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Article ; Online: Anti-inflammatory effects of new human histamine H

Honkisz-Orzechowska, Ewelina / Popiołek-Barczyk, Katarzyna / Linart, Zuzanna / Filipek-Gorzała, Jadwiga / Rudnicka, Anna / Siwek, Agata / Werner, Tobias / Stark, Holger / Chwastek, Jakub / Starowicz, Katarzyna / Kieć-Kononowicz, Katarzyna / Łażewska, Dorota

Inflammation research : official journal of the European Histamine Research Society ... [et al.

2022 Volume 72, Issue 2, Page(s) 181–194

Abstract: Objective: Microglia play an important role in the neuroinflammation developed in response to various pathologies. In this study, we examined the anti-inflammatory effect of the new human histamine H: Material and methods: The affinity of flavonoids ( ...

Abstract	Objective: Microglia play an important role in the neuroinflammation developed in response to various pathologies. In this study, we examined the anti-inflammatory effect of the new human histamine H Material and methods: The affinity of flavonoids (E243 -flavone and IIIa-IIIc-chalcones) for human H Results: Chalcone derivatives showed high affinity at human H Conclusions: These results emphasize the importance of further research to accurately identify the anti-inflammatory mechanism of action of chalcones.
MeSH term(s)	Mice ; Humans ; Animals ; Histamine/metabolism ; Neuroinflammatory Diseases ; Flavonoids/pharmacology ; Flavonoids/therapeutic use ; Chalcones/metabolism ; Chalcones/pharmacology ; Chalcones/therapeutic use ; Microglia/metabolism ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Receptors, Histamine/metabolism ; Cytokines/metabolism ; Lipopolysaccharides/pharmacology ; Inflammation/drug therapy ; Inflammation/metabolism
Chemical Substances	Histamine (820484N8I3) ; Flavonoids ; Chalcones ; Anti-Inflammatory Agents ; Receptors, Histamine ; Cytokines ; Lipopolysaccharides
Language	English
Publishing date	2022-11-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1221794-3
ISSN	1420-908X ; 1023-3830
ISSN (online)	1420-908X
ISSN	1023-3830
DOI	10.1007/s00011-022-01658-z
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Article ; Online: Targeting the Microglial Signaling Pathways: New Insights in the Modulation of Neuropathic Pain.

Popiolek-Barczyk, Katarzyna / Mika, Joanna

Current medicinal chemistry

2016 Volume 23, Issue 26, Page(s) 2908–2928

Abstract: The microglia, once thought only to be supporting cells of the central nervous system (CNS), are now recognized to play essential roles in many pathologies. Many studies within the last decades indicated that the neuro-immune interaction underlies the ... ...

Abstract	The microglia, once thought only to be supporting cells of the central nervous system (CNS), are now recognized to play essential roles in many pathologies. Many studies within the last decades indicated that the neuro-immune interaction underlies the generation and maintenance of neuropathic pain. Through a large number of receptors and signaling pathways, the microglial cells communicate with neurons, astrocytes and other cells, including those of the immune system. A disturbance or loss of CNS homeostasis causes rapid responses of the microglia, which undergo a multistage activation process. The activated microglia change their cell shapes and gene expression profiles, which induce proliferation, migration, and the production of pro- or antinociceptive factors. The cells release a large number of mediators that can act in a manner detrimental or beneficial to the surrounding cells and can indirectly alter the nociceptive signals. This review discusses the most important microglial intracellular signaling cascades (MAPKs, NF-kB, JAK/STAT, PI3K/Akt) that are essential for neuropathic pain development and maintenance. Our objective was to identify new molecular targets that may result in the development of powerful tools to control the signaling associated with neuropathic pain.
MeSH term(s)	Central Nervous System/metabolism ; Humans ; Microglia/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Neuralgia/metabolism ; Neuralgia/pathology ; Neurons/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; STAT Transcription Factors/metabolism ; Signal Transduction
Chemical Substances	NF-kappa B ; STAT Transcription Factors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2016-06-04
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1319315-6
ISSN	1875-533X ; 0929-8673
ISSN (online)	1875-533X
ISSN	0929-8673
DOI	10.2174/0929867323666160607120124
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Article ; Online: Dual Piperidine-Based Histamine H

