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Altered monocyte and NK cell phenotypes correlate with posttrauma infection
Anupamaa Seshadri1, Gabriel A Brat, Brian K Yorkgitis
1From the Department of Surgery, Brigham and Women's Hospital and Harvard Medical School (A.S., B.K.Y., M.G., J.K., J.P.N., W.L., Y.N., T.W., A.S., R.A., J.A.L.); Boston, Massachusetts; Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School (G.A.B. C.H.), Boston, MA.
Trauma alters immune cell markers like CD86 on monocytes and CD39 on NK cells, potentially predicting infection risk. These findings offer insights into immune responses following severe injury.
Area of Science:
- Immunology
- Systems Biology
- Trauma Research
Background:
- Trauma triggers complex immune responses requiring systems biology analysis.
- Multicellular changes in trauma patients are not fully understood.
- Identifying immune correlates of infection post-trauma is crucial.
Purpose of the Study:
- To investigate time-dependent immune cell changes in trauma patients.
- To identify immune cell subset alterations correlating with post-traumatic infection.
- To apply a systems biology approach to trauma-induced immune dysregulation.
Main Methods:
- Peripheral blood samples collected from trauma patients (Injury Severity Score > 20) and controls at Days 1, 3, and 5 post-injury.
- Mass cytometry by time-of-flight (CyTOF) with a 33-marker panel for immunophenotyping.
- Statistical analysis using one-way ANOVA with multiple comparisons.
Main Results:
- Significant decrease in CD86 expression on monocytes at all post-injury time points.
- Trend towards decreased CD86 on monocytes in patients who developed infection.
- Significant increase in CD39 expression on NK cells exclusively in patients who developed infection.
Conclusions:
- Trauma impacts innate immune cell function, evidenced by decreased CD86 on monocytes.
- Increased CD39 on NK cells in infected trauma patients suggests a role for adenosine-mediated immunosuppression.
- Identified immune cell changes may serve as biomarkers or therapeutic targets for post-traumatic infections.
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