intestinal muscle contraction induced by CCh but not by SP. The selective synthetic TrkB agonists LM 22A4 and 7,8-dihydroxyflavone produced similar effects to BDNF. The Trk antagonist K-252a, a TrkB antibody but not p75NTR antibody, blocked the effect of BDNF. The enhancement of CCh-induced contraction by BDNF was blocked by the phospholipase C (PLC) antagonist U73122, but not by ERK1/2 or Akt antagonists. Direct measurement in muscle strips and isolated muscle cells showed that BDNF caused phosphorylation of TrkB receptors and PLC-␥, but not ERK1/2 or Akt. We conclude that exogenous BDNF augments the CCh-induced contraction of longitudinal muscle from rabbit intestine by activating TrkB receptors and subsequent PLC activation.neurotrophins; smooth muscle contraction; Trk receptors BRAIN DERIVED-NEUROTROPHIC FACTOR (BDNF) belongs to the neurotrophin family of peptides that includes nerve growth factor, neurotrophin-3, and neurotrophin-4/5. Neurotrophins are best known for their prolonged effects and role in neuronal survival, development, differentiation, migration, and synaptic plasticity (47, 56). BDNF mediates its biological functions by activating two distinct cell membrane receptors: p75NTR, a low-affinity receptor to which all neurotrophins bind, and tropomyosin-related kinase B (TrkB), a high-affinity receptor that preferentially binds BDNF (46). BDNF binding to TrkB induces autophosphorylation of the receptor intracellular tyrosine kinase domain that leads to activation of one or more of three canonical and independent intracellular signaling pathways: the Ras/extracellular signal-regulated kinase (ERK) pathway, the phosphatidylinositol-3-OH kinase (PI3K)/Akt pathway, and the phospholipase C-␥1 (PLC-...

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“…Tumor necrosis factor (TNF)-a has been proved to be a key cytokine of the pathogenesis of IBD [34,35]. Increased TNF-a mRNA expression level in UC had been confirmed and TNF-a level was well related to endoscopic inflammation score [36].…”

Section: Introductionmentioning

confidence: 97%

Role of miR-19a targeting TNF-α in mediating ulcerative colitis

Chen

She

et al. 2013

Scandinavian Journal of Gastroenterology

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New aspects concerning ulcerative colitis and colonic carcinoma: Analysis of levels of neuropeptides, neurotrophins, and TNFalpha/TNFreceptor in plasma and mucosa in parallel with histological evaluation of the intestine

Cited by 29 publications

References 51 publications

Breaking Human Cytomegalovirus Major Immediate-Early Gene Silence by Vasoactive Intestinal Peptide Stimulation of the Protein Kinase A-CREB-TORC2 Signaling Cascade in Human Pluripotent Embryonal NTera2 Cells

Breaking Human Cytomegalovirus Major Immediate-Early Gene Silence by Vasoactive Intestinal Peptide Stimulation of the Protein Kinase A-CREB-TORC2 Signaling Cascade in Human Pluripotent Embryonal NTera2 Cells

Brain-derived neurotrophic factor enhances cholinergic contraction of longitudinal muscle of rabbit intestine via activation of phospholipase C

Role of miR-19a targeting TNF-α in mediating ulcerative colitis

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