Proinflammatory Cytokines Induce Neurotrophic Factor Expression in Enteric Glia

Boyen, Georg B T von; Steinkamp, Martin; Geerling, Irmlind; Reinshagen, Max; Schäfer, Karl Herbert; Adler, Guido; Kirsch, Joachim

doi:10.1097/01.mib.0000219350.72483.44

Cited by 94 publications

(38 citation statements)

References 42 publications

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“…All this confirms the leading role performed by the enteric glia in the inflammation and therefore it could be regarded as an important source of cytokines in the neuroimmune network of the intestine [1-5]. …”

Section: Introductionmentioning

confidence: 61%

“…Therefore, changes in the nervous functions could represent an important link between inflammation and neurodegeneration, and this link could be represented by the glial cells, which have demonstrated to control the enteric neuronal functions [1-5]. In particular, alterations of the glial cells may be responsible of the increase of the mucosal barrier permeability, of the neuronal cells' proliferation and of the production of neurokines.…”

Section: Introductionmentioning

confidence: 99%

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Interaction between Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium avium subspecies paratuberculosis with the enteric glia and microglial cells

et al. 2011

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BackgroundWe investigated the interaction of Mycobacterium avium subspecies paratuberculosis, M. bovis and M. tuberculosis and different glial cells (enteric glial and microglial cells) in order to evaluate the infecting ability of these microorganisms and the effects produced on these cells, such as the evaluation of cytokines expression.ResultsOur experiments demonstrated the adhesion of M. paratuberculosis to the enteroglial cells and the induction of IL-1A and IL-6 expression; M. tuberculosis and M. bovis showed a good adhesive capability to the enteric cell line with the expression of the following cytokines: IL-1A and IL-1B, TNF-α, G-CSF and GM-CSF; M. bovis induced the expression of IL-6 too.The experiment performed with the microglial cells confirmed the results obtained with the enteroglial cells after the infection with M. tuberculosis and M. bovis, whereas M. paratuberculosis stimulated the production of IL-1A and IL-1B.ConclusionEnteroglial and microglial cells, could be the target of pathogenic mycobacteria and, even if present in different locations (Enteric Nervous System and Central Nervous System), show to have similar mechanism of immunomodulation.

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Section: Introductionmentioning

confidence: 61%

Section: Introductionmentioning

confidence: 99%

Interaction between Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium avium subspecies paratuberculosis with the enteric glia and microglial cells

et al. 2011

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“…Recent molecular and biochemical analysis as well as cell biology approaches demonstrated important regulatory functions of mucosal EGC in the assembly and maintenance of intestinal mucosa integrity [9,10]. This is underscored by the potential of EGC to secrete key cytokines and growth factors such as interleukin-6 (IL-6), and TGF-ß1 [15,16], which ensure cell communication with the microenvironment.…”

Section: Discussionmentioning

confidence: 99%

“…Neurotrophins has been identified as antiapoptotic substances for the colonic epithelial cells [8,9]. The source of neurotrophins and neurotrophic factors could be identified as the enteric glia cells (EGC) of the mucosal plexus [10]. On the other hand, it was shown that in Crohn's disease (CD) the amount of glial cells is reduced [11,12].…”

Section: Introductionmentioning

confidence: 99%

GDNF protects enteric glia from apoptosis: evidence for an autocrine loop

et al. 2012

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BackgroundEnteric glia cells (EGC) play an important role in the maintenance of intestinal mucosa integrity. During the course of acute Crohn's disease (CD), mucosal EGC progressively undergo apoptosis, though the mechanisms are largely unknown. We investigated the role of Glial-derived neurotrophic factor (GDNF) in the regulation of EGC apoptosis.MethodsGDNF expression and EGC apoptosis were determined by immunofluorescence using specimen from CD patients. In primary rat EGC cultures, GDNF receptors were assessed by western blot and indirect immunofluorescence microscopy. Apoptosis in cultured EGC was induced by TNF-α and IFN-γ, and the influence of GDNF on apoptosis was measured upon addition of GDNF or neutralizing anti-GDNF antibody.ResultsIncreased GDNF expression and Caspase 3/7 activities were detected in in specimen of CD patients but not in healthy controls. Moreover, inactivation of GDNF sensitized in EGC cell to IFN-γ/TNF-α induced apoptosis.ConclusionsThis study proposes the existence of an autocrine anti-apoptotic loop in EGC cells which is operative in Crohn's disease and dependent of GDNF. Alterations in this novel EGC self-protecting mechanism could lead to a higher susceptibility towards apoptosis and thus contribute to disruption of the mucosal integrity and severity of inflammation in CD.

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“…diabetic gastroparesis) (Thazhath et al, 2013), infection (achalasia and colon dysmotility in Chagas disease (Machado et al, 2012), varicella zoster (Chen et al, 2011; Holland-Cunz et al, 2006)), toxins (e.g., ethanol) (Krecsmarik et al, 2006), or local inflammation (causing inflammatory bowel disease associated dysmotility (Mawe, 2015; Mawe et al, 2009; Vasina et al, 2006) and post-infectious irritable bowel syndrome (Spiller and Garsed, 2009)). In part, post-inflammatory changes in the ENS may be mediated by cytokines that induce GDNF and NGF synthesis in enteric glia or alter glial phenotypes (von Boyen et al, 2006a; von Boyen et al, 2004, 2006b). Enteric glia modulate neuronal function to regulate motility, and can affect neuron survival and bowel epithelial barrier function, among other roles (Brown et al, 2016; Ochoa-Cortes et al, 2016; Sharkey, 2015).…”

Section: Non-hscr Motility Disordersmentioning

confidence: 99%

Gene-environment interactions and the enteric nervous system: Neural plasticity and Hirschsprung disease prevention

Heuckeroth

Schäfer

2016

Developmental Biology

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Intestinal function is primarily controlled by an intrinsic nervous system of the bowel called the enteric nervous system (ENS). The cells of the ENS are neural crest derivatives that migrate into and through the bowel during early stages of organogenesis before differentiating into a wide variety of neurons and glia. Although genetic factors critically underlie ENS development, it is now clear that many non-genetic factors may influence the number of enteric neurons, types of enteric neurons, and ratio of neurons to glia. These non-genetic influences include dietary nutrients and medicines that may impact ENS structure and function before or after birth. This review summarizes current data about gene-environment interactions that affect ENS development and suggests that these factors may contribute to human intestinal motility disorders like Hirschsprung disease or irritable bowel syndrome.

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Proinflammatory Cytokines Induce Neurotrophic Factor Expression in Enteric Glia

Cited by 94 publications

References 42 publications

Interaction between Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium avium subspecies paratuberculosis with the enteric glia and microglial cells

Interaction between Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium avium subspecies paratuberculosis with the enteric glia and microglial cells

GDNF protects enteric glia from apoptosis: evidence for an autocrine loop

Gene-environment interactions and the enteric nervous system: Neural plasticity and Hirschsprung disease prevention

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