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Updated: Jun 8, 2026

Murine Model of Epicutaneously-Induced Immunomodulation
Published on: June 24, 2025
Effect of anaphylactic shock on suppressors of cytokine signaling
Zhenyu Li1, Yanbing Liang, Hao Tang
1Department of General Internal Medicine, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Abstract:
The pathophysiologic mechanisms of anaphylactic shock still remain unclear. In this study, we investigated the changes of expression and translation of SOCS1/SOCS3 in the heart, lungs, kidney, liver and spleen from patients who died of anaphylactic shock. Samples from the same viscera of 8 patients who died of anaphylactic shock and 8 healthy controls who died from accidents were collected in the present study. The level of IgE was measured in heart, and SOCS1/ SOCS3 mRNA and protein expression were determined by RT-PCR and immunohistochemistry, respectively. As a result, the higher IgE level was detected in the blood samples from the patients' heart than the control. SOCS1 and SOCS3 protein were significantly increased in the kidney and liver than the control. After anaphylactic shock, the expression of SOCS1 and SOCS3 mRNA were also increased. The expression level of SOCS3 mRNA was higher than that of SOCS1 in all viscera, and both were the highest in liver and kidney. There was a positive correlation between SOCS1 mRNA and SOCS3 mRNA in liver and kidney after anaphylactic shock. Our results indicate that SOCS1 and SOCS3 may play a regulatory role in anaphylactic shock viscera injury processes during anaphylactic shock.
Insights
Anaphylactic shock mechanisms remain unclear. This study found increased SOCS1 and SOCS3 proteins and mRNA in organs like the kidney and liver, suggesting their role in anaphylactic shock organ injury.
Area of Science:
- Immunology
- Pathophysiology
- Molecular Biology
Background:
- The precise pathophysiologic mechanisms underlying anaphylactic shock are not fully understood.
- Suppressor of Cytokine Signaling (SOCS) proteins, including SOCS1 and SOCS3, are critical regulators of immune responses.
- Investigating SOCS1/SOCS3 expression may elucidate their role in anaphylactic shock-induced organ damage.
Purpose of the Study:
- To investigate the expression and translation of SOCS1 and SOCS3 in visceral organs of patients who died from anaphylactic shock.
- To compare SOCS1/SOCS3 levels with healthy controls to identify changes associated with anaphylactic shock.
- To explore the potential involvement of SOCS1 and SOCS3 in the organ injury observed during anaphylactic shock.
Main Methods:
- Analysis of visceral organ samples (heart, lungs, kidney, liver, spleen) from 8 anaphylactic shock fatalities and 8 accidental death controls.
- Measurement of immunoglobulin E (IgE) levels in heart blood.
- Determination of SOCS1/SOCS3 mRNA and protein expression using RT-PCR and immunohistochemistry, respectively.
Main Results:
- Elevated IgE levels were detected in the heart blood of anaphylactic shock patients compared to controls.
- Significant increases in SOCS1 and SOCS3 protein expression were observed in the kidney and liver.
- Both SOCS1 and SOCS3 mRNA levels were elevated post-anaphylactic shock, with SOCS3 expression higher than SOCS1, particularly in the liver and kidney.
Conclusions:
- SOCS1 and SOCS3 expression is altered in visceral organs following anaphylactic shock.
- The increased expression of SOCS1 and SOCS3, especially in the liver and kidney, suggests a potential regulatory role in anaphylactic shock-induced organ injury.
- Further research is warranted to fully elucidate the specific mechanisms by which SOCS1 and SOCS3 contribute to anaphylactic shock pathophysiology.
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