Comparative Transcriptomic and Metabolomic Analyses Reveal the Mechanism by Which Foam Macrophages Restrict Survival of Intracellular <i>Mycobacterium Tuberculosis</i>.

Xiao PENG; Yuan Yuan LIU; Li Yao CHEN; Hui YANG; Yan CHANG; Ye Ran YANG; Xuan ZHANG; An Na JIA; Yong Bo YU; Yong Li GUO; Jie LU

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Comparative Transcriptomic and Metabolomic Analyses Reveal the Mechanism by Which Foam Macrophages Restrict Survival of Intracellular Mycobacterium Tuberculosis.

Author: Xiao PENG ¹ ; Yuan Yuan LIU ¹ ; Li Yao CHEN ¹ ; Hui YANG ¹ ; Yan CHANG ¹ ; Ye Ran YANG ¹ ; Xuan ZHANG ¹ ; An Na JIA ¹ ; Yong Bo YU ¹ ; Yong Li GUO ¹ ; Jie LU ¹
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1. Beijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Publication Type:Comparative Study
Keywords: Foam macrophages; Metabolomic; Transcriptomic; Tuberculosis; cAMP signal pathway
MeSH: Mycobacterium tuberculosis/physiology*; Transcriptome; Metabolomics; Foam Cells/microbiology*; Humans; Metabolome; Tuberculosis/microbiology*; Gene Expression Profiling
From: Biomedical and Environmental Sciences 2025;38(7):781-791
CountryChina
Language:English
Abstract: OBJECTIVES:This study aimed to investigate the impact of foam macrophages (FMs) on the intracellular survival of Mycobacterium tuberculosis (MTB) and identify the molecular mechanisms influencing MTB survival.
METHODS:An in vitro FM model was established using oleic acid induction. Transcriptomic and metabolomic analyses were conducted to identify the key molecular pathways involved in FM-mediated MTB survival.
RESULTS:Induced FMs effectively restricted MTB survival. Transcriptomic and metabolomic profiling revealed distinct changes in gene and metabolite expression in FMs during MTB infection compared with normal macrophages. Integrated analyses identified significant alterations in the cyclic adenosine monophosphate (cAMP) signaling pathway, indicating that its activation contributes to the FM-mediated restriction of MTB survival.
CONCLUSIONS:FMs inhibit MTB survival. The cAMP signaling pathway is a key contributor. These findings enhance the understanding of the role of FMs in tuberculosis progression, suggest potential targets for host-directed therapies, and offer new directions for developing diagnostic and therapeutic strategies against tuberculosis.