Abstract
Objective: To assess the relationship between IL-10 release and anti-inflammatory response following blunt trauma. Design: Prospective longitudinal clinical study. Setting: Departments of trauma and anaesthetics in a university teaching hospital Patients: Forty-eight adult patients with a mean injury severity score of 14.5 (range 9–57) were prospectively studied following blunt trauma. Measurements and results: Venous blood samples were collected on arrival and at 16 and 24 h, and at 3, 5, and 7 days. Peripheral blood mononuclear cell (HLA-DR) expression on CD14 + monocytes was quantified by flow cytometry and serum IL-10 was assayed by ELISA. Anti-inflammatory response was defined as monocyte HLA-DR expression of less than 30 % of that seen in healthy controls. Serum IL-10 levels in trauma patients on arrival was significantly elevated, 70.0 [48.0–92.1, 95 % confidence interval, (CI)] compared to the control group, 3 (0–5) (P < 0.0001), and monocyte HLA-DR expression was significantly lower, 14.2 (12.1–16.3, 95 % CI), in patients versus 25.2 (22.4–28.1) in controls (P < 0.001). Patients with low HLA-DR expression (n = 14) had significantly higher serum IL-10 levels than those whose HLA-DR expression remained above 30 % of the control value (n = 34), (P < 0.038). In patients who developed sepsis (n = 11), serum IL-10 levels were greater on admission, [143.7 (80.2–207.2) pg/ml–1], and remained elevated during the study period compared with non-complicated patients, [50.16 (33.5–66.8) pg/ml–1]. Immediate IL-10 (2 h following trauma) was negatively correlated with simultaneous HLA-DR expression, (r = –0.49, P = 0.0005). Conclusion: These findings support the view that IL-10 release regulates monocyte HLA-DR expression and may be related to an anti-inflammatory response and development of sepsis following trauma.
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Received: 1 December 1999 Final revision received: 13 April 2000 Accepted: 1 May 2000
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Giannoudis, P., Smith, R., Perry, S. et al. Immediate IL-10 expression following major orthopaedic trauma: relationship to anti-inflammatory response and subsequent development of sepsis. Intensive Care Med 26, 1076–1081 (2000). https://doi.org/10.1007/s001340051320
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DOI: https://doi.org/10.1007/s001340051320