Moderate pediatric burn injury is associated with reduced monocyte HLA-DR expression and heightened whole-blood LPS-induced TNF-α responses
作者
Whitman B. Wiggins,Jaimar C. Rincon,Miguel Hernández-Ríos,Valerie E. Polcz,Christine E. Rodhouse,Athina L. Yoham,Stefan Richter,Ana Cabral,Lyle L. Moldawer,Philip Alexander Efron,Robert Maile,Shawn D. Larson
Background Burn injury is associated with immune dysregulation and an increased risk of infection and sepsis. In children, however, the immunologic consequences of small and moderate burn injuries remain poorly defined. We compared phenotypic and functional innate immune responses in pediatric patients with small and moderate burn injuries. Methods Pediatric patients with small [<15% total body surface area (TBSA); n = 14] and moderate (15%–30% TBSA; n = 9) burns, along with healthy pediatric controls ( n = 7), were prospectively enrolled. Whole blood was collected on hospital day 2 and, when feasible, at weekly intervals thereafter. Monocyte HLA-DR expression and circulating myeloid-derived suppressor cell (MDSC) populations were quantified by flow cytometry. Whole-blood innate immune responsiveness was assessed using a TNF-α ELISpot assay following ex vivo lipopolysaccharide (LPS) stimulation. Results Monocyte HLA-DR expression on hospital day 2 was significantly reduced in patients with moderate burns compared with healthy controls, whereas patients with small burns did not differ significantly from either group. MDSC populations measured one week after injury did not differ among groups. Whole-blood LPS-induced TNF-α responses on hospital day 2 were preserved across all groups and were heightened in patients with moderate burns. Conclusions Moderate pediatric burn injury was associated with reduced monocyte HLA-DR expression and heightened acute whole-blood LPS-induced TNF-α responsiveness. Together, these findings suggest that early innate immune alterations after pediatric burn injury reflect concurrent phenotypic and functional dysregulation rather than uniform immune suppression.