Role of Purinergic Signaling in Acupuncture Therapeutics

2021 ◽  
pp. 1-15
Author(s):  
Zhi-Ying Lv ◽  
Yong-Qing Yang ◽  
Lei-Miao Yin
Keyword(s):  
Signaling Pathway ◽  
Immune Cells ◽  
Purinergic Signaling ◽  
P2 Receptors ◽  
Nerve Fibers ◽  
Systematic Research ◽  
Purine Receptors ◽  
Immune Systems ◽  
Immunosuppressive Cells

Acupuncture is a therapeutic treatment that is well recognized in many countries. However, the initiation mechanisms of acupuncture are not well understood. Purinergic signaling has been considered a key signaling pathway in acupuncture in recent years. Acupuncture-induced ATP is mainly produced by mast cells and fibroblasts, and ATP is gradually hydrolyzed into adenosine. ATP and adenosine further participate in the process of acupuncture information transmission to the nervous and immune systems through specific purine receptors. Acupuncture initiates analgesia via the down-regulation of the expression of P2 receptors or up-regulation of the expression of adenosine A1 receptors on nerve fibers. ATP also promotes the proliferation of immune cells through P2 receptors and A3 receptors, causing inflammation. In contrast, adenosine activates A2 receptors, promotes the production and infiltration of immunosuppressive cells, and causes an anti-inflammatory response. In summary, we described the role of purinergic signaling as a general signaling pathway in the initiation of acupuncture and the influence of purinergic signaling on the neuroimmune network to lay the foundation for future systematic research on the mechanisms of acupuncture therapeutics.

Role of purinergic signaling pathways in the adaptogenic-like activity of methyl jasmonate in rats exposed to unpredictable chronic mild stress

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Oritoke M. Aluko ◽  
Solomon Umukoro
Keyword(s):  
Methyl Jasmonate ◽  
Adenosine Deaminase ◽  
Signaling Pathway ◽  
Purinergic Signaling ◽  
Hematological Parameters ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Unpredictable Chronic Mild Stress ◽  
Swimming Endurance

AbstractObjectivesPurinergic signaling pathway has been implicated in maladaptation of animals subjected to chronic stress. Previous studies have shown that methyl jasmonate (MJ) exhibited adaptogenic properties in mice exposed to unpredictable chronic mild stress (UCMS) via antioxidant and neuroprotective-related mechanisms.MethodsThis study evaluated the role of purinergic system in adaptogenic-like activity of MJ. Male Wistar rats were treated intraperitoneally with vehicle (10 mL/kg) or MJ (25, 50, or 100 mg/kg) 30 min prior exposure to UCMS. Thereafter, rats were assessed for swimming endurance in forced swim test (FST) and post-swimming motor coordination on beam walk test (BWT) apparatus. The rats’ brains were processed for adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine deaminase, and arginase quantification. Hematological parameters, cholesterol, triglyceride, creatinine, and urea nitrogen were also determined.ResultsMJ prolonged swimming endurance time and reversed stress-induced post-swimming motor dysfunction. The altered hematological parameters induced by UCMS in rats were significantly (p<0.05) attenuated by MJ. MJ also reversed UCMS-induced alterations of total cholesterol, triglyceride, creatinine, and urea nitrogen levels. MJ averted UCMS-induced alterations in purinergic system by decreasing ATP and ADP hydrolysis, adenosine deaminase, and arginase activities in rats’ brains.ConclusionsOverall, these findings further suggest that MJ has adaptogenic-like activity in rats exposed to UCMS, which may be related to modulation of the purinergic signaling pathway.

scholarly journals Key chemokines direct migration of immune cells in solid tumors

2021 ◽  
Author(s):  
Karan Kohli ◽  
Venu G. Pillarisetty ◽  
Teresa S. Kim
Keyword(s):  
Solid Tumors ◽  
Immune Cells ◽  
Chemokine Receptors ◽  
Tumor Tissue ◽  
Immune Cell ◽  
Chemokine Signaling ◽  
Immune Cell Migration ◽  
Preclinical And Clinical Studies ◽  
Immunosuppressive Cells

AbstractImmune cell infiltration into solid tumors, their movement within the tumor microenvironment (TME), and interaction with other immune cells are controlled by their directed migration towards gradients of chemokines. Dysregulated chemokine signaling in TME favors the growth of tumors, exclusion of effector immune cells, and abundance of immunosuppressive cells. Key chemokines directing the migration of immune cells into tumor tissue have been identified. In this review, we discuss well-studied chemokine receptors that regulate migration of effector and immunosuppressive immune cells in the context of cancer immunology. We discuss preclinical models that have described the role of respective chemokine receptors in immune cell migration into TME and review preclinical and clinical studies that target chemokine signaling as standalone or combination therapies.

