More concerning asthma and exercise.
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Biomedical subjects
Publications and source records attributed to K M Altenburger.
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Increased permissiveness of macrophages for herpes simplex virus (HSV) replication may be a mechanism for the dissemination and severity of neonatal herpetic infection. We have assessed the replication of HSV in neonatal blood monocytes and placental macrophages using several criteria for viral permissiveness. Assay of production of infectious progeny virus indicated that cord blood monocytes, like adult monocytes, were nonpermissive for HSV (about 1% of cells producing virus). In vitro culture of cord blood monocytes resulted in increased replication of HSV, but no greater extent than virus production in cultured adult cells. HSV infection of fetal placental macrophages was weak but present (4.4% of cells). Assay of production of viral antigens and electron microscopic analysis of structural elements indicated that a larger number of cord blood monocytes and placental macrophages were abortively infected than were productively infected. These results indicate that monocytes and macrophages from human neonates do not show the enhanced permissiveness for HSV demonstrated in newborn mice and suggest that dissemination of herpetic infection in human newborns cannot be explained by increased neonatal monocyte permissiveness for HSV.
Investigation of oxidative metabolism in neutrophils (PMNs) from newborns was performed by measuring generation of superoxide anion (.O2-) and production of hydroxyl radical (.OH) in the resting state and after stimulation with opsonized zymosan or phorbol myristate acetate (PMA). Neutrophils from cord blood of ten term infants and normal adult controls were tested simultaneously. Cord PMNs generated significantly more .O2- than paired adult controls when stimulated with opsonized zymosan (P less than .01) and produced less .OH with PMA (P less than .005). When the amount of .O2- and .OH released by newborn PMNs with both stimuli was expressed as percent of values obtained from paired adult controls, there was a discrepancy in the generation of these two radicals: newborn PMNs produced relatively less .OH compared to .O2-. This decreased ability to produce .OH could underlie defective bactericidal activity in PMNs of neonates.
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