Human mucosal surfaces are colonized by diverse microbial communities. Candida albicans colonizes human mucosal surfaces and is a major systemic fungal pathogen. Biofilm formation and virulence are both linked to the ability to transition from the yeast (blastospore) growth form to the filamentous (hyphal) growth form. The aims of this research were to better understand the interactions between the oral bacteria Streptococcus gordonii and the disease associated fungus C. albicans. Specifically, we analyzed the effects of S. gordonii DL1 on activation of MAP kinases Cek1 and Mkc1 which impact C. albicans morphogenesis from blastospore to the filamentous hyphal form, and the role of H2O2 in this interactionl(1).
 C. V. Bamford et al, Infection and Immunity, Sept.2009, p3696-3704. doi:10.1128/IAI.00438-09
Co-incubation of C. albicans with S. gordonii DL1 cells led to activation of Cek1. The presence of S. gordonii cells also suppressed the H2O2-induced phosphorylation of Mkc1. Thus, the activities of these MAP kinases differentially respond to the presence of, or contact with, Streptococcus bacteria in the environment (Fig.1).
These results suggest that filamentation of C. albicans may be biochemically promoted by streptococci. In addition, in the presence of streptococci, H2O2 is unlikely to be the main cause of increased hyphal development.
Fig. 1: Western immunoblot analysis of effects of 10mM H202 on phosphorylation of C. albicans MAP kinases after 20 min in the presence or absence of S. gordonii.