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Article ; Online: Cytokine expression in subjects with

Kuenstner, J Todd / Xu, Qiang / Bull, Tim J / Foddai, Antonio C G / Grant, Irene R / Naser, Saleh A / Potula, Raghava / Zhang, Peilin / Shafran, Ira / Akhanli, Serhat Emre / Khaiboullina, Svetlana / Kruzelock, Russell

Frontiers in cellular and infection microbiology

2024 Volume 14, Page(s) 1327969

Abstract: Objectives: 1) Culture : Methods: The Temple University/Abilene Christian University (TU/ACU) study had a prospective case control design with 201 subjects including 61 CD patients and 140 non-CD controls. The culture methods included MGIT, TiKa and ... ...

Abstract	Objectives: 1) Culture Methods: The Temple University/Abilene Christian University (TU/ACU) study had a prospective case control design with 201 subjects including 61 CD patients and 140 non-CD controls. The culture methods included MGIT, TiKa and Pozzato broths, and were deemed MAP positive, if IS900 PCR positive. A phage amplification assay was also performed to detect MAP. Cytokine analysis of the TU/ACU samples was performed using Simple Plex cytokine reagents on the Ella ELISA system. Statistical analyses were done after log transformation using the R software package. The meta-analysis combined three studies. Results: Most subjects had MAP positive blood cultures by one or more methods in 3 laboratories. In our cytokine study comparing CD to non-CD controls, IL-17, IFNγ and TNFα were significantly increased in CD, but IL-2, IL-5, IL-10 and GM-CSF were not increased. In the meta-analysis, IL-6, IL-8 and IL-12 were significantly increased in the CD patients. Conclusion: Most subjects in our sample had MAP infection and 8 of 9 subjects remained MAP positive one year later indicating persistent infection. While not identical, cytokine expression patterns in MAP culture positive CD patients in the TU/ACU study showed similarities (increased IL-17, IFNγ and TNFα) to patterns of patients with Tuberculosis in other studies, indicating the possibilities of similar mechanisms of pathogen infection and potential strategies for treatment.
MeSH term(s)	Animals ; Humans ; Crohn Disease/microbiology ; Paratuberculosis/microbiology ; Interleukin-17 ; Cytokines ; Mycobacterium avium subsp. paratuberculosis ; Tumor Necrosis Factor-alpha ; Blood Culture ; Tuberculosis
Chemical Substances	Interleukin-17 ; Cytokines ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2024-02-13
Publishing country	Switzerland
Document type	Meta-Analysis ; Journal Article
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2024.1327969
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Article ; Online: Troriluzole inhibits methamphetamine place preference in rats and normalizes methamphetamine-evoked glutamate carboxypeptidase II (GCPII) protein levels in the mesolimbic pathway.

Wiah, Sonita / Roper, Abigail / Zhao, Pingwei / Shekarabi, Aryan / Watson, Mia N / Farkas, Daniel J / Potula, Raghava / Reitz, Allen B / Rawls, Scott M

Drug and alcohol dependence

2022 Volume 242, Page(s) 109719

Abstract: Riluzole, approved to manage amyotrophic lateral sclerosis, is mechanistically unique among glutamate-based therapeutics because it reduces glutamate transmission through a dual mechanism (i.e., reduces glutamate release and enhances glutamate reuptake). ...

