Evidence for Enhanced Cellular Uptake and Binding of Thyroxine In Vivo during Acute Infection with <i>Diplococcus pneumoniae</i>

Frederick R. DeRubertis; Kenneth A. Woeber

doi:10.1172/JCI106873

Evidence for Enhanced Cellular Uptake and Binding of Thyroxine In Vivo during Acute Infection with Diplococcus pneumoniae

Published April 1, 1972 - More info

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Abstract

Previous work has demonstrated that acute pneumococcal infections in man and in the rhesus monkey are accompanied by accelerated metabolic disposal of L-thyroxine (T₄). In order to study the influence of acute pneumococcal infection on the kinetics of hormone distribution, the early cellular uptake of T₄ (CT₄), reflecting the net effect of plasma and cellular binding factors, was assessed in rhesus monkeys from the differences in instantaneous distribution volumes of T₄-¹³¹I and albumin-¹²⁵I during the first 60 min after their simultaneous injection. Hepatic and renal uptakes of ¹³¹I were also determined. Plasma binding of T₄ was assessed by measuring the per cent of free T₄ (% FT₄) in serum. Six monkeys were studied 12 hr (INF-12) and seven 24 hr (INF-24) after intravenous inoculation with Diplococcus pneumoniae; seven controls were inoculated with a heat-killed culture. CT₄ at 60 min as per cent administered dose was 31.5 ±2.0 (mean ±SE) in INF-12 and 33.0±0.8 in INF-24, values significantly greater than control (22.4±1.3). By contrast, mean% FT₄ was identical in control and INF-12 (0.028 ±0.002 and 0.028 ±0.001) and variably increased in INF-24 (0.034 ±0.003). Thus, in the infected monkeys CT₄ and% FT₄ were not significantly correlated. The increased CT₄ in the infected monkeys could not be ascribed to an increase in vascular permeability and did not correlate with the magnitude of fever. Although the increased CT₄ could not be accounted for by increased hepatic or renal uptake of hormone, hepatic and renal T₄ spaces were increased, results consistent with increased binding by these tissues. Our data indicate that the cellular uptake of T₄ is increased early in acute pneumococcal infection and suggest that this results from a primary enhancement of cell-associated binding factors for T₄.