Previously it was reported that compared to surviving septic foals, non-surviving foals had a 35-fold increase in IL-10 (Pusterla et al., AJVR, 2006) and a 15-fold increase in IL-6 (Gold et al., JVIM, 2007) expression in their PBMC. As gene expression profiles can be time-consuming, we sought to determine if serum [IL-6] and [IL-10] in foals would aid in the diagnosis and prognosis of septicemia.
A prospective study of septic neonatal foals admitted to the Cornell University (CU) Equine Hospital during the spring of 2007 was performed. Septicemia was confirmed in 7 foals using a combination of blood culture results and sepsis scores. Blood samples were collected from foals at the time of admission, (T0) and again 24 (T24) and 48 (T48) hours later. All foals were treated with antibiotics, plasma and supportive therapies and outcomes were determined. Blood samples from age-matched control foals (n=15), born at the CU Equine Park (2007) were obtained at 12-72 hours of age (T0) and again 24 (T24) and 48 (T48) hours later. Serum and colostral [IL-6] and [IL-10] were also measured in samples obtained from the dams. [IL-6] was measured using an ELISA and [IL-10] was measured using a Luminex immunoassay system. Group differences were detected using a Wilcoxon rank sum test with a Bonferroni correction applied to the p value.
Relative to the controls, septic foals had significantly lower serum [IL-6] at all three time points (p = 0.0313) and a trend towards higher [IL-10]. The single septic foal that died had a 5,106-fold higher [IL-10] at T0 compared to survivors (n = 6). Serum and colostral [IL-10] in the dams were undetectable in 10 out of 13 samples. Dam serum and colostral [IL-6] were high in 18 out of 18 samples. These results are in contrast to our previous work where gene expression of IL-6 in PBMC was studied and the increased IL-6 mRNA expression in septic foals suggested production of this cytokine in response to the disease. Here, we found an increased serum [IL-6] in healthy compared to septic foals, which was likely to be the result of maternal transfer of high [IL-6] to the healthy neonates. This could be due to localization of IL-6 in PBMC rather than in serum of septic foals. Our results also suggest that IL-6 is partly derived from colostrum, whereas IL-10 was not transferred with the colostrum in most foals and is produced by the foal's own immune system. This is the first report of serum [IL-6] and [IL-10] measurement in neonatal foals and preliminary data suggest that elevated serum [IL-10] but not [IL-6] are associated with a poor prognosis.