scholarly journals PD-L1-Mediated Immunosuppression in Glioblastoma Is Associated With the Infiltration and M2-Polarization of Tumor-Associated Macrophages

2020 ◽  
Vol 11 ◽  
Author(s):  
Zhiyuan Zhu ◽  
Hongbo Zhang ◽  
Baodong Chen ◽  
Xing Liu ◽  
Shizhong Zhang ◽  
...  
Keyword(s):  
Immune Cells ◽  
Immune Checkpoint Inhibitors ◽  
Potential Role ◽  
Checkpoint Inhibitors ◽  
Clinical Information ◽  
Tumour Microenvironment ◽  
Expression Data ◽  
M2 Polarization ◽  
Immunosuppressive Cells

There has been no significant improvements for immune checkpoint inhibitors since its first use. Tumour-associated macrophages (TAMs) are critical mediators in the PD-1/PD-L1 axis, contributing to the immunosuppressive tumour microenvironment. This study aims to investigate the potential role of PD-L1 in regulating TAMs in glioblastoma. Gene expression data and clinical information of glioma patients were collected from TCGA (n = 614) and CGGA (n = 325) databases. Differentially expressed genes between PD-L1high and PD-L1low groups were identified and subjected to bioinformatical analysis. We found that PD-L1 was frequently expressed in gliomas with a grade-dependent pattern. Higher PD-L1 expression predicted shorter overall survival. Moreover, PD-L1 was positively correlated with immunosuppressive cells (macrophage, neutrophil and immature DC) and negatively correlated with cytocidal immune cells (CD8+ T cell and Th1). Importantly, PD-L1 high expression was significantly correlated with M2-polarization of macrophages (M2-TAMs). We conclude that PD-L1 is an unfavourable prognostic marker for patients with glioblastoma; PD-L1-mediated immunosuppression may attribute to the infiltration and M2-polarization of TAMs.

scholarly journals NF-κB—An Important Player in Xenoestrogen Signaling in Immune Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1799
Author(s):  
Karolina Nowak ◽  
Ewa Jabłońska ◽  
Wioletta Ratajczak-Wrona
Keyword(s):  
Immune System ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Immune Cells ◽  
Estrogen Signaling ◽  
Cellular Processes ◽  
Pathogenic Factors ◽  
Important Player ◽  
Exogenous Factors

The proper functioning of the immune system is critical for an effective defense against pathogenic factors such as bacteria and viruses. All the cellular processes taking place in an organism are strictly regulated by an intracellular network of signaling pathways. In the case of immune cells, the NF-κB pathway is considered the key signaling pathway as it regulates the expression of more than 200 genes. The transcription factor NF-κB is sensitive to exogenous factors, such as xenoestrogens (XEs), which are compounds mimicking the action of endogenous estrogens and are widely distributed in the environment. Moreover, XE-induced modulation of signaling pathways may be crucial for the proper development of the immune system. In this review, we summarize the effects of XEs on the NF-κB signaling pathway. Based on our analysis, we constructed a model of XE-induced signaling in immune cells and found that in most cases XEs activate NF-κB. Our analysis indicated that the indirect impact of XEs on NF-κB in immune cells is related to the modulation of estrogen signaling and other pathways such as MAPK and JAK/STAT. We also summarize the role of these aspects of signaling in the development and further functioning of the immune system in this paper.

scholarly journals Controlling TIME: How MNK Kinases Function to Shape Tumor Immunity

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2096
Author(s):  
Thao N.D. Pham ◽  
Christina Spaulding ◽  
Hidayatullah G. Munshi
Keyword(s):  
Systematic Review ◽  
Immune System ◽  
Side Effects ◽  
Immune Cells ◽  
Cancer Development ◽  
Interacting Protein ◽  
Immune Systems ◽  
Adaptive Immune ◽  
Adaptive Immune Systems

