Codonopsis pilosula polysaccharide attenuates the inflammatory response in macrophages induced by Brucella abortus outer membrane protein 19 via regulating ATP2A1 to modulate cell adhesion and calcium signaling - Report - MDSpire
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Codonopsis pilosula polysaccharide attenuates the inflammatory response in macrophages induced by Brucella abortus outer membrane protein 19 via regulating ATP2A1 to modulate cell adhesion and calcium signaling
Polysaccharides from Codonopsis pilosula Reduce Macrophage Inflammation
Overview
This study demonstrates that polysaccharides from Codonopsis pilosula (CPPS) significantly reduce macrophage inflammation induced by Brucella abortus outer membrane protein 19 (OMP19). CPPS achieves this by modulating ATP2A1 expression, affecting cell adhesion and calcium signaling pathways.
Background
Brucellosis is a significant zoonotic disease with a high incidence globally, particularly in endemic regions. The disease is characterized by its ability to evade host immune responses, leading to chronic infections. Understanding the mechanisms of inflammation and potential therapeutic interventions is crucial for improving treatment outcomes in brucellosis.
Data Highlights
In vivo, CPPS reduced tissue damage and downregulated HMGB1, E-cadherin, and paxillin. In vitro, it inhibited SYK/FAK/AKT phosphorylation and PKC activation, while modulating cytokine profiles by decreasing TNF-α and IL-6 and increasing IL-10.
Key Findings
CPPS alleviated tissue damage in vivo and downregulated key inflammatory markers.
In vitro, CPPS inhibited critical signaling pathways associated with inflammation.
CPPS modulated the cytokine profile, reducing pro-inflammatory cytokines and increasing anti-inflammatory cytokines.
ATP2A1 was identified as a key gene involved in the anti-inflammatory effects of CPPS.
CPPS reduced intracellular calcium ion concentrations, impacting cell adhesion and signaling.
Clinical Implications
The findings suggest that CPPS may serve as a potential therapeutic agent for managing inflammation in brucellosis. By targeting ATP2A1 and related signaling pathways, CPPS could enhance macrophage function and improve clinical outcomes in patients with brucellosis.
Conclusion
CPPS demonstrates significant anti-inflammatory effects in macrophages challenged by Brucella OMP19, highlighting its potential as a therapeutic strategy in brucellosis management.