Lipidomics revealed the global lipid responses of primary bovine alveolar macrophages to infections of Mycobacterium tuberculosis and Mycobacterium bovis

Mycobacterium tuberculosis (M. tuberculosis (MTB) and M. bovis (MB) of the Mycobacterium tuberculosis complex (MTBC) are the causative agents of the notorious infectious disease tuberculosis (TB) in a range of mammals, including bovine and human. The lipid composition of MTB/MB performed imperative function as invading host macrophage. However, the detailed variations in lipid compositions of MTB and MB were unknown, while the responses relevant to lipid metabolisms in MTB/MB-infected host were also unclear. In the present study, a dualLipidomics were used to elucidate the differences in lipid composition of MTB and MB and responses in lipid metabolisms of primary bovine alveolar macrophages infected by MTB/MB. The Lipidomics showed significant differences in lipid composition, especially differences in levels of Glycerophospholipids, Sterol Lipids, Fatty Acyls and Polyketides between these two mycobacterium species. Meanwhile, both MTB and MB could invoke various responses of lipid metabolisms in host macrophages. An infection of MTB mainly induced the increases of Polyketides and Glycerophospholipids in macrophages, whereas an MB infection induced the increases of Glycerophospholipids and Sterol. Furthermore, TAG 13:0-18:5-18:5 of MTB and PC (16:1(9E)/0:0), PI(20:2 (11Z,14Z)/22:6(4Z,7Z,10Z,13Z,16Z,19Z)), 4, 6-Decadiyn-1-ol isovalerate and LacCer (d18:1/24:1(15Z)) of MB were identified to cause variations in lipid metabolisms of macrophages, respectively. From these data, we proposed that the differential compositions of lipid compositions in MTB and MB could successfully colonize in macrophage by different mechanisms. MTB could promote the formation of foam cells of macrophage for its colonization and development, while MB mainly suppresses the macrophage autophagy to escape the immune responses of host.