Different Subtypes of GABA-A Receptors Are Expressed in Human, Mouse and Rat T Lymphocytes

Mendu, Suresh K.; Bhandage, Amol K.; Jin, Zhe; Birnir, Bryndis

doi:10.1371/journal.pone.0042959

Cited by 95 publications

(90 citation statements)

References 40 publications

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“…This is consistent with the in vitro studies of Han et al (2007) that found that pro-inflammatory effects of ENDO -mediated through NF-jB -increased host levels of TNFa, IL-6, IL-1b and iNOS, and another study that found that activation of the GABA receptor (a major target of OC pesticides; Rand et al 2010) enhanced synthesis of IL-6 and TNFa (Reyes-Garc ıa et al 2007). Mendu et al (2012) confirmed the presence of the GABAergic system in mammalian immune cells. It is known that patients with CRC have elevated levels of IL-6 in the serum and that these concentrations correlate with an increase of this cytokine in tumor tissues.…”

Section: Discussionsupporting

confidence: 58%

Chronic exposure to endosulfan induces inflammation in murine colon via β-catenin expression and IL-6 production

Téllez‐Bañuelos

Haramati

Franco-Topete

et al. 2016

Journal of Immunotoxicology

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Endosulfan (ENDO) is a widely used organochlorine (OC) pesticide and persistent organo-pollutant. Epidemiological studies have shown that high levels of OC exposure were related to colorectal cancer (CRC) incidence. The objectives of the present study were to evaluate histological changes in the colon, as well as in in situ expression of b-catenin and P-selectin, and serum levels of select pro-inflammatory cytokines in mice administered ENDO; there is a relationship between increased serum IL-6 and P-selectin levels in CRC patients and aberrant b-catenin signaling is important in initiation/maintenance of most CRCs. Mice were exposed to ENDO (at dose < LD 50 ) orally once a week for up to 24 weeks, and monitored (inclusive) for a total of 42 weeks. The experiment was comprised of three groups, one that did not receive ENDO (olive oil vehicle), one administered 2 mg ENDO/kg/week and a positive control (for induction of CRC) given a weekly 20 mg 1,2-dimethylhydrazine (DMH)/kg injection. The results indicated that oral administration of ENDO provoked moderate inflammation starting at six weeks, and severe colonic inflammation with an appearance of dysplastic formations (aberrant crypts) in mice treated with ENDO (or DMH) for 12 weeks or longer. Serum IL-6 levels significantly increased starting at six weeks and rose to a peak of 15-fold higher than in controls at 42 weeks; TNFa levels likewise significantly increased, with a later peak (%four-fold higher than controls) at 30-42 weeks. Immunohistochemical analysis of the colon also showed that expression of b-catenin and P-selectin increased with length of exposure to ENDO. Taken together, the results indicate that continued repeated oral exposure to ENDO induces increased expression of b-catenin and P-selectin, inflammation in the colon, and, ultimately, local tissue dysplasia. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 58%

Chronic exposure to endosulfan induces inflammation in murine colon via β-catenin expression and IL-6 production

Téllez‐Bañuelos

Haramati

Franco-Topete

et al. 2016

Journal of Immunotoxicology

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“…Although GABA has been described as neuroprotective by acting directly on GABA B Rs expressed on neurons (Fern et al 1995), it has recently been suggested that, by acting on cells different of neurons, this neurotransmitter may have beneficial effects by reducing neuroinflammation. In support of this notion, it has been reported the expression of GABA A Rs on CD4+ T-cells from mouse, rat and human origin (Mendu et al 2012). Interestingly, CD4+ T-cells not only sense GABA on the environment but they can also produce it and release it (Bhat et al 2010).…”

Section: Neurotransmitters As Modulators Of Encephalitogenic T-cellsmentioning

confidence: 82%

Regulation of the Neurodegenerative Process Associated to Parkinson’s Disease by CD4+ T-cells

González

Contreras

Pacheco

2015

J Neuroimmune Pharmacol

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Neuroinflammation constitutes a fundamental process involved in the physiopathology of Parkinson's disease (PD). Microglial cells play a central role in the outcome of neuroinflammation and consequent neurodegeneration of dopaminergic neurons in the substantia nigra. Current evidence indicates that CD4+ T-cells infiltrate the central nervous system (CNS) in PD, where they play a critical role determining the functional phenotype of microglia, thus regulating the progression of the neurodegenerative process. Here, we first analysed the pathogenic role of inflammatory phenotypes and the beneficial role of anti-inflammatory phenotypes of encephalitogenic CD4+ T-cells involved in the physiopathology of PD. Next, we discussed how alterations of neurotransmitter levels observed in the basal ganglia throughout the time course of PD progression could be strongly affecting the behaviour of encephalitogenic CD4+ T-cells and thereby the outcome of the neuroinflammatory process and the consequent neurodegeneration of dopaminergic neurons. Afterward, we integrated the evidence indicating the involvement of an antigen-specific immune response mediated by T-cells and B-cells against CNS-derived self-constituents in PD. Consistent with the involvement of a relevant autoimmune component in PD, we also reviewed the polymorphisms of both, class I and class II major histocompatibility complexes, associated to the risk of PD. Overall, this study gives an overview of how an autoimmune component involved in PD plays a fundamental role in the progression of the neurodegenerative process.

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“…, and CD8 ? T cells [23]. Up to now, if there is any correlation between the expressions of GABA-A receptors on human T cells and seizure development remains totally unknown.…”

Section: Changes Of Pbcs After Epileptic Seizurementioning

confidence: 99%

Some cross-talks between immune cells and epilepsy should not be forgotten

et al. 2014

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Recent studies have reported that immune cells were not always found in brain specimens from epileptic patients, then should we stop investigating the relationship between these cells and epilepsy? The answer is no! In addition to immunocyte infiltration in brain parenchyma, a flurry of papers have demonstrated that there were significant alterations in peripheral blood cells (PBCs) immediately after seizure onset, especially changes in some specific transporters of neurotransmitters expressed on the membrane of immunocyte. These transporters may regulate neuronal excitability in mature neurons. Besides, many researchers did find activated leukocytes adhered to the endothelium of blood brain barrier or infiltrated into the brain parenchyma in several types of epilepsy both in human and animal studies; moreover, it is worth noting that different immune cells play different roles in epilepsy development, which was indicated by in vitro and in vivo evidence. This review is going to summarize available evidence supporting changes in PBCs after seizures, and will also focus on some specific effects of immune cells on epilepsy development.

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Different Subtypes of GABA-A Receptors Are Expressed in Human, Mouse and Rat T Lymphocytes

Cited by 95 publications

References 40 publications

Chronic exposure to endosulfan induces inflammation in murine colon via β-catenin expression and IL-6 production

Chronic exposure to endosulfan induces inflammation in murine colon via β-catenin expression and IL-6 production

Regulation of the Neurodegenerative Process Associated to Parkinson’s Disease by CD4+ T-cells

Some cross-talks between immune cells and epilepsy should not be forgotten

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