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Sepsis-Induced Inhibition of Contractile Function of Lymphatic Nodes
M E Kosareva1, A V Chivildeev1, G I Lobov2
1I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.
Bulletin of Experimental Biology and Medicine
|February 9, 2024
Summary
Inflammation following cecal ligation and puncture (CLP) in rats reduces lymph node capsule contractility. Inflammatory mediators like nitric oxide and prostaglandins likely cause this decreased contractile function in mesenteric lymph nodes.
Area of Science:
- Immunology
- Physiology
- Vascular Biology
Background:
- Inflammation is a key component of numerous diseases.
- The lymphatic system plays a crucial role in inflammatory processes, influencing both their onset and resolution.
- Understanding lymph node function during inflammation is vital for comprehending systemic responses.
Purpose of the Study:
- To investigate the impact of cecal ligation and puncture (CLP)-induced inflammation on the contractile function of rat mesenteric lymph nodes.
- To identify the molecular mechanisms underlying changes in lymph node contractility post-CLP.
Main Methods:
- Cecal ligation and puncture (CLP) model in rats to induce abdominal inflammation.
- Ex vivo assessment of mesenteric lymph node contractile function using a myograph.
- Analysis of the expression of key inflammatory mediators, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and cystathionine-γ-lyase (CSE).
Main Results:
- Lymph nodes from CLP-operated rats exhibited significantly reduced tension compared to sham-operated controls.
- Increased expression of iNOS, COX-2, and CSE was detected in the lymph nodes of CLP rats.
- The inflammatory mediators nitric oxide (NO), prostaglandins, and hydrogen sulfide (H2S) were found to inhibit the contractile activity of smooth muscle cells in the lymph node capsule.
Conclusions:
- CLP-induced inflammation impairs the contractile function of rat mesenteric lymph nodes.
- The observed decrease in contractility is attributed to the inhibitory effects of inflammatory mediators (NO, prostaglandins, H2S) on lymph node smooth muscle cells.
- These findings highlight a novel mechanism by which inflammation affects lymphatic system function.
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