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1

CFA-induced inflammation influences neurochemical properties of trigeminal ganglion neurons

100%
Kuzawinska O., Cudna A., Lis K., Balkowiec-Iskra E.
Acta Neurobiologiae Experimentalis
|
2013
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tom 73
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nr Suppl.1
Despite of many years of research, the evidence for interactions between the peripheral nervous system and the immune system remains incomplete. Our recent studies have shown that the proinflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF) play a critical role in the pathogenesis of the immune response within the peripheral endings of trigeminal ganglion neurons. The goal of the current project was to determine whether peripheral inflammation leads to changes in BDNF expression in trigeminal ganglia. In order to examine the effects of peripheral inflammation on the regulation of BDNF content in trigeminal ganglion neurons in vivo, a model of CFA-evoked inflammation in the TMJ of C57BL mice was employed. BDNF levels in trigeminal ganglia ipsilateral to the CFA-induced inflammation were compared with BDNF levels in the control ganglia from the contralateral (intact) side, on day 3 and 7 after induction of inflammation. A standard sandwich ELISA methodology was used to compare levels of BDNF in the trigeminal ganglion that supplies the tissue that has been affected by the inflammatory process with BDNF levels in the contralateral ganglion. These in vivo data further support the notion that BDNF is a likely key player of trigeminal inflammatory pain.
2

Gender differences in the neurochemical response of trigeminal ganglion neurons to peripheral inflammation in mice

100%
Kuzawinska O., Lis K., Cudna A., Balkowiec-Iskra E.
Acta Neurobiologiae Experimentalis
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2014
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tom 74
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nr 2
It is well established that the majority of headache and other trigeminal nerve-associated disorders have higher prevalence in females than in males. However, the pathogenesis of many chronic trigeminal pain conditions, such as trigeminal neuralgia, migraine and temporo-mandibular disorders, is still not known. One of the proposed mechanisms involve calcitonin gene-related peptide (CGRP), which is considered the most important neuropeptide in the trigeminal system. In various animal models of trigeminal nerve-associated disorders concentration of CGRP has been shown to be increased in trigeminal ganglia (TG). Moreover, intraganglionic release of CGRP has been shown to modulate neuronal transmission of pain signals. In most of these models, pathological changes in the trigeminal system are accompanied by inflammation within peripheral endings of TG neurons. The aim of the present study was to investigate the relation between gender and neurochemical changes in trigeminal ganglia evoked by peripheral inflammation, induced by Complete Freund Adjuvant (CFA) administration. Our studies show significant increase in CGRP expression in female mice, comparing to male mice. Furthermore, we demonstrate, that activation of trigeminal nociceptors by peripheral inflammation causes significant increase in expression of IL-ip, IL-6, TNF and BDNF in male mice, comparing to female mice. This phenomenon may be involved in clinically observed gender-dependent differences in the frequency of both migraine and other trigeminal nerve- related facial pain disorders.
3

Different immune response of brain areas and the inolvement of inflammatory cytokines (IL-1, IL-6, TNFalfa) in spatial learning and memory deficits after MPTP injury in mice

88%
Zaremba M., Kurkowska-Jastrzebska I., Cudna A., Piechal A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2011
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tom 71
|
nr S
Parkinson’s disease (PD) is a neurodegenerative disorders causing not only motor dysfunction, but also cognitive disturbance. The pattern of cognitive deficits in PD often includes: executive impairments, episodic memory deficits and visuospatial dysfunctions. It also became evident that inflammatory processes play an important role in the pathophysiology of PD. Neurodegeneration intense brain immune activation and “cytokine storm” which might induce hyper-excitability of neuronal circuits and might reduce neuronal plasticity and cause impairments in learning and memory abilities. The role of cytokines in regulation of inflammatory responses in different brain regions during PD is unclear. It still remains to be fully understood as to how cytokines participate in the molecular and cellular mechanisms of deficits in learning, memory and cognition in PD. Loss of dopaminergic neurons in acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models is associated with massive and prolonged glial response and increased production and release of inflammatory mediators. To assess the inflammatory response following MPTP intoxication, we measured the IL-6, IL-1β and TNFα gene expression by real-time quantitative RT-PCR following the Morris water maze behavioral test that was provided at 7 days, 3 and 6 months from the intoxication. Our results indicate that neuroinflammatory activity in MPTP model was not restricted to the nigrostriatal system but also involved hippocampal and cortical areas, regions there are essential for cognitive functions such as working and long - term memory, not only in mice. To evaluate spatial learning and memory abilities of mice the mean latency of reaching the platform, the swimming distance, the time spent in the goal quadrant and crossing parameters were estimated. We found that these parameters correlated with level of mRNA expression of cytokines in hippocampus and cortex.
4

