Journal of Microbiology

Journal Articles

Secretions from Serratia marcescens Inhibit the Growth and Biofilm Formation of Candida spp. and Cryptococcus neoformans: Caiyan Xin , Fen Wang , Jinping Zhang , Quan Zhou , Fangyan Liu , Chunling Zhao , Zhangyong Song; J. Microbiol. 2023;61(2):221-232. Published online February 21, 2023; DOI: https://doi.org/10.1007/s12275-022-00007-3

Abstract: Candida spp. and Cryptococcus are conditional pathogenic fungi that commonly infect immunocompromised patients. Over the past few decades, the increase in antifungal resistance has prompted the development of new antifungal agents. In this study, we explored the potential antifungal effects of secretions from Serratia marcescens on Candida spp. and Cryptococcus neoformans. We confirmed that the supernatant of S. marcescens inhibited fungal growth, suppressed hyphal and biofilm formation, and downregulated the expression of hyphae-specific genes and virulence-related genes in Candida spp. and C. neoformans. Furthermore, the S. marcescens supernatant retained biological stability after heat, pH, and protease K treatment. The chemical profile of the S. marcescens supernatant was characterized by ultra-high-performance liquid chromatography–linear ion trap/orbitrap high resolution mass spectrometry analysis and a total of 61 compounds with an mzCloud best match of greater than 70 were identified. In vivo, treatment with the S. marcescens supernatant reduced the mortality of fungi-infected Galleria mellonella. Taken together, our results revealed that the stable antifungal substances in the supernatant of S. marcescens have promising potential applications in the development of new antifungal agents.

Caspase-3 inhibitor inhibits enterovirus D68 production: Wenbo Huo , Jinghua Yu , Chunyu Liu , Ting Wu , Yue Wang , Xiangling Meng , Fengmei Song , Shuxia Zhang , Ying Su , Yumeng Liu , Jinming Liu , Xiaoyan Yu , Shucheng Hua; J. Microbiol. 2020;58(9):812-820. Published online September 1, 2020; DOI: https://doi.org/10.1007/s12275-020-0241-y

Abstract: Enterovirus D68 (EVD68) is an emerging pathogen that recently caused a large worldwide outbreak of severe respiratory disease in children. However, the relationship between EVD68 and host cells remains unclear. Caspases are involved in cell death, immune response, and even viral production. We found that caspase-3 was activated during EVD68 replication to induce apoptosis. Caspase-3 inhibitor (Z-DEVDFMK) inhibited viral production, protected host cells from the cytopathic effects of EVD68 infection, and prevented EVD68 from regulating the host cell cycle at G0/G1. Meanwhile, caspase-3 activator (PAC-1) increased EVD68 production. EVD68 infection therefore activates caspase-3 for virus production. This knowledge provides a potential direction for the prevention and treatment of disease related to EVD68.

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