Szczepańska, Katarzyna / Karcz, Tadeusz / Dichiara, Maria / Mogilski, Szczepan / Kalinowska-Tłuścik, Justyna / Pilarski, Bogusław / Leniak, Arkadiusz / Pietruś, Wojciech / Podlewska, Sabina / Popiołek-Barczyk, Katarzyna / Humphrys, Laura J / Ruiz-Cantero, M Carmen / Reiner-Link, David / Leitzbach, Luisa / Łażewska, Dorota / Pockes, Steffen / Górka, Michał / Zmysłowski, Adam / Calmels, Thierry /

Cobos, Enrique J / Marrazzo, Agostino / Stark, Holger / Bojarski, Andrzej J / Amata, Emanuele / Kieć-Kononowicz, Katarzyna

Journal of medicinal chemistry

2023 Volume 66, Issue 14, Page(s) 9658–9683

Abstract: In search of new dual-acting histamine ... ...

Abstract	In search of new dual-acting histamine H
MeSH term(s)	Humans ; Histamine ; Receptors, Histamine H3/chemistry ; Ligands ; Nociception ; Receptors, sigma ; Piperazine ; Piperidines/pharmacology ; Piperidines/therapeutic use ; Piperidines/chemistry ; Neuralgia/drug therapy ; Structure-Activity Relationship ; Sigma-1 Receptor
Chemical Substances	Histamine (820484N8I3) ; Receptors, Histamine H3 ; Ligands ; Receptors, sigma ; Piperazine (1RTM4PAL0V) ; Piperidines
Language	English
Publishing date	2023-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.3c00430
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Article ; Online: Botulinum Toxin Type A-A Modulator of Spinal Neuron-Glia Interactions under Neuropathic Pain Conditions.

Rojewska, Ewelina / Piotrowska, Anna / Popiolek-Barczyk, Katarzyna / Mika, Joanna

Toxins

2018 Volume 10, Issue 4

Abstract: Neuropathic pain represents a significant clinical problem because it is a chronic condition often refractory to available therapy. Therefore, there is still a strong need for new analgesics. Botulinum neurotoxin A (BoNT/A) is used to treat a variety of ... ...

Abstract	Neuropathic pain represents a significant clinical problem because it is a chronic condition often refractory to available therapy. Therefore, there is still a strong need for new analgesics. Botulinum neurotoxin A (BoNT/A) is used to treat a variety of clinical diseases associated with pain. Glia are in continuous bi-directional communication with neurons to direct the formation and refinement of synaptic connectivity. This review addresses the effects of BoNT/A on the relationship between glia and neurons under neuropathic pain. The inhibitory action of BoNT/A on synaptic vesicle fusion that blocks the release of miscellaneous pain-related neurotransmitters is known. However, increasing evidence suggests that the analgesic effect of BoNT/A is mediated through neurons and glial cells, especially microglia. In vitro studies provide evidence that BoNT/A exerts its anti-inflammatory effect by diminishing NF-κB, p38 and ERK1/2 phosphorylation in microglia and directly interacts with Toll-like receptor 2 (TLR2). Furthermore, BoNT/A appears to have no more than a slight effect on astroglia. The full activation of TLR2 in astroglia appears to require the presence of functional TLR4 in microglia, emphasizing the significant interaction between those cell types. In this review, we discuss whether and how BoNT/A affects the spinal neuron-glia interaction and reduces the development of neuropathy.
MeSH term(s)	Analgesics/pharmacology ; Analgesics/therapeutic use ; Animals ; Botulinum Toxins, Type A/pharmacology ; Botulinum Toxins, Type A/therapeutic use ; Humans ; Neuralgia/drug therapy ; Neuroglia/drug effects ; Neuroglia/physiology ; Neurons/drug effects ; Neurons/physiology ; Spine/cytology
Chemical Substances	Analgesics ; Botulinum Toxins, Type A (EC 3.4.24.69)
Language	English
Publishing date	2018-04-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2518395-3
ISSN	2072-6651 ; 2072-6651
ISSN (online)	2072-6651
ISSN	2072-6651
DOI	10.3390/toxins10040145
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Article: Traumatic brain injury in mice induces changes in the expression of the XCL1/XCR1 and XCL1/ITGA9 axes.

