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Host-strain compatibility shapes host transcriptional responses in macrophage in vitro infection models of Mycobacterium tuberculosis.

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Τίτλος: Host-strain compatibility shapes host transcriptional responses in macrophage in vitro infection models of Mycobacterium tuberculosis.
Συγγραφείς: Ruiz-Rodriguez P; Institute for Integrative Systems Biology (ISysBio), University of Valencia-CSIC, FISABIO Joint Research Unit Infection and Public Health, Valencia, Spain., Caballer-Gual M; Institute for Integrative Systems Biology (ISysBio), University of Valencia-CSIC, FISABIO Joint Research Unit Infection and Public Health, Valencia, Spain., Santamaria G; Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Esch-Belval Esch-sur-Alzette, Luxembourg., Hiza H; Institute for Integrative Systems Biology (ISysBio), University of Valencia-CSIC, FISABIO Joint Research Unit Infection and Public Health, Valencia, Spain., Coscollá M; Institute for Integrative Systems Biology (ISysBio), University of Valencia-CSIC, FISABIO Joint Research Unit Infection and Public Health, Valencia, Spain.
Πηγή: Microbial genomics [Microb Genom] 2026 Sep; Vol. 12 (9).
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Microbiology Society Country of Publication: England NLM ID: 101671820 Publication Model: Print Cited Medium: Internet ISSN: 2057-5858 (Electronic) Linking ISSN: 20575858 NLM ISO Abbreviation: Microb Genom Subsets: MEDLINE
Imprint Name(s): Publication: Oct. 2015- : [London] : Microbiology Society
Original Publication: [London] : Society for General Microbiology, [2015]-
Ιατρικοί όροι (MeSH): Mycobacterium tuberculosis*/pathogenicity , Mycobacterium tuberculosis*/genetics , Macrophages*/microbiology , Macrophages*/metabolism , Macrophages*/immunology , Host-Pathogen Interactions*/genetics , Tuberculosis*/microbiology , Tuberculosis*/genetics, Type C Phospholipases/metabolism ; Type C Phospholipases/genetics ; Humans ; Animals ; Cattle ; Transcriptome ; THP-1 Cells
Περίληψη: Differences in host distribution are observed across Mycobacterium tuberculosis complex (MTBC) lineages, but investigating the molecular basis of host compatibility in vivo is challenging. Here, we establish an epidemiology-guided in vitro framework to operationalize 'host compatibility' as a theoretical parameter that can be approximated experimentally using macrophage infection readouts. We infected two widely used but biologically distinct models, human THP-1-derived macrophages (THP-1m) and bovine macrophages (BoMac), with four MTBC human and animal strains. We quantified infected-cell frequency, intracellular bacterial burden dynamics, cell death and host transcriptome by RNA-seq. Across both models, infection phenotypes were concordant with the a priori epidemiology-informed reference pairings: the most compatible strain showed a higher late intracellular bacterial burden in its respective host, and the corresponding transcriptomes were enriched for replication, repair and cell-cycle signatures, whereas the opposite pairings showed lower bacterial burdens and stronger enrichment for endosomal, antigen-presentation and immune-signalling pathways in each cell type. Given the role of phospholipase C and virulence, we assessed plc expression and performed pharmacological inhibition experiments. These analyses revealed lineage- and macrophage-context-dependent expression patterns and reduced intracellular burden and cytotoxicity in THP-1m but not in BoMac. This framework links MTBC strain diversity to macrophage infection phenotypes and prioritizes candidate pathways potentially involved in bacterial-host interactions.
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Contributed Indexing: Keywords: Mycobacterium tuberculosis; RNA-seq; host–pathogen interactions; phospholipase; transcriptomics
Substance Nomenclature: EC 3.1.4.- (Type C Phospholipases)
Entry Date(s): Date Created: 20260923 Date Completed: 20260923 Latest Revision: 20260925
Update Code: 20260925
PubMed Central ID: PMC13600463
DOI: 10.1099/mgen.0.001826
PMID: 42776569
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:2057-5858
DOI:10.1099/mgen.0.001826