Abstract	Riluzole, approved to manage amyotrophic lateral sclerosis, is mechanistically unique among glutamate-based therapeutics because it reduces glutamate transmission through a dual mechanism (i.e., reduces glutamate release and enhances glutamate reuptake). The profile of riluzole is favorable for normalizing glutamatergic dysregulation that perpetuates methamphetamine (METH) dependence, but pharmacokinetic and metabolic liabilities hinder repurposing. To mitigate these limitations, we synthesized troriluzole (TRLZ), a third-generation prodrug of riluzole, and tested the hypothesis that TRLZ inhibits METH hyperlocomotion and conditioned place preference (CPP) and normalizes METH-induced changes in mesolimbic glutamate biomarkers. TRLZ (8, 16 mg/kg) reduced hyperlocomotion caused by METH (1 mg/kg) without affecting spontaneous activity. TRLZ (1, 4, 8, 16 mg/kg) administered during METH conditioning (0.5 mg/kg x 4 d) inhibited development of METH place preference, and TRLZ (16 mg/kg) administered after METH conditioning reduced expression of CPP. In rats with established METH place preference, TRLZ (16 mg/kg) accelerated extinction of CPP. In cellular studies, chronic METH enhanced mRNA levels of glutamate carboxypeptidase II (GCPII) in the ventral tegmental area (VTA) and prefrontal cortex (PFC). Repeated METH also caused enhancement of GCPII protein levels in the VTA that was prevented by TRLZ (16 mg/kg). TRLZ (16 mg/kg) administered during chronic METH did not affect brain or plasma levels of METH. These results indicate that TRLZ, already in clinical trials for cerebellar ataxia, reduces development, expression and maintenance of METH CPP. Moreover, normalization of METH-induced GCPII levels in mesolimbic substrates by TRLZ points toward studying GCPII as a therapeutic target of TRLZ.
MeSH term(s)	Rats ; Animals ; Methamphetamine/pharmacology ; Central Nervous System Stimulants/pharmacology ; Glutamate Carboxypeptidase II/therapeutic use ; Riluzole/therapeutic use ; Amphetamine-Related Disorders/drug therapy ; Glutamates/therapeutic use
Chemical Substances	Methamphetamine (44RAL3456C) ; Central Nervous System Stimulants ; Glutamate Carboxypeptidase II (EC 3.4.17.21) ; Riluzole (7LJ087RS6F) ; Glutamates
Language	English
Publishing date	2022-12-05
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	519918-9
ISSN	1879-0046 ; 0376-8716
ISSN (online)	1879-0046
ISSN	0376-8716
DOI	10.1016/j.drugalcdep.2022.109719
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Article: Automated blood culture testing: A retrospective study indicates that a three-day incubation period is sufficient.

Potula, Raghava / Dadhania, Vipul / Truant, Allan L

MLO: medical laboratory observer

2015 Volume 47, Issue 9, Page(s) 8, 10, 12 passim; quiz 16

MeSH term(s)	Autoanalysis ; Bacteremia/diagnosis ; Bacteriological Techniques ; Education, Continuing ; Humans ; Retrospective Studies
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	603205-9
ISSN	0580-7247
ISSN	0580-7247
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Zs.B 2587: Show issues

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Article ; Online: Correction to: Extracellular Microvesicles Released From Brain Endothelial Cells are Detected in Animal Models Of HIV‑1 Signifying Unresolved Inflammation.

Ramirez, Servio H / Buzhdygan, Tetyana P / Hale, Jonathan F / Cheng, Liang / Li, Guangming / Hoover-Hankerson, Bryson / Razmpour, Roshanak / Sriram, Uma / Su, Lishan / Potula, Raghava / Andrews, Allison M

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2021 Volume 16, Issue 4, Page(s) 888–889

Language	English
Publishing date	2021-10-01
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-021-10024-5
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Article ; Online: Purinergic P2X7 receptor antagonist inhibits methamphetamine-induced reward, hyperlocomotion, and cortical IL-7A levels in mice: A role for P2X7/IL-17A crosstalk in methamphetamine behaviors?

Potula, Raghava / Gentile, Taylor A / Meissler, Joseph J / Shekarabi, Aryan / Wiah, Sonita / Farkas, Daniel J / Inan, Saadet / Eisenstein, Toby K / Rawls, Scott M

Brain, behavior, and immunity

2022 Volume 107, Page(s) 47–52

Abstract: P2X7 receptors are dysregulated during psychostimulant exposure. Furthermore, P2X7 receptors enhance endogenous systems (e.g., cytokines, dopamine, and glutamate) that facilitate psychostimulant addiction. Therefore, using mouse locomotor, conditioned ... ...