Ciechanowska, Agata / Popiolek-Barczyk, Katarzyna / Ciapała, Katarzyna / Pawlik, Katarzyna / Oggioni, Marco / Mercurio, Domenico / de Simoni, Maria-Grazia / Mika, Joanna

Pharmacological reports : PR

2020 Volume 72, Issue 6, Page(s) 1579–1592

Abstract: Background: Every year, millions of people suffer from various forms of traumatic brain injury (TBI), and new approaches with therapeutic potential are required. Although chemokines are known to be involved in brain injury, the importance of X-C motif ... ...

Abstract	Background: Every year, millions of people suffer from various forms of traumatic brain injury (TBI), and new approaches with therapeutic potential are required. Although chemokines are known to be involved in brain injury, the importance of X-C motif chemokine ligand 1 (XCL1) and its receptors, X-C motif chemokine receptor 1 (XCR1) and alpha-9 integrin (ITGA9), in the progression of TBI remain unknown. Methods: Using RT-qPCR/Western blot/ELISA techniques, changes in the mRNA/protein levels of XCL1 and its two receptors, in brain areas at different time points were measured in a mouse model of TBI. Moreover, their cellular origin and possible changes in expression were evaluated in primary glial cell cultures. Results: Studies revealed the spatiotemporal upregulation of the mRNA expression of XCL1, XCR1 and ITGA9 in all the examined brain areas (cortex, thalamus, and hippocampus) and at most of the evaluated stages after brain injury (24 h; 4, 7 days; 2, 5 weeks), except for ITGA9 in the thalamus. Moreover, changes in XCL1 protein levels occurred in all the studied brain structures; the strongest upregulation was observed 24 h after trauma. Our in vitro experiments proved that primary murine microglial and astroglial cells expressed XCR1 and ITGA9, however they seemed not to be a main source of XCL1. Conclusions: These findings indicate that the XCL1/XCR1 and XCL1/ITGA9 axes may participate in the development of TBI. The XCL1 can be considered as one of the triggers of secondary injury, therefore XCR1 and ITGA9 may be important targets for pharmacological intervention after traumatic brain injury.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Brain Injuries, Traumatic/physiopathology ; Chemokines, C/genetics ; Chemokines, C/metabolism ; Disease Models, Animal ; Disease Progression ; Integrin alpha Chains/genetics ; Integrin alpha Chains/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/metabolism ; Receptors, Chemokine/metabolism
Chemical Substances	Chemokines, C ; Integrin alpha Chains ; Receptors, Chemokine ; XC chemokine receptor 1, mouse ; Xcl1 protein, mouse ; integrin alpha9
Language	English
Publishing date	2020-11-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2186248-5
ISSN	1734-1140
ISSN	1734-1140
DOI	10.1007/s43440-020-00187-y
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Article ; Online: The blockade of CC chemokine receptor type 1 influences the level of nociceptive factors and enhances opioid analgesic potency in a rat model of neuropathic pain.

Pawlik, Katarzyna / Piotrowska, Anna / Kwiatkowski, Klaudia / Ciapała, Katarzyna / Popiolek-Barczyk, Katarzyna / Makuch, Wioletta / Mika, Joanna

Immunology

2020 Volume 159, Issue 4, Page(s) 413–428

Abstract: A growing body of evidence has indicated that the release of nociceptive factors, such as interleukins and chemokines, by activated immune and glial cells has crucial significance for neuropathic pain generation and maintenance. Moreover, changes in the ... ...

