Normal Expression and Function of CR3 (CD11b/CD18) on Neonatal Neutrophils(PMN) and Monocytes. • 1295

Abstract

It is well known that neonates are more susceptible to bacterial infections, probably secondary to immaturity of the immune system. Previous studies have shown that neonatal PMN express less membrane and cytoplasmic CR3(iC3b-receptor) than adult PMN, and it has been suggested that this may render neonatal PMN deficient in their ability to kill iC3b-opsonized microorganisms. The current investigation examined PMN and monocytes from cord blood versus adult blood for CR3 expression and function. CR3 was measured with unseparated leukocytes using 3-color flow cytometry in which monocytes and PMN were defined as CD14+CD15- and CD14-CD15+, respectively. Although it was confirmed that neonatal PMN bore less CR3 than did adult PMN, neonatal PMN were more heterogenous, with some PMN expressing low amounts of CR3 and other PMN expressing higher adult levels of CR3. As the result of higher total PMN counts in cord blood versus adult blood (6.7 vs. 3.7 × 103/cu.mm, n=11), there were actually similar numbers of PMN in cord blood and adult blood expressing high amounts of CR3 per cell (4.7 vs. 3.7 × 103). A similar finding was made in the comparison of cord blood and adult blood monocytes for levels of CR3 expression (4.5 vs. 1.1 × 103 total monocytes; 1.87 vs. 1.0 × 103 monocytes expressing high CR3). Another flow cytometry assay was used to assess the ability of PMN and monocytes to generate a CR3-dependent respiratory burst in response to particulate β-glucan as a function of the level of CR3 per cell. The magnitude of such CR3-specific bursts was found to correlate directly with levels of CR3 expression with both PMN and monocytes. With cells expressing comparable amounts of CR3, there was no difference between neonatal and adult PMN or monocytes in this CR3 function. In conclusion, these data suggest that there is no numerical or functional deficiency of CR3 on neonatal PMN or monocytes that explains the higher susceptibility of newborns to bacterial infections. Supported by NIH grant AI-27771