Premature infants respond to early-onset and late-onset sepsis with leukocyte activation.

OBJECTIVE: Leukocyte differentiation antigens are expressed on the cell membrane during activation. The purpose of this study was to evaluate leukocyte activation in premature neonates with sepsis. Paired blood samples from the same individual while sick and while convalescent were examined to quantify the expression of leukocyte antigens in these clinical states. METHODS: Mononuclear blood cells from 21 premature infants (24 to 30 weeks' gestation) were analyzed. The "sick" samples were drawn at the time of workup for sepsis; "convalescent" samples were drawn 20 days later. Samples were incubated with monoclonal antibodies to the lymphocyte antigens CD3, CD19, CD25, CD26, CD71, and CD69 and neutrophil antigens CD11b, CD11c, CD13, CD15, CD33, and CD66b. The cells were lysed, fixed, and analyzed by flow cytometry. RESULTS: Twenty-one infants enrolled in the study had multiple sepsis evaluations and had more than one sample available for a paired observation. CD33, CD66b, and CD19 levels were significantly elevated in both the presumed sepsis and culture-proven sepsis groups when compared with the samples drawn from those same patients when healthy. Expression of CD33 and expression of CD66b were correlated, and in a multivariate analysis the elevation of antigen expression was predictive of sepsis. CONCLUSIONS: Leukocytes from preterm newborn infants respond to infection with an increased expression of CD19, CD33, and CD66b on their cell surfaces.

Prenatal diagnosis by analysis of fetal cells in maternal blood.

The data accumulated thus far indicate that fetal NRBCs are the target cell type of choice in maternal blood for most investigators, although some groups continue to work with the trophoblast. Reports of persistent circulation of hematopoietic stem cells, lymphoid/myeloid progenitors, and lymphocytes mandate that removal of these cell types must occur before clinical diagnosis of the current pregnancy can be made. In selected cases, accurate detection of fetal aneuploidy has been made from fetal cells in maternal blood; the clinical evaluation sponsored by the National Institute of Child Health and Human Development will determine the sensitivity and specificity of cytogenetic diagnosis in a larger group of pregnant women, but this information will not be available for several years. At present, detection of uniquely fetal, paternally inherited gene polymorphisms or mutations such as the Rh(D) antigen is possible only because the mother lacks these genes; hence, maternal cell contamination does not hinder diagnosis. Currently the presence of large numbers of maternal cells in enriched samples precludes single-gene diagnosis for conditions in which the mother carries a mutant gene, because her cells are preferentially amplified and difficult to distinguish from those of the fetus. It is likely, however, that as techniques of individual fetal cell isolation are perfected, maternal cell contamination will no longer be an issue, and the entire fetal genome will become available for diagnosis and therapy. Pediatricians need to be aware of the progress of research in this field, because fetal cell isolation from maternal blood not only could change prenatal diagnosis but would change the amount of genetic information that arrives with a newborn infant at birth. The ultimate goal of this work is to diagnose noninvasively, in the first trimester, the common fetal aneuploidies and single-gene disorders, to permit in utero treatment, or to allow low-risk pregnant women carrying an abnormal fetus an opportunity for reproductive choice.