As such, KP related changes in depression may be independent of inflammation, and our findings support this notion based on the observations of: (a) an inverse relationship between IL-6 and depressive symptoms, (b) no inverse correlation between tryptophan and its downstream metabolites or differential in KYN/TRP ratio, an indicator of host IDO/TDO activity, (c) limited associations between the pro-inflammatory and KP markers, and (d) KA was the only biomarker to remain a significant predictor of depression severity in a model accounting for covariates including IL-6. This evidence concerns the gene IL6 and depressive symptom measurement.