Fusarium proliferatum as a filamentous fungal pathogen can produce mycotoxins that can contaminate postharvest fruits and thus impact risks on human health. The extracellular proteomes of F . proliferatum grown in the absence and presence of butylated hydroxyanisole (BHA) were analyzed comparatively. A total of 66 significantly different expressed secreted proteins were identified by LC-ESI-MS/MS analysis. The BHA treatment suppressed the accumulation of some pathogenic factors such as aspartic protease , cell wall degradation enzymes , porin , superoxide dismutase and glyceraldehyde-3-phosphate dehydrogenase. On the contrary, the BHA treatment increased the abundances of some proteins, such as ATP binding cassette transporter substrate-binding protein and lipopolysaccharide-assembly lipoprotein , involved in the growth of F . proliferatum . These findings suggest that BHA treatment could influence the pathogenic ability of F . proliferatum via inhibiting the levels of virulence factors and cell wall degradation-associated enzymes . Moreover, the induction of the growth-related proteins after the BHA treatment suggests that the livelihood of F . proliferatum might depend on the cost of reduced pathogenic ability. This study has provided some evidence for understanding the complicated mechanisms of F . proliferatum infection in an effort to develop new targets for the control of this fungal pathogen. Biological significance To better understand the inhibitory mechanism of F . proliferatum by butylated hydroxyanisole (BHA) treatment, a comprehensive proteomic analysis of the secreted proteins of F . proliferatum was firstly conducted. Among the 66 identified spots, 34 and 32 proteins were down- and up-accumulated significantly by BHA treatment, respectively. Many of the identified key protein species were involved in the pathogenic ability and the growth of F . proliferatum . This study is helpful for broadening our knowledge of the pathogenic mechanism of F . proliferatum .
Background The role of fungal pathogenic factors and the immune response of the vaginal epithelium in vulvovaginal candidiasis (VVC) and recurrent vulvovaginal candidiasis (RVVC) are still unclear. Our study wants to clarify whether there are differences in pathogenic factors between VVC and RVVC strains, confirm the roles of pathogenic factors in the pathogenesis of RVVC, and analyze the influence of pathogenic factors on vaginal host immunity. Methods VVC- and RVVC-causing Candida albicans strains were genotyped with 25S rDNA. Drug susceptibility assays using a modified alamarBlue broth microdilution method were carried out. Milk culture medium and egg yolk culture medium were used to measure the secreted aspartate protease (Sap) and phospholipase (Plb) activity of the samples. We used C. albicans with different Sap activity levels to induce RVVC in mice and measured interleukin 4 (IL4), interleukin 8 (IL8), and interleukin 17 (IL17) in vaginal lavage fluid at different stages of RVVC infection. Results There were no significant differences between VVC and RVVC fungi except that the Sap activity was lower for RVVC-causing C. albicans than for VVC-causing C. albicans . C. albicans with both strong Sap and weak Sap induced RVVC in mice. C. albicans with strong Sap had a reduced RVVC infection rate. In addition, C. albicans with strong Sap stimulated the vaginal epithelium to secrete more IL4, IL8, and IL17. Conclusion Compared with that of VVC-causing C. albicans , the Sap activity of RVVC-causing C. albicans was lower. C. albicans with strong Sap was less capable of causing repeated vaginal infections than that with weak Sap and stimulated the vaginal epithelium to produce more cytokines.
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