The influence of phosphodiesterase inhibitors on degradation and neuroinflammation in the mouse model of Parkinson's disease

76%
Schwenkgrub J., Zaremba M., Joniec-Maciejak I., Cudna A., Mirowska-Guzel D., Kurkowska-Jastrzebska I.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
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nr Supl.
BACKGROUND AND AIMS: A neuroprotective or disease modifying treatment of Parkinson’s disease (PD) still remains an unmet need. The non-clinical and clinical studies have indicated that cyclic nucleotide phosphodiesterase (PDE) inhibitors represent a novel class of drugs which may be useful in treating neuroinflammation disorders. The present study was designed to examine the efficacy of PDE inhibitors, ibudilast (IBD) and vinpocetine (VPC) in the mice model of PD induced by 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP). METHODS: 3 months-old male C57Bl/10Tar mice were treated with IBD (0, 20, 30, 40 or 50 mg/kg) BID for 9 days or VPC (0, 10, 20 or 30 mg/kg) once daily for 8 consecutive days (beginning 2 days or 1 day prior to MPTP (60 mg/kg) intoxication, respectively). Rotarod test was conducted on day 3 post MPTP injection. Mice were sacrificed 7 days after MPTP intoxication. IL-1β, IL-6, TNF-α and GDNF mRNA expression in the striatum was examined by the Real Time RT-PCR method. Western blot analysis was used to estimate tyrosine hydroxylase (TH) expression, micro- and astroglia activation markers (Iba1 and GFAP, respectively). Dopamine (DA) metabolism was evaluated by HPLC method. RESULTS: Chronic administration of PDE inhibitors attenuated astroglial reactivity and increased glial cell-derived neurotrophic factor (GDNF) gene expression in the striatum. IBD reduced TNF-α, IL-6 and IL-1β expressions, whereas VPC had no impact on elevated levels of TNF-α. Moreover,  mice receiving 40 mg/ kg IBD showed significant improvement in the locomotor activity compared to control. However, PDE inhibitors did not change DA metabolism and TH expression in the striatum. CONCLUSIONS: The findings provide evidence for the glia-derived protective properties of PDE inhibitors in the MPTP-induced model of PD. This response may be promising for the better outcome in the later stages of neurodegeneration. However, the further study is needed to confirm such possibility.
5

