AI Article Synopsis
- Neurogenic inflammation is a local inflammatory response influenced by neuropeptide release in various organs, affecting leukocyte behavior in the knee joint's microcirculation.
- The study shows that stimulating the saphenous nerve can alter leukocyte rolling in the synovial microcirculation, with the frequency of stimulation playing a critical role.
- Pre-treatment with specific antagonists suggests that endocannabinoids are involved in modulating this inflammatory response, highlighting their potential therapeutic role in managing inflammation.
Article Abstract
Neurogenic inflammation is a local inflammatory response that is driven by the peripheral release of neuropeptides from small diameter afferents which occurs in many organs including joints. The knee joint has a rich endocannabinoid system which has been shown to decrease acute synovitis. The aim of this study was to investigate the influence of joint afferents on leukocyte-endothelial interactions within the synovial microcirculation of mice and determine the role of endocannabinoids on this inflammatory response. Electrical, antidromic stimulation of the saphenous nerve decreased leukocyte rolling at the lowest frequency tested (0.5Hz), while increasing leukocyte rolling at higher frequencies (2.0 and 5.0Hz). The leukocyte rolling effect of nerve stimulation was completely abolished by pre-treating the knee with the vasoactive intestinal peptide antagonist VIP; however, neither calcitonin gene related peptide nor substance P antagonism had an effect on this neurogenic inflammatory response. Treating knees with the endocannabinoid breakdown inhibitor URB597 completely blocked leukocyte rolling and this effect could be reversed with the non-canonical cannabinoid antagonist O-1918. These results provide evidence that antidromic stimulation of the mouse saphenous nerve promotes leukocyte rolling within the synovial microcirculation, and that endocannabinoids can attenuate this neurogenic inflammatory response.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.npep.2016.08.007 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CRP deposition in human abdominal aortic aneurysm is associated with transcriptome alterations toward aneurysmal pathogenesis: insights from spatial whole transcriptomic analysis.
Front Immunol
December 2024
Department of Thoracic and Cardiovascular Surgery, Seoul Metropolitan Government-Seoul National University (SMG-SNU) Boramae Medical Center, Seoul National University College of Medicine, Seoul, Republic of Korea.
Background: We investigated the effects of C-reactive protein (CRP) deposition on the vessel walls in abdominal aortic aneurysm (AAA) by analyzing spatially resolved changes in gene expression. Our aim was to elucidate the pathways that contribute to disease progression.
Methods: AAA specimens from surgically resected formalin-fixed paraffin-embedded tissues were categorized into the AAA-high CRP [serum CRP ≥ 0.
Targeting P-selectin and interleukin-1β in mice with sickle cell disease: effects on vaso-occlusion, liver injury and organ iron deposition.
Haematologica
November 2024
Hematology Center, University of Campinas - UNICAMP, Campinas - São Paulo.
Continuous vaso-occlusive and inflammatory processes cause extensive end-organ damage in adults with sickle cell disease (SCD), and there is little evidence that longterm hydroxyurea therapy prevents this. In initial trials, P-selectin blockade with crizanlizumab reduced SCD vaso-occlusive crisis frequency, and interleukin (IL)-1β inhibition in SCD patients, using canakinumab, lowered inflammatory markers. We used murine SCD models to examine the effects of acute and chronic blockade of Pselectin and of IL-1β on vaso-occlusive events, their inflammatory profile and organ health.
View Article and Find Full Text PDFType 2 diabetes remodels collateral circulation and promotes leukocyte adhesion following ischemic stroke.
bioRxiv
October 2024
Department of Neurological Surgery, University of California San Francisco, San Francisco, CA, USA.
Article Synopsis
- Type 2 diabetes mellitus (T2DM) leads to smaller pial vessels and lower blood flow velocity before and after a stroke, contributing to poor recovery outcomes.
- After a stroke, T2DM mice showed persistent deficits in blood flow and increased leukocyte adhesion to blood vessel walls, highlighting chronic inflammation's role in complicating recovery.
- The study used two-photon microscopy to analyze blood flow dynamics, vessel remodeling, and inflammation in the brain, suggesting that T2DM-induced changes worsen stroke effects.
Gingival inflammation and leukocyte-endothelium cell interactions in women with polycystic ovary syndrome.
J Periodontol
October 2024
Department of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research, Valencia, Spain.
Article Synopsis
- This study explores the impact of gingivitis on inflammation and cardiovascular risks in women with polycystic ovary syndrome (PCOS).
- The research involved three groups of participants: two with PCOS (one with gingivitis and one without) and a control group, all assessed for various health indicators and inflammatory markers.
- Results indicated that PCOS patients, especially those with gingivitis, had higher levels of systemic inflammation and more aggressive neutrophil behavior, which may increase the risk of atherosclerosis.
Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy.
J Vis Exp
September 2024
Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main;
Article Synopsis
- Intestinal ischemia-reperfusion (I/R) injury is a severe condition caused by reduced blood flow to the intestines, leading to significant tissue damage and poor health outcomes.
- The study uses a microsurgical model combined with intravital microscopy to observe the behaviors of immune cells (like leukocytes) during I/R injury, particularly focusing on the role of the endothelial PAR1 receptor.
- Results show that mice lacking the PAR1 receptor had less leukocyte adhesion and reduced formation of neutrophil extracellular traps (NETs), suggesting that PAR1 is a critical factor in the inflammatory response during I/R injury.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!