Molecular mechanisms of bacteria-host interactions
financed by the Swedish Research Council.
The overarching objective is to comprehend how bacteria might influence host cell processes and pathways through released components, such as bacterial proteins and membrane vesicles. The study integrates findings from our previous investigations into how Vibrio cholerae and Escherichia coli interact with one another and with their hosts, as well as how these factors impact epigenetic regulation, apoptosis, and autophagy, and how these factors affect anti-viral immune signaling.
The primary objective is to investigate how bacterial factors impact host cell processes. Regardless of the host, virulence factors are generally necessary for pathogenicity to develop. MakABE tripartite toxin, a bacterial fitness factor, was found in V. cholerae utilizing C. elegans as a predatory model. MakA alone modulate autophagy and apoptosis in mammalian cells, as well as tube-like superstructures when lipids are present at low pH, revealing a novel tubulation mechanism for a bacterial toxin. MakA is capable of functioning as an effector in both non-vertebrate and vertebrate hosts.
We also highlight the biological functions of bacterial membrane vesicles (BMVs) in host interactions. BMVs play several functions in bacterial pathogenicity and may have medical and biotechnological implications. A greater knowledge of commensal BMVs and their activities in hosts is necessary for precision medicine for infectious and non-infectious diseases including cancer.