Inflammation-Associated Co-morbidity Between Depression and Cardiovascular Disease

Current topics in behavioral neurosciences, Journal Year: 2016, Volume and Issue: unknown, P. 45 - 70

Published: Jan. 1, 2016

Language: Английский

---

Chronic stress promotes gastric cancer progression and metastasis: an essential role for ADRB2

Cell Death and Disease, Journal Year: 2019, Volume and Issue: 10(11)

Published: Oct. 17, 2019

An increasing number of studies indicate that adrenergic signalling plays a fundamental role in chronic stress-induced tumour progression and metastasis. However, its function gastric cancer (GC) potential mechanisms remain unknown. The expression levels β-adrenergic receptor (ADRB) GC cell lines were examined by using real-time polymerase chain reaction (RT-PCR) western blotting. effects β2 (ADRB2) activation blockade investigated vitro cells proliferation, migration, invasion, cycle apoptosis assays. Chronic restraint stress (CRS) increased the plasma catecholamines cortisol also induced metastasis vivo. Furthermore, immunohistochemical staining TUNEL assay employed to observe regulation viability ADRB2 100 human samples measured RT-PCR immunohistochemistry. hormones epinephrine norepinephrine significantly accelerated invasion culture, as well growth These reversed ADRB antagonists propranolol ICI118,551 (an ADRB2-specific antagonist). Moreover, selective ADRB1 antagonist atenolol had almost no effect on proliferation suppressed inhibiting ERK1/2-JNK-MAPK pathway transcription factors, such NF-κB, AP-1, CREB STAT3. Analysis xenograft models revealed inhibited metastasis, antagonized these inhibitory effects. In addition, VEGF, MMP-2, MMP-7 MMP-9 transplanted tissue, catecholamine enhanced metastasis-related proteins. was upregulated tissues positively correlated with size, histological grade, lymph node clinical stage samples. Stress hormone-induced crucial findings regulates suggest novel strategy complement existing therapies for GC.

Language: Английский

---

The Anti-Inflammatory Actions and Mechanisms of Acupuncture from Acupoint to Target Organs via Neuro-Immune Regulation

Journal of Inflammation Research, Journal Year: 2021, Volume and Issue: Volume 14, P. 7191 - 7224

Published: Dec. 1, 2021

Inflammation plays a significant role in the occurrence and development of multiple diseases. This study comprehensively reviews presents literature from last five years, showing that acupuncture indeed exerts strong anti-inflammatory effects biological systems, namely, immune, digestive, respiratory, nervous, locomotory, circulatory, endocrine, genitourinary systems. It is well known localized acupuncture-mediated involve regulation populations functions immune cells, including macrophages, granulocytes, mast T cells. In stimulation, macrophages transform M1 to M2 phenotype negative TLR4 regulator PPARγ activated inhibit intracellular TLR/MyD88 NOD signaling pathways. The downstream IκBα/NF-κB P38 MAPK pathways are subsequently inhibited by acupuncture, followed suppressed production inflammasome proinflammatory mediators. Acupuncture also modulates balance helper cell populations. Furthermore, it inhibits oxidative stress enhancing SOD activity via Nrf2/HO-1 pathway eliminates generation oxygen free radicals, thereby preventing inflammatory infiltration. on different systems specific individual organ microenvironments. As part its action, deforms connective tissue upregulates secretion various molecules acupoints, further activating NF-κB, MAPK, ERK fibroblasts, keratinocytes, monocytes/macrophages. somatic afferents present acupuncture-activated acupoints convey sensory signals spinal cord, brainstem, hypothalamic neurons. Upon information integration brain, stimulates neuro-immune pathways, cholinergic anti-inflammatory, vagus-adrenal medulla-dopamine, sympathetic as hypothalamus-pituitary-adrenal axis, ultimately acting cells release crucial neurotransmitters hormones. review provides scientific reliable basis viewpoints for clinical application conditions.

Language: Английский

---

Manipulation of the inflammatory reflex as a therapeutic strategy

Cell Reports Medicine, Journal Year: 2022, Volume and Issue: 3(7), P. 100696 - 100696

Published: July 1, 2022

The cholinergic anti-inflammatory pathway is the efferent arm of inflammatory reflex, a neural circuit through which CNS can modulate peripheral immune responses. Signals communicated via vagus and splenic nerves use acetylcholine, produced by Choline acetyltransferase (ChAT)+ T cells, to downregulate actions macrophages expressing α7 nicotinic receptors. Pre-clinical studies using transgenic animals, agonists, vagotomy, nerve stimulation have demonstrated this pathway's role therapeutic potential in numerous diseases. In review, we summarize what understood about reflex. We also demonstrate how pre-clinical findings are being translated into promising clinical trials, draw particular attention innovative bioelectronic methods harnessing for use.

