At first the fungi engage with a succession of innate-immunity leukocytes then later lymphocytes, all involved in a complex chemical cross-talk based at the earliest stages on production of a mixture of chemokines and cytokines by host leukocytes, and of surface polysaccharides and secreted proteins by the fungus. At any temporal stage, the balance between elimination of the fungal cells and local damage at the site of infection will depend on the responses both of the leukocytes and the fungus to this array of effector LOUREIRIN-B molecules and cells. When an immune response is characterized as predominantly Th1 or Th2, this reflects the overall outcome of the fungus-host interaction, but does not indicate the component events that led to that outcome. 
We hypothesized that a more detailed picture of the host-fungus interactions that occur in a kidney infected with C. albicans could be obtained by measurement of a greater number of chemokines and cytokines than has previously been attempted, and by semiquantitative histopathological analysis of the lesions. By infecting mice with a set of C. albicans strains chosen to Catharanthine sulfate represent examples known to be of high and low virulence in the mouse model we aimed to differentiate host responses and lesion parameters that correlate with survival and non-survival of the experimental infection. Because the available evidence suggests that the early stages of host-C. albicans interactions determine gross clinical outcomes, we confined our monitoring of events to the first 48 h after IV challenge. This study demonstrates that, in the mouse intravenous C. albicans challenge model, early interactions between the fungus and host predict the level of gross progression of disease in the kidney, the major organ affected in the model. Our study is the first we are aware of to link cytokine or chemokine production with refined histopathological measurements of lesion development in the mouse model. Because we measured immune effector concentrations at different stages in the progression of renal disease, we can hypothesize the sequence of activation of these molecules from the statistical associations between their concentrations and the four parameters relating to lesion development in the kidney. The significant and ubiquitous association of 12 h kidney KC concentrations with subsequent kidney lesion parameters strongly implicates this chemokine.