Peripheral inflammation affects function of trigeminal ganglion neurons

76%
Kuzawinska O., Lis K., Grygorowicz T., Cudna A., Dabrowska M., Mirowska-Guzel D., Balkowiec-Iskra E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Our previous studies showed that inflammatory reaction in the area of trigeminal ganglion (TG) nociceptive endings affects neurochemical properties of TG, causing increase in concentration of both brain-derived neurotrophic factor (BDNF) and calcitonin gene-related peptide (CGRP). In the present study we have employed CFA-induced TG inflammation model to begun investigating the underlying molecular mechanisms of the inflammation-induced changes in trigeminal neurons properties. METHODS: A model of orofacial inflammation was obtained by local injection of CFA to the mice whisker pad. Pain reaction was assessed every day by von-Frey filaments. 7 and 14 days after CFA injection mice were euthanized. Both TG were removed for ELISA and quantitative PCR analysis of differences in concentration and expression of BDNF, CGRP and selected proinflammatory cytokines, both in male and female mice. After perfusion with 4% paraformaldehyde, TG were removed from the sculls, crioprotected and cut on the 20 μm sections. Tissue was immunostained using primary antibodies against BDNF and TRPV1 and then with secondary antibodies conjugated with Alexa Fluor. RESULTS: Expression of proinflammatory cytokines, BDNF and CGRP was different in male and female mice. Our results indicate that response of TG to peripheral inflammatory reaction is genderdependent, what may explain differences in frequency and severity of trigeminal nerve-associated disorders observed between women and men. CONCLUSIONS: TG neurons in female mice showed increased expression of CGRPa, this neuropeptide may act as the main mediator of trigeminal signaling during migraine. This project has been supported by the Polish National Science Center, based on the Decision No. DEC-2012/05/B/NZ4/02385. Research subject implemented with CePT infrastructure financed by the European Union – the European Regional Development Fund within the Operational Programme “Innovative economy” for 2007-2013”
6

Dose-dependent neuroprotection by 17Betta-estradiol following MPTP intoxication in male mice:role of the neuroinBetta ammatory reaction in estrogen-mediated neuroprotection

76%
Ciesielska A., Joniec I., Cudna A., Kurkowska-Jastrzebska I., Zaremba M., Czlonkowska A.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
|
nr 1
17β-estradiol (E2) have been shown to reduce damage of the nigrostriatal system following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The immunosuppressive properties of this hormone may be involved in estrogen-mediated nigro-striatal neuroprotection. We studied the chronic effects of two doses of E2: 0.25 and 2.5 mg per pellet (21-days release) administered 7 days prior MPTP treatment in C57BL male mice (12 months old) on MPTP-induced dopaminergic neurons degeneration and infl ammatory reaction in nigrostriatal pathway. We estimated striatal: tyrosine hydroxylase (TH) and dopamine (DA) level; glial fi brillary acidic protein (GFAP), cytokines (IL-1β, IL-6, TNFα, TGFβ1, IFNg), trophic factor (GDNF) and adhesion molecules (ICAM-1 and VCAM-1) gene expression at 1,7 and 21 days post MPTP intoxication. We showed that only the lower E2 dose (0.25 mg) exerted a neuroprotective effect upon nigrostriatal system. E2 0.25 pre-treatment attenuated the MPTP-induced loss of striatal DA at 1 day time-point and TH at 7- and 21-day time-points. E2 0.25 also diminished the early MPTP-induced increase of the striatal IFNg, IL-1β, TGFβ, ICAM-1, VCAM-1 and GFAP levels but failed to suppress the MPTP-induced increase of striatal TNFα. E2 0.25 also induced an increase of the striatal GDNF and IL-6 gene expression. In contrast, higher E2 doses did not affect the expression of the investigated infl ammatory mediators, expect the GFAP gene expression (increase of the GFAP expression after E2 2.5 administration). We conclude that E2 has a critical dosing effect on dopaminergic neurons survival, only physiologic levels of E2 are neuroprotective in male mice. The neuroprotective effects of E2 might mediate through a modulation of molecular factors of neuroinfl ammatory reaction.
7

Hippocampal and cortical neuroinflammation in experimental autoimmune encephalomyelitis is not accompanied by deficits of spatial memory in a late phase of the disease

