Hydrogen Sulfide and Neurogenic Inflammation in Sepsis
Author Information
Author(s): Ang Seah-Fang, Moochhala Shabbir M., MacAry Paul A., Bhatia Madhav
Primary Institution: National University of Singapore
Hypothesis
Is substance P an important neural element that implicates in H2S-induced neurogenic inflammation in sepsis in a TRPV1-dependent manner?
Conclusion
H2S regulates TRPV1-mediated neurogenic inflammation in polymicrobial sepsis through enhancement of substance P production and activation of the ERK-NF-κB pathway.
Supporting Evidence
- H2S was shown to induce neurogenic inflammation in polymicrobial sepsis.
- Capsazepine significantly attenuated H2S-induced substance P production.
- Administration of NaHS resulted in increased pulmonary and plasma substance P levels in sepsis.
Takeaway
This study shows that a gas called hydrogen sulfide can make inflammation worse during a serious infection called sepsis by affecting a special protein that helps send pain signals.
Methodology
Male Swiss mice were subjected to cecal ligation and puncture (CLP)-induced sepsis and treated with various substances to assess the effects on inflammation and organ dysfunction.
Potential Biases
Potential bias in the selection of animal models and the interpretation of results based on specific treatment groups.
Limitations
The study primarily focused on male Swiss mice, which may limit the generalizability of the findings to other populations.
Participant Demographics
Male Swiss mice, weighing 25-30 g.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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