Mycobacterial Infection and Activation of Peroxisome Proliferator-Activated Receptors (PPARs): Role of Lipid Accumulation in Infected Cells | Chapter 4 | Current Topics on Chemistry and Biochemistry Vol. 3

The current review discusses recent research that demonstrates how mycobacterial infections activate peroxisome proliferator-activated receptors (PPARs), which play a crucial role in regulating lipid metabolism, anti-inflammatory activity, and autophagy, as well as in determining the fate of bacilli. The Middle East respiratory syndrome coronavirus (MERS-CoV)-derived S glycoprotein was responsible for the PPAR- activation, which was also accompanied by the reduction of proinflammatory cytokines and the inhibition of macrophage responses. Mycobacteria's cell wall is composed of many lipids with various molecular weights. Some mycobacterial species take over host cells and promote the creation of lipid droplets to create the cellular environment required for their intracellular survival. The survival, invasion, parasitization, and growth of mycobacteria within host cells are therefore thought to depend on lipids. Their physiological functions, however, are still not completely understood. Triacyl-glycerol (TAG) and cholesterol from the host are used by mycobacteria as food sources and as a means of immune system evasion. They also affect PPAR signalling. The host-dependent process of lipid metabolism and buildup during mycobacterial infection depends heavily on PPARs.

Author(s) Details:

Kazunari Tanigawa,
Department of Molecular Pharmaceutics, Faculty of Pharma-Science, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan.

Yasuhiro Nakamura,
Department of Molecular Pharmaceutics, Faculty of Pharma-Science, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan.

Yuqian Luo,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japana and Department of Laboratory Medicine, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.

Akira Kawashima,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan.

Mitsuo Kiriya,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan.

Mariko Sugawara-Mikami,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan and  West Yokohama Sugawara Dermatology Clinic, Yokohama, Kanagawa 221-0835, Japan.

Ken Karasawa,
Department of Molecular Pharmaceutics, Faculty of Pharma-Science, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan.

Koichi Suzuki,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Itabashi-Ku, Tokyo 173-8605, Japan.

Please see the link here: https://stm.bookpi.org/CTCB-V3/article/view/7498