Scholarlink

<p>The protective efficacy of the Bacillus Calmette-Guérin (BCG) vaccine against <i>Mycobacterium tuberculosis</i> (Mtb) is variable, and the systemic mechanisms linking cellular immunity with host metabolism remain poorly understood. This study employed high-dimensional mass cytometry (CyTOF) within the splenic compartment and serum lipidomics to map the integrated immuno-metabolic landscape in BCG-vaccinated and non-vaccinated mice following infection with the H37Rv strain. We report that BCG vaccination was associated with a distinct phenotype characterised by the priming of antimicrobial myeloid subsets (CD11b+ Mac2+/Mac3+) and lipidomic pathways away from stress-induced inflammatory responses. In contrast, non-vaccinated hosts exhibited a dysregulated response, characterised by a systemic cortisol surge, a lipidomic profile suggestive of reduced bioactive lipids (including PPARγ ligands such as 13-HODE and 19,20-DiHDPA), and the reactive mobilisation of CD103 + CD4+/CD8 + T cells and activated B cell subsets to the spleen. These findings reveal that protection is not solely cellular but relies on a stable metabolic environment that supports immune function. While infection in naive hosts drives a resource-depleting stress response that likely compromises macrophage efficacy, BCG vaccination establishes an integrated multiparametric defence, preventing pathogen-driven metabolic manipulation and maintaining the necessary lipid mediators for effective inflammation resolution and bacterial control.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Comprehensive CyTOF and lipidomic analysis of splenic immune and serum lipid responses to BCG vaccination and H37Rv challenge in BALB/c mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月26日

查看全文
  • Matthieu Van-Tilbeurgh,
  • Wei Yang,
  • Ernesto Marcos Lopez,
  • Anne-Sophie Gallouët,
  • Belinda Dagg,
  • Sara Goulding,
  • James Keeble,
  • Mei Mei Ho,
  • Amy Harms,
  • Roger Le Grand,
  • Bhagwati Khatri

摘要

The protective efficacy of the Bacillus Calmette-Guérin (BCG) vaccine against Mycobacterium tuberculosis (Mtb) is variable, and the systemic mechanisms linking cellular immunity with host metabolism remain poorly understood. This study employed high-dimensional mass cytometry (CyTOF) within the splenic compartment and serum lipidomics to map the integrated immuno-metabolic landscape in BCG-vaccinated and non-vaccinated mice following infection with the H37Rv strain. We report that BCG vaccination was associated with a distinct phenotype characterised by the priming of antimicrobial myeloid subsets (CD11b+ Mac2+/Mac3+) and lipidomic pathways away from stress-induced inflammatory responses. In contrast, non-vaccinated hosts exhibited a dysregulated response, characterised by a systemic cortisol surge, a lipidomic profile suggestive of reduced bioactive lipids (including PPARγ ligands such as 13-HODE and 19,20-DiHDPA), and the reactive mobilisation of CD103 + CD4+/CD8 + T cells and activated B cell subsets to the spleen. These findings reveal that protection is not solely cellular but relies on a stable metabolic environment that supports immune function. While infection in naive hosts drives a resource-depleting stress response that likely compromises macrophage efficacy, BCG vaccination establishes an integrated multiparametric defence, preventing pathogen-driven metabolic manipulation and maintaining the necessary lipid mediators for effective inflammation resolution and bacterial control.