Abstract	A growing body of evidence has indicated that the release of nociceptive factors, such as interleukins and chemokines, by activated immune and glial cells has crucial significance for neuropathic pain generation and maintenance. Moreover, changes in the production of nociceptive immune factors are associated with low opioid efficacy in the treatment of neuropathy. Recently, it has been suggested that CC chemokine receptor type 1 (CCR1) signaling is important for nociception. Our study provides evidence that the development of hypersensitivity in rats following chronic constriction injury (CCI) of the sciatic nerve is associated with significant up-regulation of endogenous CCR1 ligands, namely, CCL2, CCL3, CCL4, CCL6, CCL7 and CCL9 in the spinal cord and CCL2, CCL6, CCL7 and CCL9 in dorsal root ganglia (DRG). We showed that single and repeated intrathecal administration of J113863 (an antagonist of CCR1) attenuated mechanical and thermal hypersensitivity. Moreover, repeated administration of a CCR1 antagonist enhanced the analgesic properties of morphine and buprenorphine after CCI. Simultaneously, repeated administration of J113863 reduced the protein levels of IBA-1 in the spinal cord and MPO and CD4 in the DRG and, as a consequence, the level of pronociceptive factors, such as interleukin-1β (IL-1β), IL-6 and IL-18. The data obtained provide evidence that CCR1 blockade reduces hypersensitivity and increases opioid-induced analgesia through the modulation of neuroimmune interactions.
MeSH term(s)	Analgesics/pharmacology ; Animals ; Buprenorphine/pharmacology ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/immunology ; Chemokine CCL2/genetics ; Chemokine CCL2/immunology ; Disease Models, Animal ; Drug Synergism ; Ganglia, Spinal/drug effects ; Ganglia, Spinal/immunology ; Ganglia, Spinal/physiopathology ; Gene Expression Regulation ; Hyperalgesia/drug therapy ; Hyperalgesia/genetics ; Hyperalgesia/immunology ; Hyperalgesia/physiopathology ; Interleukin-18/genetics ; Interleukin-18/immunology ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; Interleukin-6/genetics ; Interleukin-6/immunology ; Male ; Microfilament Proteins/genetics ; Microfilament Proteins/immunology ; Morphine/pharmacology ; Neuralgia/drug therapy ; Neuralgia/genetics ; Neuralgia/immunology ; Neuralgia/physiopathology ; Nociception/drug effects ; Peroxidase/genetics ; Peroxidase/immunology ; Protein Isoforms/genetics ; Protein Isoforms/immunology ; Rats ; Rats, Wistar ; Receptors, CCR1/antagonists & inhibitors ; Receptors, CCR1/genetics ; Receptors, CCR1/immunology ; Sciatic Nerve/drug effects ; Sciatic Nerve/injuries ; Sciatic Nerve/physiopathology ; Signal Transduction ; Xanthenes/pharmacology
Chemical Substances	Aif1 protein, rat ; Analgesics ; Calcium-Binding Proteins ; Ccl2 protein, rat ; Ccr1 protein, rat ; Chemokine CCL2 ; IL1B protein, rat ; Il6 protein, rat ; Interleukin-18 ; Interleukin-1beta ; Interleukin-6 ; Microfilament Proteins ; Protein Isoforms ; Receptors, CCR1 ; Xanthenes ; Buprenorphine (40D3SCR4GZ) ; Morphine (76I7G6D29C) ; UCB 35625 (E32U2ESR7J) ; Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2020-02-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.13172
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Article ; Online: Changes in macrophage inflammatory protein-1 (MIP-1) family members expression induced by traumatic brain injury in mice.

Ciechanowska, Agata / Popiolek-Barczyk, Katarzyna / Pawlik, Katarzyna / Ciapała, Katarzyna / Oggioni, Marco / Mercurio, Domenico / De Simoni, Maria-Grazia / Mika, Joanna

Immunobiology

2020 Volume 225, Issue 3, Page(s) 151911

Abstract: A deep knowledge of the profound immunological response induced by traumatic brain injury (TBI) raises the possibility of novel therapeutic interventions. Existing studies have highlighted the important roles of C-C motif ligands in the development of ... ...

