There are major gaps in our understanding of the immunopathogenesis ofClostridium difficile infections (CDIs). In this study, 36 different biomarkerswere examined in the stools of CDI and non-CDI patients using the ProteomeProfiler human cytokine array assay and quantitative enzyme-linked immunosorbent assay. Diarrheal stools from patients with CDI (CDI-positive diarrheal stools)showed higher relative amounts of the following inflammatory markers than thediarrheal stools from CDI-negative patients (CDI-negative diarrheal stools): C5a,CD40L, granulocyte colony-stimulating factor, I-309, interleukin-13 (IL-13),IL-16, IL-27, monocyte chemoattractant protein 1, tumor necrosis factor alpha,and IL-8. IL-8 and IL-23 were present in a larger number of CDI-positivediarrheal stools than CDI-negative diarrheal stools. Th1 and Th2 cytokines werenot significantly different between the CDI-positive and CDI-negative diarrhealstools. Lactoferrin and calprotectin concentrations were also higher in theCDI-positive diarrheal stools. Our results demonstrate that CDI elicits aproinflammatory host response, and we report for the first time that IL-23 is amajor marker in CDI-positive diarrheal stools. IL-23 may explain the lack of arobust immunological response exhibited by a proportion of CDI patients and mayrelate to recurrence; the IL-23 levels induced during CDI in these patients maybe inadequate to sustain the cellular immunity conferred by this cytokine inpromoting the induction and proliferation of effector memory T cells.
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