To the Editor: We read with interest the article by Schultz et al. (1), who present data on the neonatal inflammatory response.

As detection of intracellular cytokines may not necessarily correlate with extracellular cytokine concentrations, we do not totally agree with the authors' conclusions on the neonatal immune system extracted from these data.

As well, there may be concern about some methodical issues:

  1. 1

    The authors stored blood samples for up to 24 hours at room temperature. Reinsberg et al. (2) showed that IL-8 concentrations in whole blood lysate increased significantly after 3 hours of storage at room temperature. The authors do not show data on the influences of sample storage.

  2. 2

    Differences in storage time between the groups may have affected the results.

  3. 3

    Van Langevelde et al. (3) reported a maximum endotoxin concentration of 18 pg/ml in adult febrile patients. In this study a maximal LPS stimulus of 30,000 pg/ml has been used. The effect on intracellular cytokine production may not reflect in vivo conditions.

  4. 4

    It has been shown that labor induces cytokine production in term and preterm infants (4). Modification of cytokine synthesis by labor may differ in neonatal cells from preterm and term infants. The diminished spontaneous production of intracellular cytokines as well as the production after ex vivo stimulation in preterm infants <32 weeks gestational age could well have resulted from the 100% cesarean section rate in this group.

  5. 5

    The authors demonstrate a dose related inhibition of ex vivo monocyte cytokine expression by incubation with dexamethasone. They do not comment on the possible effects of the different rates of corticosteroid pretreatment between the study groups (50%, 96%, 100%). There is no information on the number of doses and the type of steroid used for prophylaxis of RDS.

  6. 6

    The diagnosis of neonatal infection has been based on single parameters. This is not a commonly used definition.

  7. 7

    Anti-inflammatory activity has not been investigated. Data on IL-10 derived from different study designs are compared in the discussion.

On the background of these questions, the hypothesis of an enhanced neonatal inflammatory response remains at least debatable. Evaluation of imbalances of pro- and antiinflammatory components in neonatates may be more effective by investigation of a larger cytokine panel.