MTN Deficiency Attenuates Bacterial Biofilms and Adherence to the Extracellular Matrix
Abstract
The enzyme methylthioadenosine nucleosidase (MTN) and its downstream pathways play a role in promoting many potent virulence phenotypes among gram negative bacterial pathogens. These phenotypes include both the formation of biofilms and adherence to mammalian extracellular matrix proteins (ECM) during infection that promote pathogenicity and infection. The role of MTN in these processes was examined by studying the effect of MTN inhibitors and genetic knock-out strains to reduce biofilms and ECM adherence in two model pathogens of Escherichia coli O157:H7 and Klebsiella pneumonia. The results of our studies indicate that deficiency of MTN activity decreases biofilms and ECM adherence, and supports virulence attenuation as a mechanism of action for MTN inhibitors.
MTN Deficiency Attenuates Bacterial Biofilms and Adherence to the Extracellular Matrix
The enzyme methylthioadenosine nucleosidase (MTN) and its downstream pathways play a role in promoting many potent virulence phenotypes among gram negative bacterial pathogens. These phenotypes include both the formation of biofilms and adherence to mammalian extracellular matrix proteins (ECM) during infection that promote pathogenicity and infection. The role of MTN in these processes was examined by studying the effect of MTN inhibitors and genetic knock-out strains to reduce biofilms and ECM adherence in two model pathogens of Escherichia coli O157:H7 and Klebsiella pneumonia. The results of our studies indicate that deficiency of MTN activity decreases biofilms and ECM adherence, and supports virulence attenuation as a mechanism of action for MTN inhibitors.