A number of studies have clearly established the oncogenic role for MAPK-interacting protein kinases (MNK) in human malignancies. Modulation of MNK activity affects translation of mRNAs involved in cancer development, progression, and resistance to therapies. As a result, there are ongoing efforts to develop and evaluate MNK inhibitors for cancer treatment. However, it is important to recognize that MNK activity also plays an important role in regulating the innate and adaptive immune systems. A better understanding of the role of MNK kinases and MNK-mediated signals in regulating the immune system could help mitigate undesired side effects while maximizing therapeutic efficacy of MNK inhibitors. Here, we provide a systematic review on the function of MNK kinases and their substrates in immune cells.

scholarly journals The Controversial Role of Microglia in Malignant Gliomas

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Jun Wei ◽  
Konrad Gabrusiewicz ◽  
Amy Heimberger
Keyword(s):  
Immune Cells ◽  
Malignant Gliomas ◽  
Therapeutic Strategies ◽  
Activated Microglia ◽  
Immunosuppressive Cells ◽  
Glioma Microenvironment

Malignant gliomas contain stroma and a variety of immune cells including abundant activated microglia/macrophages. Mounting evidence indicates that the glioma microenvironment converts the glioma-associated microglia/macrophages (GAMs) into glioma-supportive, immunosuppressive cells; however, GAMs can retain intrinsic anti-tumor properties. Here, we review and discuss this duality and the potential therapeutic strategies that may inhibit their glioma-supportive and propagating functions.

Nitric Oxide-Cyclic GMP Signaling Pathway in the Regulation of Rabbit Clitoral Cavernosum Tone1

2002 ◽  
Vol 227 (11) ◽  
pp. 1022-1030 ◽  
Author(s):  
Jong Kwan Park ◽  
Jung Ui Kim ◽  
Soon Oak Lee ◽  
Pyoung Han Hwang ◽  
Ho Keun Yi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Electrical Field Stimulation ◽  
Nerve Fibers ◽  
Nadph Diaphorase ◽  
Rt Pcr ◽  
Electrical Field ◽  
Cgmp Signaling ◽  
Polymerase Chain

We investigated the role of nitric oxide (NO)-guanosine 3′,5′-cyclic monophosphate (cGMP) signaling in the regulation of rabbit clitoral cavernosum (CC) tone. Tension measurements, reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and NADPH-diaphorase staining were performed in CC. In the precontracted CC strips with phenylephrine (10–5 M), acetylcholine (ACh) relaxed, dependent on dosage. Pretreatment with atropine, Nω nitro-l-arginine-methyl ester (NAME) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), guanylate cyclase inhibitor abolished the ACh-induced relaxations, but tetrodotoxin (TTX) did not. Sodium nitroprusside relaxed the strips in the presence of atropine and NAME, but not in the presence of ODQ. Electrical field stimulation (EFS) relaxed the strips dependent on stimulus strength. Pretreatment with TTX, NAME, or ODQ abolished the EFS-induced relaxation, but atropine did not. l-Arginine partially restored the inhibited response to ACh and EFS. The inducible NO synthase (iNOS) and neuronal NOS (nNOS) mRNAs and iNOS and endothelial NOS (eNOS) proteins were identified in the CC. NADPH-diaphorase staining revealed the positivity on the nerve trunks and fine nerve fibers in the CC. Finally, results demonstrate that the nNOS, ENOS, and the NO-cGMP signaling pathway are involved in the regulation of clitoral tumescence.

scholarly journals Content of cells of innate and acquired immunity in peripheral blood in brain tumors

2019 ◽  
pp. 397-408
Author(s):  
Mykola Lisianyi ◽  
Iryna Hnidkova ◽  
Liudmyla Belska ◽  
Anastasiia Palamarchuk ◽  
Viktoriia Vaslovych
Keyword(s):  
Brain Tumors ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Comparison Group ◽  
Malignant Tumors ◽  
Benign Tumors ◽  
Acquired Immunity ◽  
Mesenchymal Tumors ◽  
Immune Systems

