Physiological Sources of Essential Lipids for Mycoplasma pneumoniae via Protein P116: Innovative Biotechnological Tools for Targeting Atherosclerotic and Hepatic Lesions

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Abstract

Mycoplasma pneumoniae ( MPN ) is a bacterial pathogen in humans that primarily causes atypical pneumonia. MPN cannot synthesize several lipids crucial for its cell membrane structure and needs to extract them from the lung of the host to survive. The protein responsible for extracting essential lipids from cell membranes is P116. MPN has been detected in increased quantities within ruptured atherosclerotic plaques and the question is how MPN survives in the blood and in the plaques and obtains the lipids necessary for its membrane. Here we show that P116 can uptake essential lipids from LDL and HDL and when targeting its C-terminal domain via a monoclonal antibody there is growth inhibition in vitro . Phase contrast epifluorescence microscopy of human arteries also revealed that this antibody blocks MPN binding to human atherosclerotic lesions ex vivo . Furthermore, injection of MPN in the blood results in accumulation of MPN within the liver and atheroma plaques in a hyperlipidemic mouse model. We conclude that P116 plays a critical role in extracting essential lipids from physiological circulating lipoproteins and from host cells and regulates MPN localization to liver and atheromatous plaques. These results suggest new strategies for managing mycoplasma infections and addressing the potential complications of MPN infections in atherosclerotic lesions. They also open avenues for utilizing biotechnological tools in the treatment of atherosclerotic and hepatic lesions.

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