Pathogenesis and involvement of Interleukin-11 in response to Candida albicans in a murine intravenous challenge model

Abstract

IntroductionSystemic candidiasis remains a significant cause of morbidity and mortality even in patients treated with antifungal agents, with Candida albicans remains the most causative agent. Differences in the virulence of Candida albicans strains used and mice species differ in their susceptibility to systemic infection. Hence, in this study, we characterized the pathogenesis of a clinical Candida albicans isolate from Malaysia in an immunocompetent balb/c mice model. ObjectiveTo evaluate the pathogenesis and involvement of interleukin-11 in response to Candida albicans in a murine intravenous challenge model. MethodsMice were challenged intravenously with Candida albicans via lateral tail vein and parameters such as mortality study, quantitative yeast culture, histopathology, were adopted to evaluate the pathogenesis of systemic Candida albicans infection. Besides that, transcript levels from kidney and brain on day 3 post infection were quantified via real time RT-PCR. Results & DiscussionMice infected systemically with Candida albicans resulted in high mortality. Kidney and brain have higher fungal recovery rates as compared to other organs and extensive yeast infiltration with moderate to severe inflammation were seen in kidney and brain tissues. Interleukin-11 was up-regulated in the brain and kidney. Involvement of interleukin-11 might reduce the host resistance against systemic Candida albicans infection as it involves in modulating and antagonizing the proinflammatory immune responses and maintenance of Th2 response which is detrimental during systemic candidiasis. ConclusionThis study demonstrated the pathological evidence of systemic infection caused by Candida albicans and involvement of IL-11 which could be of clinical relevance during systemic Candida albicans infection.