Abstract	A deep knowledge of the profound immunological response induced by traumatic brain injury (TBI) raises the possibility of novel therapeutic interventions. Existing studies have highlighted the important roles of C-C motif ligands in the development of neuroinflammation after brain injury; however, the participation of macrophage inflammatory protein-1 (MIP-1) family members in this phenomenon is still undefined. Therefore, the goal of our study was to evaluate changes in macrophage inflammatory protein-1 (MIP-1) family members (CCL3, CCL4, and CCL9) and their receptors (CCR1 and CCR5) in a mouse model of TBI (induced by controlled cortical impact (CCI)). We also investigated the pattern of activation of immunological cells (such as neutrophils, microglia and astroglia), which on one hand express CCR1/CCR5, and on the other hand might be a source of the tested chemokines in the injured brain. We investigated changes in mRNA (RT-qPCR) and/or protein (ELISA and Western blot) expression in brain structures (the cortex, hippocampus, thalamus, and striatum) at different time points (24 h, 4 days, 7 days, 2 weeks, and/or 5 weeks) after trauma. Our time-course studies revealed the upregulation of the mRNA expression of all members of the MIP-1 family (CCL3, CCL4, and CCL9) in all tested brain structures, mainly in the early stages after injury. A similar pattern of activation was observed at the protein level in the cortex and thalamus, where the strongest activation was observed 1 day after CCI; however, we did not observe any change in CCL3 in the thalamus. Analyses of CCR1 and CCR5 demonstrated the upregulation of the mRNA expression of both receptors in all tested cerebral structures, mainly in the early phases post injury (24 h, 4 days and 7 days). Protein analysis showed the upregulation of CCR1 and CCR5 in the thalamus 24 h after TBI, but we did not detect any change in the cortex. We also observed the upregulation of neutrophil marker (MPO) at the early time points (24 h and 7 days) in the cortex, while the profound activation of microglia (IBA-1) and astroglia (GFAP) was observed mainly on day 7. Our findings highlight for the first time that CCL3, CCL4, CCL9 and their receptors offer promising targets for influencing secondary neuronal injury and improving TBI therapy. The results suggest that the MIP-1 family is an important target for pharmacological intervention for brain injury.
MeSH term(s)	Animals ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Brain Injuries, Traumatic/etiology ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/pathology ; Disease Models, Animal ; Disease Susceptibility ; Gene Expression Profiling ; Gene Expression Regulation ; Macrophage Inflammatory Proteins/genetics ; Macrophage Inflammatory Proteins/metabolism ; Mice ; Microglia/metabolism ; Multigene Family ; Neurons/metabolism ; Neutrophils/immunology ; Neutrophils/metabolism
Chemical Substances	Biomarkers ; Macrophage Inflammatory Proteins
Language	English
Publishing date	2020-02-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	563292-4
ISSN	1878-3279 ; 0171-2985
ISSN (online)	1878-3279
ISSN	0171-2985
DOI	10.1016/j.imbio.2020.151911
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Article ; Online: The CCL2/CCL7/CCL12/CCR2 pathway is substantially and persistently upregulated in mice after traumatic brain injury, and CCL2 modulates the complement system in microglia.

Popiolek-Barczyk, Katarzyna / Ciechanowska, Agata / Ciapała, Katarzyna / Pawlik, Katarzyna / Oggioni, Marco / Mercurio, Domenico / De Simoni, Maria-Grazia / Mika, Joanna

Molecular and cellular probes

2020 Volume 54, Page(s) 101671

Abstract: Traumatic brain injury (TBI) is the leading cause of death in the global population. Disturbed inflammatory processes after TBI exacerbate secondary brain injury and contribute to unfavorable outcomes. Multiple inflammatory events that accompany brain ... ...

