Showing papers by "Barbara J. Stoll published in 1992"

Characterization of the fetal inflammatory response to cytomegalovirus placentitis. An immunohistochemical study.

Abstract: The histopathologic features of cytomegalovirus placentitis, an established cause of chronic villitis, are well documented. However, the immunologic features of the fetal inflammatory response to placental cytomegalovirus infection are largely unknown. The characterization of the fetal-derived inflammatory cell reaction may be important in our understanding of both the intrauterine as well as the antenatal immunological response of the neonate to this important viral infection. We examined formalin-fixed placentas from four cases of confirmed congenital cytomegalovirus infection using an in situ DNA probe to cytomegalovirus, and a variety of antibodies to leukocyte antigens, including anti-CD68, CD45RO, CDw75, CD74, IgG, IgM, and IgA. All four placentas showed marked hyperplasia of fetal-derived placental macrophages, termed Hofbauer cells. A lymphocytic villitis was present in all placentas, which was characterized by positive staining in all cases with T-cell antibodies. There was no evidence of positive staining of lymphocytes using B-cell antibodies in any of the cases. Two placentas showed plasmacellular villitis, which stained positively for both IgG- and IgM-secreting cells, that was present as early as the second trimester of gestation. No IgA positivity of plasma cells was observed. These data are presented in light of current theories of fetal viral immunity.

Anisoosmostic liver perfusion: redox shifts and modulation of alpha-ketoisocaproate and glycine metabolism

Abstract: 1) In isolated perfused rat liver, 14CO2 production from [1-14C]alpha-ketoisocaproate or [1-14C]glycine as well as ketogenesis from alpha-ketoisocaproate were stimulated upon exposure to hypoosmotic perfusion media, whereas hyperosmotic exposure inhibited. The effects of anisotonicity were preserved when ketogenesis from alpha-ketoisocaproate and 14CO2 production from [1-14C]glycine were already stimulated by glucagon. On the other hand, ketogenesis from tyrosine (2 mM) or octanoate (0.1 mM) were almost unaffected by anisoosmotic exposure. 2) With all ketogenic substrates studied, hypoosmotic (hyperosmotic) cell swelling (shrinkage) decreased (increased) the beta-hydroxybutyrate/acetoacetate ratio in effluent perfusate. A shift of the mitochondrial and cytosolic NADH systems to a more oxidized (reduced) state following hypoosmotic (hyperosmotic) exposure was also found upon infusion of beta-hydroxybutyrate/acetoacetate and lactate/pyruvate as redox indicator metabolite couples. The effects of anisotonicity on the beta-hydroxybutyrate/acetoacetate ratio were reversible upon normoosmotic reexposure and persisted throughout anisoosmotic exposure despite completion of volume regulatory K+ fluxes within 10-15 min. Hepatic oxygen consumption decreased by about 10% during hyperosmotic cell shrinkage and was transiently stimulated during hypoosmotic exposure. 3) There was a close relationship between ketogenesis from alpha-ketoisocaproate (0.5 mM) and the mitochondrial redox state, as assessed by the beta-hydroxybutyrate/acetoacetate ratio in effluent, regardless of whether the pathway was modulated by anisotonicity or glucagon. 4) Isoosmotic cell swelling induced by addition of glutamine (3 mM) was without significant effect on ketogenesis from octanoate and stimulated ketogenesis and 14CO2production from [1-14C]alpha-ketoisocaproate only slightly (i.e. by less than 10%); however, in each case the hydroxybutyrate/acetoacetate ratio in effluent perfusate decreased by about 20% upon addition of glutamine. 5) Stimulation of 14CO2production from [1-14C]glycine by hypoosmotic exposure and glucagon was only slightly affected when the accompanying decrease of the beta-hydroxybutyrate/acetoacetate ratio was reversed by addition of beta-hydroxybutyrate. 6) The data are compatible with a hypotonicity (hypertonicity)-induced shift of the mitochondrial NADH system to a more oxidized (reduced) state, probably due to a alterations of respiration. Mitochondrial swelling probably also occurs under the influence of glutamine. Modulation of ketogenesis from alpha-ketoisocaproate, but not of glycine oxidation by anisoosmotic exposure and glucagon can be related to the accompanying redox shifts. The observations support the concept that cell volume may be an important parameter determining liver cell function.

Prevention of perinatal transmission of the hepatitis B virus. Outcome of infants in a community prevention program.

Abstract: • Objective. —To assess the outcome of infants born to hepatitis B surface antigen (HBSAg)-positive mothers who received prenatal and infant care in a large, public health care system. Design. —Follow-up of a cohort of infants born to HBsAg-positive mothers. Setting. —Large, urban hospital providing prenatal care and obstetric services to county health departments. Participants. —Forty-two infants born to HBsAg-positive women. Interventions. —Prental testing of women and immunoprophylaxis of infants with hepatitis B immune globulin at birth and hepatitis B vaccine at birth and ages 1 and 6 months. Results. —All 42 infants received hepatitis B immune globulin and the first dose of vaccine. Of forty-one infants (98%) who received the second dose of vaccine, 37 received it by age 4 months. Thirty-two infants (76%) completed the three-dose vaccine series by age 12 months, and 34 infants (81%) completed the series by age 18 months. The rate of completion of the hepatitis B vaccine series was comparable to that of infants receiving the third dose of diphtheriapertussis-tetanus vaccine. Of 26 infants who completed the hepatitis B vaccine series and had follow-up serologic testing, 24 (92%) had adequate levels of antibody to HBsAg. Only one infant who did not complete the vaccine series had serologic evidence of hepatitis B virus infection. No infant was HBsAg-positive. Conclusions. —Public programs serving urban populations can effectively deliver hepatitis B immunoprophylaxis to infants born to HBsAg-positive mothers. (AJDC. 1992;146:793-796)

CD5+ B cells in normal newborns and infants, and in those with HIV and intrauterine infections.

Abstract: Human B cells comprise at least two subsets that can be characterized as reacting with an antLCD5 mAb as CD5+. An accurate enumeration of these subsets is problematic because of the poor demarcation from CD5B cells. We have developed reproducible and reliable means for enumerating CD5+ and CD5B cells using the two-color direct immunofluorescence and a whole-blood staining technique with the appropriate monoclonal antibody and flow cytometry. We have obtained improved results by first gating > 90% of lymphocytes with the SimulTest Leucogate (CD45/CD14), Becton Dickinson, San Jose, California. Relative percentages and absolute numbers of the B-cell subsets in children from birth to eight years of age were compared to adult levels; the same was also done in infants infected with HIV perinatally compared to age-matched controls. A physical separation of these subsets (with magnetic beads) from HIV-seropositive adults was also functionally characterized.