Abstract
The purpose of this study was to determine whether decreased FcγRIII expression on the PMN of extremely low birth weight infants (ELBW) is due to decreased receptor synthesis or increased receptor shedding from the PMN surface. 42 ELBW, 12 larger infants and 14 adults were enrolled. Plasma and total cellular FcγRIII were measured by ELISA, and PMN FcγRIII expression was measured by flow cytometry. ELBW PMN plasma membrane expression of FcγRIII as measured by log mean channel fluorescence (5.00 ± 1.98 vs. 10.68 ± 1.61, p < 0.050) and plasma FcγRIII levels were both lower (7.5 ± 6.1 vs. 82.4 ± 64.8 nM, p < 0.05) than in adult controls. In follow-up studies, 14 ELBW (age = 29 ± 14 days, range = 14-56 days) increased PMN expression of FcγRIII (p < 0.001) but not plasma FcγRIII. ELBW had lower total PMN-associated FcγRIII than adults (2.3 ± 0.9 vs. 6.8 ± 2.2 ng/l06 PMN, p = 0.006). ELBW’s PMN produce less FcγRIII than adults’ PMN, and expression of this receptor is developmentally regulated.