76%
Kurkowska-Jastrzebska I., Swiatkiewicz M., Zaremba M., Piechal A., Cudna A., Oderfeld-Nowak B.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Cognitive dysfunctions are common features of multiple sclerosis. The exact mechanism of their appearance is unknown. The disconnection of some parts of the cortex reflecting an axonal loss, neuronal damage and alterations in synaptic transmission, have been postulated. In the present study, an autoimmune encephalomyelitis (EAE), a common model of multiple sclerosis, was induced passively by lymphocytes transfer, to evoke a one-phase disease in Lewis rats. The inflammatory reactions and neural injury in the hippocampus and frontal cortex were investigated. We found a decrease of the number of CA1 and CA4 pyramidal neurons by about 25% on 30 dpi and by about 50% in CA1 region on 90 dpi. This was accompanied by prolonged astroglial activation and by a rise of the pro-inflammatory cytokine mRNA expression (IL-1β, IL-6 and TNFα). A significant rise of NGF and BDNF was also found. In the frontal cortex, neural degeneration was not so evident. A slight astrocyte activation and a strong increase of expression of IL 6 on 30 dpi and IL1β and TNFα on 90 dpi was seen. Learning and memory abilities (Morris water-maze tests) were also evaluated 30 and 90 dpi. The mean latency of reaching the platform, the swimming distance, the time spent in the goal quadrant and crossing parameters were estimated. The reaction of animals suffering from EAE was not different from that of the control group, in any of the tasks except 20% higher chance for reaching the platform on 30 dpi. We demonstrated therefore the lack of correlation between strong neuroinflammation in the hippocampus and cortex and the deficits in memory and learning ability at a late phase of the disease. However, the severity of motor impairment during earlier stages of the disease made difficult identification of any early cognitive deficits. The possibility exists that early deficits could be later compensated due to simultaneously occurring compensatory processes involving activity of neurotrophic factors.
8

Inhibitory effects of 17beta-estradiol on production of both molecular and cellular factors in neuroinflammatory reaction in model of Parkinson's disease

64%
Ciesielska A., Joniec L., Cudna A., Kurkowska-Jastrzebska L., Sznejder A., Zaremba N., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
The neuroprotective action of 17β-estradiol (E2) against 1-methyl4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown in both female and male mice, however the exact mechanisms of that phenomenon remain obscured. We studied the chronic effects of E2 (0.25 mg per pellet, 21-days release) administered 7 days prior (Experiment 1) to or 3 days after (Experiment 2) MPTP intoxication (40 mg/kg, i.p.) in C57BL aged male mice on neurodegenerative and infl ammatory processes in nigrostriatal pathway. We estimated striatal: tyrosine hydroxylase (TH), glial fi brillary acidic protein (GFAP) content (Western blotting); cytokines (TNFα, TGFβ1, IFNγ), trophic factor (GDNF) gene expression (RT-PCR); CD4+ and CD8+ cells infl ux (immunohistochemistry) at 1, 7, 21 (Exp. 1) and 7, 21 (Exp. 2) days post intoxication. E2 exerted a neuroprotective effect upon nigrostriatal system when administered prior but also when administered after intoxication (E2 attenuated the MPTP-induced loss of TH). E2 also decreased the GFAP content. MPTP caused a rapid increase of TGFβ1, TNFα and IFNγ. Pre-treatment with E2 decreased the early expression of TGFβ1 and IFNγ but failed to suppress the MPTP-induced increase of TNFα. E2 pre-treatment also induced an increase of the GDNF and CD4+ cells infl ux to the injured brain areas but decreased the CD8+ cells infi ltration. The neuroprotective effects of E2 indicated in MPTP model might mediate through a modulation of neuroinfl ammatory reaction in lesioned nigrostriatal system.
9

Autoimmune encephalomyelitis is accompanied by the injury of hippocampal neurons

64%
Kurkowska-Jastrzebska L., Zaremba M., Cudna A., Piechal A., Swiatkiewicz M., Zaremba M., Czlonkowska A., Oderfeld-Nowak B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Multiple sclerosis (MS) is associated with cognitive defi cits, developing independently from motor disorders. These defi cits may be associated with brain neuronal damage. In this study, using the experimental model for MS – autoimmune encephalomyelitis (EAE), we investigated whether EAE will result in the damage of hippocampal neurons and selective defi cits in learning and memory, and whether there may be a correlation between the two phenomena. Lewis rats 3 months old were injected with 4 millions of anti-MBP CD4+ T cells to evoke EAE. Animals suffered from tail and hind limb paresis and recovered after 10 dpi. T cells infi ltrated spinal cord and many brain regions including hippocampus. We demonstrated the decrease of pyramidal neurons in CA4 region by about 20%, as evaluated by stereological measurements, at 21 dpi. This was preceded by prolonged glial activation as well as by a rise of the pro-infl ammatory cytokine mRNA expression (IL-1β, IL-6 and TNF α). However, no differences in the water maze test were detected between the EAE and control groups, on 21 dpi and on 90 dpi. In conclusion, anti-MBP CD4+ T cells are capable of injuring hippocampal pyramidal neurons during EAE, probably, through the secretion of pro-infl ammatory cytokines. However, in the studied conditions, hippocampal neurodegeneration caused by T cells did not result in memory disturbances. Supported by the grant no N401- 1293-33 of the Ministry of Scientifi c Research and Information Technology in Poland.
10

