IP-10, a Potential Driver of Neurally-Controlled IL-10 and Morbidity in Human Blunt Trauma

Crit Care Med, 2014 · DOI: 10.1097/CCM.0000000000000248 · Published: June 1, 2014

Simple Explanation

Blunt trauma and traumatic spinal cord injury (TSCI) induce systemic inflammation that contributes to morbidity. This study compares the dynamic systemic inflammatory responses of TSCI vs. non-SCI patients. The chemokine IP-10/CXCL10 drives systemic IL-10 in TSCI patients.

Study Duration

June 2008 to November 2011

Participants

21 severely-injured thoraco-cervical TSCI patients and matched 21 severely-injured blunt trauma patients without spinal cord injury (non-SCI)

Evidence Level

Retrospective study

Key Findings

1
Circulating IL-10 was significantly elevated in thoraco-cervical TSCI vs. non-SCI, whereas IL-1β, sIL-2Rα, IL-4, IL-5, IL-7, IL-13, IL-17, MIP-1α and -1β, GM-CSF, and IFN-γ were significantly reduced in TSCI vs. non-SCI.
2
Post-SCI IL-10 is driven by IP-10, whereas MCP-1 was central in non-SCI dynamic networks.
3
Individuals with plasma IP-10 levels ≥ 730 pg/ml had significantly prolonged hospital and ICU stay and days on mechanical ventilator vs. patients with plasma IP-10 < 730 pg/ml.

Research Summary

This study compares the dynamic systemic inflammatory responses of TSCI vs. non-SCI patients, suggesting a key role for IP-10 in driving systemic IL-10 and morbidity. The systemic inflammatory responses of these two cohorts of patients differ significantly and specifically: in thoraco-cervical TSCI patients, IL-10 is highly elevated, and most other inflammatory mediators measured are suppressed. The chemokine IP-10/CXCL10 drives systemic IL-10 in TSCI patients, while the chemokine MCP-1/CCL2 drives multiple mediators, including IL-6, in non-SCI patients.

Practical Implications

Biomarker for Adverse Outcomes

IP-10/CXCL10 and IL-10 may serve as biomarkers of adverse outcomes post-injury, even in the absence of TSCI.

Targeted Therapies

The insights from this study may lead to better diagnosis and targeted therapeutic modulation of inflammation post-trauma and TSCI.

Understanding Immunodepression

The study highlights the profound blunting of systemic inflammation post-TSCI, which could inform strategies to address immunodepression.

Study Limitations

1
The number of inflammatory mediators analyzed
2
Data were missing later time points of inflammatory mediators in non-SCI patients, specifically at 10, 11, and 12 days post-injury.
3
Qualitative assessment of the functional status of TSCI patients was not available; complications were used as a predictor of functional recovery.

Your Feedback

Was this summary helpful?

Back to Spinal Cord Injury