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Injury induces alterations in T-cell NFkappaB and AP-1 activation.

C B O'Suilleabhain¹, S Kim, M R Rodrick

¹Department of Surgery (Immunology), Harvard Medical School/Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Shock (Augusta, Ga.)

|June 2, 2001

Summary

Severe injury impairs T-cell immunity by altering transcription factor activation. This study reveals that changes in AP-1 and NFkappaB activation correlate with reduced IL-2 gene expression after thermal injury.

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Area of Science:

Immunology
Molecular Biology
Cellular Signaling

Background:

Severe injury triggers immune dysfunction, characterized by suppressed T-helper 1 (Th1) responses and increased T-helper 2 (Th2) cytokine production.
The molecular mechanisms underlying this injury-induced T-cell phenotypic shift remain largely unknown.

Purpose of the Study:

To investigate the molecular basis of how severe injury affects T-helper cell cytokine expression.
To determine if diminished Interleukin-2 (IL-2) gene expression after thermal injury is linked to altered induction of its regulatory transcription factors.

Main Methods:

Utilized Electrophoretic Mobility Shift Assays (EMSA) to assess nuclear expression of IL-2 gene transcription factors in T-cells.
Employed Western immunoblot analysis to confirm protein translocation.
Compared T-cells from sham-injured and burn-injured mice at 9 days post-injury.

Main Results:

Mitogen-stimulated T-cell AP-1 and NFkappaB factor activation changes correlated with defective IL-2 mRNA expression post-injury.
A loss of nuclear AP-1 activation and altered NFkappaB factor activation were observed 9 days after injury.
Burn-injured mice showed predominantly NFkappaB1 (p50) in NFkappaB EMSA complexes, with absent RelA (p65) and NFkappaB2 (p52), unlike sham-injured controls.

Conclusions:

T-cell NFkappaB and AP-1 activation pathways are implicated in injury-induced alterations of T-cell cytokine production.
These findings suggest a role for these pathways in the immune deviation observed after severe injury.