Neuroprotective effects of AAV2-h1L-10 in mouse model of Parkinson's disease

64%
Joniec L., Ciesielska A., Gladka A., Cudna A., Zaremba M., Kurkowska-Jastrzebska L., Hadaczek P., Bankiewicz H., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Parkinson’s disease (PD) is a neurodegenerative disorder which is characterized by abnormal loss of nigrostriatal dopamine (DA) neurons, accompanied by DA defi ciency in the striatum. The pathomechanism by which DA neurons degenerate is still unknown, however, there is increasing evidence that is possible immunological mechanisms involvement in the etiopathogenesis of PD. The aim of the present study was to examine the effect of an adeno-associated viral type-2 (AAV2) vector containing human interleukin-10 (hIL-10) gene on dopaminergic system restoration in the murine model of PD induced by by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Male C57BL/6 mice 12 months-old were used in this study. MPTP was injected in four intraperitoneal injections at 1-h intervals. AAV2-hIL-10 vector was bilaterally administered into striatum at 14, 21 or 28 days prior to MPTP intoxication. Animals were sacrifi ced at 7 days following MPTP injection. Striatal DA, DOPAC, HVA concentrations were quantifi ed by HPLC method; tyrosine hydroxylase (TH) mRNA expression was measured by RT-PCR method. MPTP treatment dramatically decreased DA concentration, signifi cantly decreased TH mRNA gene expression. AAV2-hIL-10 exerted a neuroprotective effect upon dopaminergic system (lower decrease in DA concentration). Additionally, viral vector administration prevented depletion of TH mRNA expression induced by MPTP. Our data suggest that AAV2-hIL-10 may play a neuroprotective role in MPTP mouse model of PD.
11

Effect of AAF-2-h1L-10 on immune response following toxic degeneration caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in micep.345

64%
Joniec L., Ciesielska A., Gladka A., Schwenkgrub J., Sznejder A., Cudna A., Hadaczek P., Bankiewicz K., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Interleukine 10 (IL-10) – an antiinfl ammatory cytokine produced by lymphocytes and mononuclear phagocytes including microglia. IL10 modulates the biological activities of immune cells resulting in a decreased production of pro-infl ammatory mediators including cytokines, chemokines and adhesion molecules. The aim of the present study was to examine the effect of an adeno-associated viral type-2 (AAV2) vector containing human interleukin-10 (hIL-10) gene to evaluation of immune response to the AAV2-hIL-10 (measured as IFN-γ, GFAP and TGFβ mRNA expression) in the murine model of Parkinson’s disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Male C57BL/6 mice 12 months-old were used in this study. MPTP (40 mg/kg) was injected in four intraperitoneal injections at 1-h intervals. AAV2-hIL-10 vector was bilaterally administered into striatum at 14, 21 or 28 days prior to MPTP intoxication. Animals were sacrifi ced by spinal cords dislocation at 7 days following MPTP injection. TGFβ, IFN-γ and GFAP mRNA expression was examined by RT-PCR method. MPTP treatment signifi cantly increased IFN-γ mRNA expression. AAV2-hIL-10 administration strongly increased IFN-γ as well as TGFβ and GFAP (21 and 28 day) gene expression compared to control and MPTP group. Our results point to the necessity of the reinterpretation of the role of the infl ammatory reaction in nerodegenerative processes
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