Abstract	Traumatic brain injury (TBI) is the leading cause of death in the global population. Disturbed inflammatory processes after TBI exacerbate secondary brain injury and contribute to unfavorable outcomes. Multiple inflammatory events that accompany brain trauma, such as glial activation, chemokine release, or the initiation of the complement system cascade, have been identified as potential targets for TBI treatment. However, the participation of chemokines in the complement activation remains unknown. Our studies sought to determine the changes in the expression of the molecules involved in the CCL2/CCL7/CCL12/CCR2 pathway in the injured brain and the effect of CCL2, CCL7, and CCL12 (10, 100, and 500 ng/mL) on the classic and lectin complement pathways and inflammatory factors in microglial cell cultures. Brain injury in mice was modeled by controlled cortical impact (CCI). Our findings indicate a time-dependent upregulation of CCL2, CCL7, and CCL12 at the mRNA and protein levels within the cortex, striatum, and/or thalamus beginning 24 h after the trauma. The analysis of the expression of the receptor of the tested chemokines, CCR2, revealed its substantial upregulation within the injured brain areas mainly on the mRNA level. Using primary cortical microglial cell cultures, we observed a substantial increase in the expression of CCL2, CCL7, and CCL12 after 24 h of LPS (100 ng/mL) treatment. CCL2 stimulation of microglia increased the level of IL-1β mRNA but did not influence the expression of IL-18, IL-6, and IL-10. Moreover, CCL2 significantly increased the expression of Iba1, a marker of microglia activation. CCL2 and CCL12 upregulated the expression of C1qa but did not influence the expression of C1ra and C1s1 (classical pathway); moreover, CCL2 increased ficolin A expression and reduced collectin 11 expression (lectin pathway). Additionally, we observed the downregulation of pentraxin 3, a modulator of the complement cascade, after CCL2 and CCL12 treatment. We did not detect the expression of ficolin B, Mbl1, and Mbl2 in microglial cells. Our data identify CCL2 as a modulator of the classical and lectin complement pathways suggesting that CCL2 may be a promising target for pharmacological intervention after brain injury. Moreover, our study provides evidence that CCL2 and two other CCR2 ligands may play a role in the development of changes in TBI.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Brain Injuries, Traumatic/genetics ; Cells, Cultured ; Chemokine CCL2/genetics ; Chemokine CCL2/metabolism ; Chemokine CCL7/genetics ; Chemokine CCL7/metabolism ; Complement System Proteins/metabolism ; Inflammation Mediators/metabolism ; Lipopolysaccharides ; Male ; Mice, Inbred C57BL ; Microglia/metabolism ; Monocyte Chemoattractant Proteins/genetics ; Monocyte Chemoattractant Proteins/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, CCR2/genetics ; Receptors, CCR2/metabolism ; Signal Transduction ; Time Factors ; Up-Regulation
Chemical Substances	Ccl12 protein, mouse ; Chemokine CCL2 ; Chemokine CCL7 ; Inflammation Mediators ; Lipopolysaccharides ; Monocyte Chemoattractant Proteins ; RNA, Messenger ; Receptors, CCR2 ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2020-11-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639082-1
ISSN	1096-1194 ; 0890-8508
ISSN (online)	1096-1194
ISSN	0890-8508
DOI	10.1016/j.mcp.2020.101671
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Article ; Online: CCR4 antagonist (C021) influences the level of nociceptive factors and enhances the analgesic potency of morphine in a rat model of neuropathic pain.

Bogacka, Joanna / Popiolek-Barczyk, Katarzyna / Pawlik, Katarzyna / Ciechanowska, Agata / Makuch, Wioletta / Rojewska, Ewelina / Dobrogowski, Jan / Przeklasa-Muszynska, Anna / Mika, Joanna

European journal of pharmacology

2020 Volume 880, Page(s) 173166

Abstract: Neuropathic pain is a chronic condition which significantly reduces the quality of life and serious clinical issue that is in general resistant to available therapies. Therefore looking for new analgesics is still critical issue. Recent, studies have ... ...

