Changes in mitogen responsiveness lymphocyte subsets after traumatic injury: relation to development of sepsis

• Published in: Clinical immunology and immunopathology Vol. 32; no. 2; p. 224
• Main Authors: Levy, E M, Alharbi, S A, Grindlinger, G, Black, P H
• Format: Journal Article
• Language: English
• Published: United States 01-01-1984
• Subjects: Adult; Aged; Antibodies, Monoclonal; Female; Humans; Lymphocyte Activation; Male; Middle Aged; Sepsis - etiology; Sepsis - immunology; T-Lymphocytes - classification; T-Lymphocytes, Helper-Inducer - immunology; T-Lymphocytes, Regulatory - immunology; Wounds and Injuries - complications; Wounds and Injuries - immunology
• ISSN: 0090-1229
• DOI: 10.1016/0090-1229(84)90123-5

Head injury and multiple trauma patients were evaluated for mitogen responsiveness and lymphocyte subset frequencies within the first few days after injury. The profile obtained was compared to the patient's clinical course to see if there was a relation between early immune abnormalities and the subsequent development of unanticipated sepsis. Lymphocytes from multiple trauma patients were generally hyporesponsive to in vitro stimulation with a suboptimal dose of the mitogen phytohemagglutinin (PHA). In contrast, the response of head injured patients was comparable to that of the control group. There was a significant decrease in the relative number of multiple trauma patient's T4 (29.3 vs 48.6%) and T11 (48.9 vs 74.7%) positive populations (P less than 0.01). There was no change in the percentage of T8-positive cells (19.0 vs 20.5%). Patients with head injuries also had a decrease in T4-positive cells (35.9%). The percentage of cells with B cell and natural killer (NK) markers remained normal. Thus trauma patients appeared to have an increase in null cells. Six patients whose PHA responses were among the lowest developed sepsis early after trauma. The changes in subset distributions although possibly contributing to a decreased responsiveness did not predict the ability to respond to PHA or the development of sepsis.