Abstract
ABSTRACT: Several deficiencies in antibacterial defense have been described in neonates. Among those best characterized are delayed maturation of B cells into antibody producing cells, deficient T-cell maturation, and delayed cycling of hematopoietic progenitor cells after an infectious challenge. No unifying theory has been forwarded, however, to explain the concomitance of these three developmental deficiencies. IL-6, a cytokine produced primarily by monocytes and macrophages in response to stimulation by IL-1, is involved in the regulation of these three processes. Thus, we postulated that defective production of IL-6 could be a mechanism underlying these immune deficiencies of neonates. Indeed, we observed that at peak production, cells of five term neonates produced only one half as much IL-6 (14 120 ± 2590 pg IL-6/108 monocytes) as those of five adults (28 940 ± 1680 pg, p < 0.001). Peak production was lower still by monocytes of six preterm neonates (7190 ± 1400 pg, p < 0.001 versus term). Production of IL-6 protein was inhibited by actinomycin D and the IL-6 mRNA content of monocytes from neonates, as assessed by competitive polymerase chain reaction, was less than that of adult monocytes. We speculate that defective IL-6 transcription might underlie some of the defects in immune regulation observed in neonates.
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Schibler, K., Liechty, K., White, W. et al. Defective Production of Interleukin-6 by Monocytes: A Possible Mechanism Underlying Several Host Defense Deficiencies of Neonates. Pediatr Res 31, 18–21 (1992). https://doi.org/10.1203/00006450-199201000-00003
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DOI: https://doi.org/10.1203/00006450-199201000-00003
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