Abstract	Neuropathic pain is a chronic condition which significantly reduces the quality of life and serious clinical issue that is in general resistant to available therapies. Therefore looking for new analgesics is still critical issue. Recent, studies have indicated that chemokine signaling pathways are crucial for the development of neuropathy; however, the role of CC chemokine receptor 4 (CCR4) in this process has not yet been studied. Therefore, the aim of our research was to investigate the influence of C021 (a CCR4 antagonist) and CCR4 CC chemokine ligands 17 and 22 (CCL17 and CCL22) on the development of hypersensitivity and the effectiveness of morphine induced analgesia in naive animals and/or animals exposed to chronic constriction injury (CCI) of the sciatic nerve. Firstly, we demonstrated that the intrathecal administration of CCL17 and CCL22 induced pain-related behavior in naive mice. Secondly, we revealed that the intrathecal injection of C021 significantly reduced CCI-induced hypersensitivity after nerve injury. In parallel, C021 reduced microglia/macrophages activation and the level of some pronociceptive interleukins (IL-1beta; IL-18) in the spinal cord 8 days after CCI. Moreover, C021 not only attenuated mechanical and thermal hypersensitivity but also enhanced the analgesic properties of morphine. Our research indicates that CCR4 ligands might be important factors in the early stages of neuropathy, when we observe intense microglia/macrophages activation. Moreover, pharmacological blockade of CCR4 may serve as a potential new target for better understanding the mechanisms of neuropathic pain development.
MeSH term(s)	Analgesics, Opioid/administration & dosage ; Animals ; Cold Temperature ; Cytokines/genetics ; Cytokines/metabolism ; Disease Models, Animal ; Drug Synergism ; Ganglia, Spinal/drug effects ; Ganglia, Spinal/metabolism ; Hyperalgesia/drug therapy ; Male ; Mice ; Morphine/administration & dosage ; Neuralgia/drug therapy ; Peripheral Nerve Injuries/drug therapy ; Quinazolines/administration & dosage ; Rats, Wistar ; Receptors, CCR4/antagonists & inhibitors ; Receptors, CCR4/genetics ; Sciatic Nerve/injuries ; Spinal Cord/drug effects ; Spinal Cord/metabolism ; Touch
Chemical Substances	Analgesics, Opioid ; C 021 compound ; Cytokines ; Quinazolines ; Receptors, CCR4 ; Morphine (76I7G6D29C)
Language	English
Publishing date	2020-05-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2020.173166
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Article ; Online: Biphalin, a Dimeric Enkephalin, Alleviates LPS-Induced Activation in Rat Primary Microglial Cultures in Opioid Receptor-Dependent and Receptor-Independent Manners.

Popiolek-Barczyk, Katarzyna / Piotrowska, Anna / Makuch, Wioletta / Mika, Joanna

Neural plasticity

2017 Volume 2017, Page(s) 3829472

Abstract: Neuropathic pain is relatively less responsive to opioids than other types of pain, which is possibly due to a disrupted opioid system partially caused by the profound microglial cell activation that underlines neuroinflammation. We demonstrated that ... ...

Abstract	Neuropathic pain is relatively less responsive to opioids than other types of pain, which is possibly due to a disrupted opioid system partially caused by the profound microglial cell activation that underlines neuroinflammation. We demonstrated that intrathecally injected biphalin, a dimeric enkephalin analog, diminished symptoms of neuropathy in a preclinical model of neuropathic pain in rats (CCI, chronic constriction injury of the sciatic nerve) at day 12 postinjury. Using primary microglial cell cultures, we revealed that biphalin did not influence cell viability but diminished NO production and expression of Iba1 in LPS-stimulated cells. Biphalin also diminished MOP receptor level, as well as pronociceptive mediators (iNOS, IL-1
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ZDB-ID	1454938-4
ISSN	1687-5443 ; 2090-5904 ; 0792-8483
ISSN (online)	1687-5443
ISSN	2090-5904 ; 0792-8483
DOI	10.1155/2017/3829472
Database	MEDical Literature Analysis and Retrieval System OnLINE

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