Abstract	P2X7 receptors are dysregulated during psychostimulant exposure. Furthermore, P2X7 receptors enhance endogenous systems (e.g., cytokines, dopamine, and glutamate) that facilitate psychostimulant addiction. Therefore, using mouse locomotor, conditioned place preference (CPP), and intracranial self-stimulation (ICSS) assays, we tested the hypothesis that methamphetamine (METH) reward and acute locomotor activation requires P2X7 receptor activity. We also investigated effects of P2X7 blockade on METH-induced changes in cytokine levels in brain reward regions. A438079 (5, 10, 50 mg/kg), a P2X7 antagonist, did not affect spontaneous locomotor activity but reduced hyperlocomotion caused by acute METH (1 mg/kg) exposure. A438079 (10 mg/kg) also prevented expression of METH CPP without causing aversive or rewarding effects. For ICSS experiments, METH (1 mg/kg) facilitated brain reward function as interpreted from reductions in baseline threshold. In the presence of A438079 (50 mg/kg), METH-induced facilitation of ICSS was reduced. Repeated METH exposure (1 mg/kg × 7 d) caused enhancement of IL-17A levels in the prefrontal cortex (PFC) that was normalized by A438070 (10 mg/kg × 7 d). The present data suggest that P2X7 receptor activity contributes to rewarding and locomotor-stimulant effects of METH through a potential mechanism involving IL-17A, which has recently been implicated in anxiety.
MeSH term(s)	Animals ; Mice ; Methamphetamine/pharmacology ; Receptors, Purinergic P2X7 ; Purinergic P2X Receptor Antagonists ; Interleukin-17
Chemical Substances	Methamphetamine (44RAL3456C) ; Receptors, Purinergic P2X7 ; Purinergic P2X Receptor Antagonists ; Interleukin-17
Language	English
Publishing date	2022-09-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2022.09.012
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 327: Show issues

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Article ; Online: Relative Role of Akt, ERK and CREB in Alcohol-Induced Microglia P2X4R Receptor Expression.

Gofman, Larisa / Fernandes, Nicole C / Potula, Raghava

Alcohol and alcoholism (Oxford, Oxfordshire)

2016 Volume 51, Issue 6, Page(s) 647–654

Abstract: Aims: Previously we have demonstrated altered microglia P2X4R expression in response to alcohol and pharmacological blockade with a selective P2X4R antagonist can reverse the action, suggesting that P2X4R play a role in mediating alcohol-induced effects ...

Abstract	Aims: Previously we have demonstrated altered microglia P2X4R expression in response to alcohol and pharmacological blockade with a selective P2X4R antagonist can reverse the action, suggesting that P2X4R play a role in mediating alcohol-induced effects on microglia. In the present study, we investigated the underlying signaling mediators, which may play a role in modulating P2X4R expression in microglia cells in response to alcohol. Methods: Embryonic stem cell-derived microglia (ESdM) cells were used to investigate the potential mechanisms involved in the regulation of P2X4R in response to alcohol. Selective P2X4R antagonist and kinase inhibitors were used to further corroborate the signal transduction pathway through which alcohol modulates P2X4R expression in microglia. Results: Alcohol (100 mM) suppressed phosphorylated AKT and ERK cascades in native ESdM cells. This alcohol-induced suppression was confirmed to be P2X4R-dependent through the use of a selective P2X4R antagonist and knockdown of P2XR4 by siRNA. Alcohol increased transcriptional activity of CREB. P2X4R antagonist blocked alcohol-induced effects on CREB, suggesting a P2X4R-mediated effect. Conclusion: These findings provide important clues to the underlying mechanism of purinoceptors in alcohol-induced microglia immune suppression.
MeSH term(s)	Blotting, Western ; Brain-Derived Neurotrophic Factor/physiology ; Cyclic AMP Response Element-Binding Protein/physiology ; Ethanol/pharmacology ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Gene Knockdown Techniques ; Human Embryonic Stem Cells ; Humans ; MAP Kinase Signaling System/physiology ; Microglia/drug effects ; Microglia/physiology ; Oncogene Protein v-akt/physiology ; Real-Time Polymerase Chain Reaction ; Receptors, Purinergic P2X4/metabolism ; Receptors, Purinergic P2X4/physiology ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Brain-Derived Neurotrophic Factor ; CREB1 protein, human ; Cyclic AMP Response Element-Binding Protein ; Receptors, Purinergic P2X4 ; Ethanol (3K9958V90M) ; Oncogene Protein v-akt (EC 2.7.11.1)
Language	English
Publishing date	2016-03-05
Publishing country	England
Document type	Journal Article
ZDB-ID	604956-4
ISSN	1464-3502 ; 0309-1635 ; 0735-0414
ISSN (online)	1464-3502
ISSN	0309-1635 ; 0735-0414
DOI	10.1093/alcalc/agw009
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Zs.B 798: Show issues