In this work, the level of cells of the innate and acquired immunity, namely leukocytes, neutrophils, platelets and lymphocytes in the peripheral blood of 168 patients with brain tumors of different histogenesis and anaplasia degree at different stages of surgical treatment was researched. Studies have found that the content of cells of innate and acquired immunity, namely neutrophils, platelets and lymphocytes in the peripheral blood of patients with brain tumors depends on the histogenesis of the tumor and the degree of anaplasia. In neuroectodermal and mesenchymal tumors, neutrophil count is increased and lymphocyte levels are reduced, while in neuroepithelial brain tumors (pituitary adenomas), the ratios between the cells of the innate and acquired immune systems in relation to the comparison group are not changed. In case of malignant glial tumors (glioblastomas) and brain metastases, the absolute content of neutrophils and platelets increases significantly, so does the ratio of N / Lf and Р/Lf cells in the blood compared with benign tumors. In the postoperative period, despite the removal of the bulk of the tumor during surgery, there is no restoration of the content of the studied subpopulations of cells in peripheral blood, which indicates the role of both immunoregulatory tumor and other extra-tumor factors and mechanisms that cause an imbalance of individual parts of the immune system. With repeated operations, the imbalance in the composition of immune cells in the peripheral blood changes depending on the degree of anaplasia: with malignant tumors of glial origin, this imbalance remains at the same level as during primary operations while with benign astrocytomas it increases and approaches the indicators observed in malignant tumors. Indicators of the які спостерігаються при злоякісних пухлинах. Показники співвідношення рівня імунних клітин периферичної крові (Тр / ЛФ, Тр / Нф, Нф / ЛФ) відображають стан вродженого і набутого імунітету і можуть слугувати додатковими показниками особливостей порушень в різних ланках імунної системи та прогнозу клінічного перебігу пухлинного процесу. Ключові слова: пухлини головного мозку, вроджений і набутий імунітет, нейтрофіли, тромбоцити і лімфоцити. Для цитування: Лісяний МІ, Гнідкова ІО, Бєльська ЛМ, Паламарчук АВ, Васлович ВВ. Вміст клітин вродженого та набутого імунітету в периферичній крові при пухлинах головного мозку. Журнал Національної академії медичних наук України. 2019;25(4):397–408.

scholarly journals Purinergic Signaling in Neutrophils During Inflammatory Diseases

2020 ◽  
Author(s):  
Hui Sun ◽  
Gang Xu ◽  
Pingsong Li ◽  
Yumei Li ◽  
Bingwei Sun
Keyword(s):  
Immune System ◽  
Immune Cells ◽  
Inflammatory Disease ◽  
Inflammatory Diseases ◽  
Purinergic Signaling ◽  
Regulatory Function ◽  
Potential Contribution ◽  
Complex Events ◽  
Inflammatory Molecules

Purinergic signaling is that nucleotides (especially ATP) and adenosine are utilized as transmitter molecules, which play an important role in the immune system. In the extracellular ventricle, ATP plays a significant role of pro-inflammatory molecules mainly through activating P2 receptors, while adenosine plays the role of anti-inflammatory molecules mainly through activating P1 receptors. As we know，neutrophils are the most abundant immune cells in our circulation and have become an essential part of coordinating a series of complex events during inflammatory diseases. However, due to the destruction of inflammatory substances from neutrophils, the activation of neutrophils is fine-tuned, and purinergic signaling is associated with this process. As a matter of fact, altering the balance between P2 and P1 signals is of great importance for neutrophils to exert immune activities properly. Here, we review the role of purinergic signaling in regulatory function of neutrophils during inflammatory disease, and then discuss the potential contribution of targeted purinergic signals in the treatment of the neutrophil during inflammatory diseases.

scholarly journals The Role of Immune Cells in Oxi-Inflamm-Aging

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2974
Author(s):  
Irene Martínez de Toda ◽  
Noemi Ceprián ◽  
Estefanía Diaz-Del Cerro ◽  
Mónica De la Fuente
Keyword(s):  
Oxidative Stress ◽  
Immune System ◽  
Immune Cells ◽  
Low Grade ◽  
Inflammatory Stress ◽  
Immune Systems ◽  
Age Related ◽  
Chronic Oxidative Stress ◽  
Inflammatory State

Aging is the result of the deterioration of the homeostatic systems (nervous, endocrine, and immune systems), which preserve the organism’s health. We propose that the age-related impairment of these systems is due to the establishment of a chronic oxidative stress situation that leads to low-grade chronic inflammation throughout the immune system’s activity. It is known that the immune system weakens with age, which increases morbidity and mortality. In this context, we describe how the function of immune cells can be used as an indicator of the rate of aging of an individual. In addition to this passive role as a marker, we describe how the immune system can work as a driver of aging by amplifying the oxidative-inflammatory stress associated with aging (oxi-inflamm-aging) and inducing senescence in far tissue cells. Further supporting our theory, we discuss how certain lifestyle conditions (such as social environment, nutrition, or exercise) can have an impact on longevity by affecting the oxidative and inflammatory state of immune cells, regulating immunosenescence and its contribution to oxi-inflamm-aging.

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