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Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
Published on: June 6, 2011
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Single-Cell Transcriptomics Reveals Compartment-Specific Differences in Immune Responses and Contributions for
Guang Fu1,2, Tianmeng Chen2,3, Junru Wu1,2
1Department of General Surgery, the Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Shock (Augusta, Ga.)
|March 12, 2021
Summary
Hemorrhagic shock with tissue trauma (HS/T) alters immune cell gene expression across blood, liver, and spleen. Complement factor 3 (C3) plays a key role in modulating these immune responses, impacting cell migration and interferon signaling.
Area of Science:
- Immunology
- Systems Biology
- Transcriptomics
Background:
- Hemorrhagic shock with tissue trauma (HS/T) triggers a systemic immune-inflammatory response.
- Single-cell analysis enables comprehensive immune cell profiling across multiple tissues.
Purpose of the Study:
- To investigate immune cell transcriptomic changes in response to HS/T across different body compartments.
- To elucidate the role of complement factor 3 (C3) in modulating HS/T-induced immune responses.
Main Methods:
- Single-cell RNA sequencing of leukocytes from blood, liver, and spleen in a mouse HS/T model.
- Analysis of gene expression patterns in wild-type and C3 knockout mice.
Main Results:
- HS/T induced significant gene expression shifts in monocytes, B cells, and T cells.
- Monocytes showed increased migration genes and decreased interferon signaling genes.
- C3 knockout altered monocyte gene expression and promoted interferon signaling in B and T cells.
Conclusions:
- HS/T profoundly impacts immune cell transcriptomes systemically.
- C3 is a critical regulator of monocyte activation and B/T cell interferon responses post-trauma.
- This study provides a detailed immune cell landscape of trauma response.

