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Updated: Sep 27, 2026

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis
Published on: August 12, 2020
Surgical infants on total parenteral nutrition have impaired cytokine responses to microbial challenge
A Cruccetti1, A Pierro, H Uronen
1Surgery Unit and the Infectious Disease and Microbiology Unit, Institute of Child Health and Great Ormond Hospital for Children, London, England.
Background/Purpose:
Cytokines are essential for the prevention of microbial infections. Total parenteral nutrition (TPN) in infancy is associated with an increased risk of infection, and this could be related to altered cytokine production. The aim of the study was to determine if cytokine production is altered in monocytes from surgical infants receiving TPN.
Methods:
There were 3 study groups: (a) infants receiving TPN, (b) enterally fed healthy control infants, and (c) enterally fed healthy control adults. Blood samples were incubated with either Escherichia coli LPS, Staphylococcus epidermidis, or with medium alone. Flow cytometry was used to measure monocyte intracellular cytokine: tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1beta.
Results:
After LPS stimulation, the percent of monocytes producing TNF-alpha and IL-6 were lower in infants on TPN than both control infants and adults. This was most apparent for TNF-alpha. The difference for IL-1beta was significant only between infant on TPN and control adults. When blood was stimulated with S. epidermidis, all 3 cytokines were significantly lower in the TPN group compared with control adults. However, the differences between infants on TPN and infant controls only reached statistical significance for IL-6.
Conclusions:
The inflammatory response to bacterial challenge is impaired in infants on TPN compared with enterally fed infants or adults. The pattern of this response may be dependent on the nature of the microbial challenge. Our results indicate that the susceptibility of TPN-fed surgical infants to bacterial infections may in part be caused by impaired cytokine responses after bacterial invasion.
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