Cairo M S
Division of Hematology/Oncology Research, Childrens Hospital of Orange County, California.
Clin Perinatol. 1991 Jun;18(2):343-59.
Numerous abnormalities in neonatal host-defense mechanisms have been documented over the past decade. Profound disturbances in myeloid progenitor proliferation, bone marrow neutrophil storage pools, a tendency to peripheral neutropenia and significant in vitro abnormalities of mature neutrophil cell effector function all predispose the neonate to a high mortality rate during bacterial sepsis. The recent use of hematopoietic CSFs and other cytokines to enhance host defense mechanisms in the adult has suggested a role for this new form of immunotherapy in the newborn. Several studies over the past 2 years have indicated that a number of these cytokines may in fact enhance neonatal myeloid progenitor proliferation, modulate neonatal bone marrow neutrophil storage and proliferative pools, induce peripheral neutrophilia and protect against the high mortality rate associated with experimental bacterial sepsis to enhance neonatal host defense against overwhelming bacterial infection.