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Article: Presence of Infection by

Kuenstner, J Todd / Potula, Raghava / Bull, Tim J / Grant, Irene R / Foddai, Antonio / Naser, Saleh A / Bach, Horacio / Zhang, Peilin / Yu, Daohai / Lu, Xiaoning / Shafran, Ira

Microorganisms

2020 Volume 8, Issue 12

Abstract: Mycobacterium ... ...

Abstract	Mycobacterium avium
Language	English
Publishing date	2020-12-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8122054
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Article: Methamphetamine alters T cell cycle entry and progression: role in immune dysfunction.

Potula, Raghava / Haldar, Bijayesh / Cenna, Jonathan M / Sriram, Uma / Fan, Shongshan

Cell death discovery

2018 Volume 4, Page(s) 44

Abstract: We and others have demonstrated that stimulants such as methamphetamine (METH) exerts immunosuppressive effects on the host's innate and adaptive immune systems and has profound immunological implications. Evaluation of the mechanisms responsible for T- ... ...

Abstract	We and others have demonstrated that stimulants such as methamphetamine (METH) exerts immunosuppressive effects on the host's innate and adaptive immune systems and has profound immunological implications. Evaluation of the mechanisms responsible for T-cell immune dysregulation may lead to ways of regulating immune homeostasis during stimulant use. Here we evaluated the effects of METH on T cell cycle entry and progression following activation. Kinetic analyses of cell cycle progression of T-cell subsets exposed to METH demonstrated protracted G1/S phase transition and differentially regulated genes responsible for cell cycle regulation. This result was supported by in vivo studies where mice exposed to METH had altered G1 cell cycle phase and impaired T-cell proliferation. In addition, T cells subsets exposed to METH had significant decreased expression of cyclin E, CDK2 and transcription factor E2F1 expression. Overall, our results indicate that METH exposure results in altered T cell cycle entry and progression. Our findings suggest that disruption of cell cycle machinery due to METH may limit T-cell proliferation essential for mounting an effective adaptive immune response and thus may strongly contribute to deleterious effect on immune system.
Language	English
Publishing date	2018-03-19
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-018-0045-6
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Article ; Online: Extracellular Microvesicles Released From Brain Endothelial Cells are Detected in Animal Models Of HIV-1 Signifying Unresolved Inflammation.

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2021 Volume 16, Issue 4, Page(s) 785–795

Abstract: Treatment of HIV-infected patients with antiretroviral therapy (ART) has effectively suppressed viral replication; however, the central nervous system is still a major target and reservoir of the virus leading to the possible development of HIV- ... ...

