Biomedical subjects
A S Kent
Publications and source records attributed to A S Kent.
Puerperal sepsis: a disease of the past?
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Transfer of cytokines through human fetal membranes.
Intact human fetal membranes (amnion, chorion and decidua) were incubated with 125I-labelled cytokines added to the fetal or maternal sides of the membrane. The transfer of 125I-labelled interleukin-6 (IL-6), 125I-labelled tumour necrosis factor alpha (TNF-alpha), 125I-labelled interleukin-1 alpha (IL-1 alpha) and 125I-labelled interleukin-1 beta (IL-1 beta) was determined by measurement of radioactivity in a gamma counter and the integrity of the cytokines was assessed by acid precipitation and by radioimmunoassay. IL-1 alpha and IL-1 beta were transferred through human fetal membranes in both feto-maternal and materno-fetal directions at similar rates. Only 2-4% of the cytokine originally added appeared to be intact on the opposing side of the membrane after 24 h of culture. Transfer of intact TNF-alpha (5-7%) and IL-6 (8-17%) was greater than that of the IL-1 isomers. Low but variable amounts of the four cytokines tested may be transferred through the human fetal membrane. This finding suggested that concentrations of cytokines in amniotic fluid would not reflect those produced by decidua if the fetal membranes are intact.
The effects of interleukins 1 alpha and 1 beta on prostaglandin production by cultured human fetal membranes.
The effects of IL-1 alpha and IL-1 beta on cultured human fetal membranes were studied. These cytokines are known to regulate prostaglandin synthesis by the separated components of the fetal membranes (amnion, chorion and decidua), but their effects on intact tissue are unknown. IL-1 alpha increased PGE2 levels on the fetal side of the membrane, indicating increased production of prostaglandin from the amnion, but had little effect on levels of PGE2 on the maternal side of the membrane. Low levels of IL-1 beta (0.1-1.0 ng/ml) increased PGE2 levels on the fetal side of the membrane, and also increased the production of PGE2 metabolites and PGF2 alpha, suggesting that this cytokine stimulated the decidua as well as the amnion. High concentrations of both cytokines appeared able to stimulate prostaglandin production by the side of the membrane opposing that to which they were added, but it is not clear whether this was mediated by factors released by the stimulated membrane, or by direct transfer of small quantities of cytokines through the membrane. Taken together, these results indicate that IL-1 beta was a potent stimulator of the synthesis of prostaglandins by decidua and by amnion, whereas IL-1 alpha only stimulated the amnion.
Effects of interleukin-6 and tumor necrosis factor-alpha on prostaglandin production by cultured human fetal membranes.
In this study we investigated the effects of the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) on prostaglandin production by cultured human fetal membranes. These cytokines stimulate prostaglandin synthesis by isolated components of human fetal membranes, but their effects on the intact tissue comprising amnion, chorion and decidua were not known. TNF-alpha added to the maternal side of the membrane activated decidual production of PGF2 alpha but had no effects on synthesis of PGE2 or PGE2 metabolites. Addition of TNF-alpha to the fetal side of the membrane increased production of PGE2 by amnion and PGE2 metabolites from chorion. The addition of IL-6 to the fetal or the maternal side of the membrane increased production of PGE2 from amnion and PGE2m from chorion, suggesting that IL-6 might pass through the fetal membrane. IL-6 had no effect on decidual PGF2 alpha production. These results suggest that TNF-alpha may be involved in labor by increasing decidual prostaglandin synthesis, whereas IL-6 is less likely to have a role.
The amnion produces little of the prostaglandin E2 detected on the decidual side of human fetal membranes.
Cultured intact fetal membrane disks initially produced high levels of prostaglandin E2 (PGE2) on the fetal and maternal sides which declined during four days of culture. The transfer of a bolus of PGE2 from the fetal side to the maternal side of the membrane ranged from 1% to 3% after 24 hours of culture, and was a minimum over the period of 48-72 hours from the start of the incubation. To assess the handling of PGE2 synthesized by the amnion, 3H-arachidonic acid was incorporated into cultured amnion and into the amnion side of cultured intact fetal membrane disks. Labelled amnion released 3H-PGE2 on both sides of the tissue, whereas similarly labelled cultured intact fetal membrane only had detectable levels of 3H-PGE2 on the fetal side. It was calculated that no more than 9.7 +/- 1.4% of the PGE2 synthesised by the amnion crossed to the maternal side of the membrane without being metabolised during the transfer through the membrane. These results are consistent with similar indirect methods which suggested that PGE2 from the amnion may have only a limited role in human labor, and indicates the importance of using appropriate culture systems to investigate intra-uterine prostaglandin production.
Susceptibility of Bos indicus and Bos taurus to Anaplasma marginale and Babesia bigemina infections.
The reaction of Bos taurus and pure-bred Bos indicus heifers to infection with the intraerythrocytic parasites Anaplasma marginale and Babesia bigemina was studied. B. bigemina infection at 18 months and A. marginale infection at 13 or 24 months resulted in slightly less severe reactions in pure-bred Bos indicus cattle than in Bos taurus. In both breeds, the reaction to A. marginale infection was more severe in older cattle. The severity of B. bigemina infection was not affected by a previous infection with A. marginale.