Language: Английский

---

C1 neurons mediate a stress-induced anti-inflammatory reflex in mice

Nature Neuroscience, Journal Year: 2017, Volume and Issue: 20(5), P. 700 - 707

Published: March 13, 2017

Language: Английский

---

Vagal Regulation of Group 3 Innate Lymphoid Cells and the Immunoresolvent PCTR1 Controls Infection Resolution

Immunity, Journal Year: 2017, Volume and Issue: 46(1), P. 92 - 105

Published: Jan. 1, 2017

Language: Английский

---

Vagal afferent activation suppresses systemic inflammation via the splanchnic anti-inflammatory pathway

Brain Behavior and Immunity, Journal Year: 2018, Volume and Issue: 73, P. 441 - 449

Published: June 5, 2018

Language: Английский

---

Vagal tone: effects on sensitivity, motility, and inflammation

Neurogastroenterology & Motility, Journal Year: 2016, Volume and Issue: 28(4), P. 455 - 462

Published: March 24, 2016

Abstract The vagus nerve ( VN ) is a key element of the autonomic nervous system. As mixed nerve, contributes to bidirectional interactions between brain and gut, i.e., brain‐gut axis. In particular, after integration in central network peripheral sensations such as inflammation pain via vagal spinal afferents, an efferent response through modulation preganglionic parasympathetic neurons dorsal motor nucleus and/or sympathetic cord able modulate gastrointestinal nociception, motility, inflammation. A low tone, assessed by heart rate variability, marker sympatho‐vagal balance, observed functional digestive disorders inflammatory bowel diseases. To restore normal tone appears goal Among therapeutic tools, drugs targeting cholinergic system complementary medicine (hypnosis, meditation…), deep breathing, physical exercise, stimulation VNS ), either invasive or non‐invasive, innovative. There new evidence current issue this Journal supporting role functions.

Language: Английский

---

Beyond the Brain: Peripheral Interactions after Traumatic Brain Injury

Journal of Neurotrauma, Journal Year: 2020, Volume and Issue: 37(5), P. 770 - 781

Published: Feb. 11, 2020

Traumatic brain injury (TBI) is a leading cause of death and disability, there are currently no pharmacological treatments known to improve patient outcomes. Unquestionably, contributing toward lack effective the highly complex heterogenous nature TBI. In this review, we highlight recent surge research that has demonstrated various central interactions with periphery as potential major contributor heterogeneity and, in particular, breadth from Australia. We describe growing evidence how extracranial factors, such polytrauma infection, can significantly alter TBI neuropathology. addition, dysregulation autonomic nervous system systemic inflammatory response induced by have profound pathophysiological effects on peripheral organs, heart, lung, gastrointestinal tract, liver, kidney, spleen, bone. Collectively, review firmly establishes condition. Further, occur after must be further explored accounted for ongoing search treatments.

Language: Английский

---

Intrastriatal injection of preformed alpha-synuclein fibrils alters central and peripheral immune cell profiles in non-transgenic mice

Journal of Neuroinflammation, Journal Year: 2019, Volume and Issue: 16(1)

Published: Dec. 1, 2019

Abstract Parkinson’s disease (PD) is characterized by the accumulation of alpha-synuclein (α-syn) inclusions, major component Lewy bodies. Extracellular α-syn aggregates act as a damage-associated molecular pattern (DAMP) and presence autoantibodies against species in cerebrospinal fluid serum PD patients implicate involvement innate adaptive immune responses. In non-transgenic (Tg) mice, intrastriatal injection preformed fibril (PFF) results widespread pathologic inclusions CNS. While PFF model has been broadly utilized to study mechanistic relationship between transmission other neuropathological phenotypes, phenotypes this are not clearly demonstrated. This aimed characterize during propagation utilizing α-syn–injected non-tg mice. Here, we showed that prevalent various brain regions gut at 5 months post (p.i.), preceding degeneration dopaminergic neurons substantia nigra (SN). We discovered distinct inflammatory response involving both activation microglia astrocytes infiltration B, CD4+ T, CD8+ natural killer cells p.i. Moreover, mice display significant alterations frequency number leukocyte subsets spleen lymph nodes with minimum blood. Our data provide primary evidence intracerebral-initiated synucleinopathies alter cell profiles CNS peripheral lymphoid organs. Furthermore, our provides support for mouse assess connection responses synuclein pathology.

Language: Английский

---