Mycobacterium tuberculosis/Mycobacterium bovis triggered different variations in lipid composition of Bovine Alveolar Macrophages

• Published in: Scientific reports 2022-07, Vol.12 (1), p.13115-13115, Article 13115
• Main Authors: Chen, Yuqi, Ma, Huiya, Duan, Yangbo, Ma, Xueyan, Tan, Lihui, Dong, Jianjian, Jin, Chenkai, Wei, Rong
• Format: Article
• Language: English
• Subjects: 631/326; 631/80; Accumulation; Acetic acid; Alveoli; Ceramide; Humanities and Social Sciences; Immune response; Interleukin 17; Lipid composition; Lipid metabolism; Lipids; Macrophages; multidisciplinary; Mycobacterium bovis; Mycobacterium tuberculosis; Polystyrene; Science; Science (multidisciplinary); Testosterone; Transcriptomes; Tuberculosis; Tumor necrosis factor
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-022-17531-2

The lipid composition performs important functions in interaction between macropha-ge and Mycobacterium tuberculosis (MTB)/ Mycobacterium bovis (MB). Current understanding regarding the lipid responses of bovine alveolar macrophage (BAM) to MTB/MB is quite limited. The present study conducted lipidomics and transcriptome to assess alterations in BAM lipid compositions upon MB and MTB infection. We found that both MTB and MB induced glycerophospholipids accumulation in BAM, and MTB induced more alterations in lipid composition. MTB could affect the contents of various lipids, especially ceramide phosphocholines, polystyrene (PS) (17:0/0:0), testolic acid and testosterone acetate. Meanwhile, MB particularly induced accumulation of 1-alkyl,2-acylglycerophosphoinositols. Both MB and MTB suppressed the contents of palmitoleamide, N -ethyl arachidonoyl amine, N -(1,1-dimethyl-2-hydroxy-ethyl) arachidonoyll amine, eicosanoyl-EA, and PS (O-18:0/17:0) in BAM. Additionally, transcriptome analysis revealed that only MTB triggered genes involved in immune signaling and lipid related pathways in BAM. And MTB mainly activated genes CXCL2 and CXCL3 relevant to NOD-like receptor, IL-17 and TNF to further induce lipid accumulation in BAM, which in turn promoted the formation of foam cells. Meanwhile, time course RT-qPCR results showed that MTB was recognized by BAM to triggered dramatic immune responses, whereas MB could effectively escape the recognition system of BAM, leading rearrangement of lipid metabolisms in BAM at early infection stage. Altogether, the results of the present study provided evidence for changes in lipid metabolism of MTB/MB attacked BAM and contributed to the detection and treatment of zoonotic tuberculosis.