Abstract	Treatment of HIV-infected patients with antiretroviral therapy (ART) has effectively suppressed viral replication; however, the central nervous system is still a major target and reservoir of the virus leading to the possible development of HIV-associated neurocognitive disorders (HAND). Furthermore, a hallmark feature of HAND is the disruption of the blood-brain barrier that leads to loss of tight junction protein (TJP) complexes. Extracellular vesicles (EVs), released by every cell type in the body, occur in greater quantities in response to cellular activation or injury. We have found that inflammatory insults activate brain endothelial cells (EC) and induce the release of EVs containing TJPs such as Occludin. We thus hypothesized that HIV infection and unresolved neuroinflammation will result in the release of brain-EC derived EVs. Herein, our results show elevated levels of brain-EC EVs in a humanized mouse model of HIV infection. Furthermore, while ART reduced brain-EC EVs, it was unable to completely resolve increased vesicles detectable in the blood. In addition to inflammatory insults, HIV-1 viral proteins (Tat and gp120) increased the release of Occludin + vesicles from human brain microvasculature ECs. This increase in vesicle release could be prevented by knock-down of the small GTPase ARF6. ARF6 has been shown to regulate EV biogenesis in other cell types, and we provide further evidence for the involvement of ARF6 in brain EC derived EVs. Overall, this study offers insight into the process of brain vascular remodeling (via EVs) in the setting of neuroinflammation and thus provides possibilities for biomarker monitoring and targeting of ARF6.
MeSH term(s)	Animals ; Brain ; Disease Models, Animal ; Endothelial Cells ; HIV Infections ; HIV-1 ; Humans ; Inflammation ; Mice ; Neuroinflammatory Diseases
Language	English
Publishing date	2021-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-021-10008-5
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Article ; Online: P2X4 receptor regulates alcohol-induced responses in microglia.

Gofman, Larisa / Cenna, Jonathan M / Potula, Raghava

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2014 Volume 9, Issue 5, Page(s) 668–678

Abstract: Mounting evidence indicates that alcohol-induced neuropathology may result from multicellular responses in which microglia cells play a prominent role. Purinergic receptor signaling plays a key role in regulating microglial function and, more importantly, ...

Abstract	Mounting evidence indicates that alcohol-induced neuropathology may result from multicellular responses in which microglia cells play a prominent role. Purinergic receptor signaling plays a key role in regulating microglial function and, more importantly, mediates alcohol-induced effects. Our findings demonstrate that alcohol increases expression of P2X4 receptor (P2X4R), which alters the function of microglia, including calcium mobilization, migration and phagocytosis. Our results show a significant up-regulation of P2X4 gene expression as analyzed by real-time qPCR (*p < 0.002) and protein expression as analyzed by flow cytometry (p < 0.004) in embryonic stem cell-derived microglial cells (ESdM) after 48 hours of alcohol treatment, as compared to untreated controls. Calcium mobilization in ethanol treated ESdM cells was found to be P2X4R dependent using 5-BDBD, a P2X4R selective antagonist. Alcohol decreased migration of microglia towards fractalkine (CX3CL1) by 75 % following 48 h of treatment compared to control (*p < 0.001). CX3CL1-dependent migration was confirmed to be P2X4 receptor-dependent using the antagonist 5-BDBD, which reversed the effects as compared to alcohol alone (p < 0.001). Similarly, 48 h of alcohol treatment significantly decreased phagocytosis of microglia by 15 % compared to control (p < 0.05). 5-BDBD pre-treatment prior to alcohol treatment significantly increased microglial phagocytosis (***p < 0.001). Blocking P2X4R signaling with 5-BDBD decreased the level of calcium mobilization compared to ethanol treatment alone. These findings demonstrate that P2X4 receptor may play a role in modulating microglial function in the context of alcohol abuse.
MeSH term(s)	Cell Movement/drug effects ; Cell Movement/physiology ; Cells, Cultured ; Ethanol/pharmacology ; Humans ; Microglia/drug effects ; Microglia/physiology ; Phagocytosis/drug effects ; Phagocytosis/physiology ; Receptors, Purinergic P2X4/physiology
Chemical Substances	Receptors, Purinergic P2X4 ; Ethanol (3K9958V90M)
Language	English
Publishing date	2014-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-014-9559-8
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