ArticleScientific reports2020
Mce1C and Mce1D facilitate N. farcinica invasion of host cells and suppress immune responses by inhibiting innate signaling pathways.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 9 citations in OpenAlex.
- Whole-genome sequencing and analysis of Nocardia veterana isolates from keratitis patients.Molecular genetics and genomics : MGG · 2026Article
- Phylogenetic and Genomic Feature Analysis of CutaneousInfection and drug resistance · 2026Article
- Molecular mechanisms underlyingFrontiers in cellular and infection microbiology · 2026Review
- Comparative in silico analysis of mce operons across Mycobacteriaceae and Nocardiaceae: Insights into genetic arrangements and regulatory mechanisms.Archives of microbiology · 2025Article
- Genomic characteristics, virulence potential, antimicrobial resistance profiles, and phylogenetic insights into Nocardia cyriacigeorgica.Annals of clinical microbiology and antimicrobials · 2025Article
- Activation of NF-κB/MAPK signaling and induction of apoptosis by salicylate synthase NbtS inmSystems · 2024Article
- Whole Genome Sequencing Highlights the Pathogenic Profile in Nocardia Keratitis.Investigative ophthalmology & visual science · 2024Article
- Molecular, cellular and neurological consequences of infection by the neglected human pathogen Nocardia.BMC biology · 2022Article
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mammalian cell entry (Mce) family of proteins consists of invasin-like membrane-associated proteins. The roles of Mce1C and Mce1D proteins in host-pathogen interactions have not been investigated. In this study, we demonstrate that Mce1C and Mce1D protein is localized in the cell wall fraction of N. farcinica. Both N. farcinica Mce1C and Mce1D proteins are expressed at the level of protein and mRNA and elicit antibody responses during infection. Mce1C and Mce1D facilitate the internalization of Escherichia coli expressing Mce1C protein or latex beads coated with Mce1D protein by HeLa cells, respectively. We further demonstrate that Mce1C and Mce1D can suppress the secretion of the proinflammatory factors TNF-α and IL-6 in macrophages infected with Mycobacterium smegmatis expressing Mce1C or Mce1D and promote the survival of M. smegmatis expressing Mce1C or Mce1D in macrophages. In addition, Mce1C and Mce1D supress the activation of the NF-κB and MAPK signaling pathways by blocking the phosphorylation of AKT, P65, ERK1/2, JNK, or P38 in macrophages. These findings suggest that Mce1C and Mce1D proteins facilitate N. farcinica invasion of HeLa cells and suppress host innate immune responses by manipulating NF-κB and MAPK signaling pathways, which may provide a target for N. farcinica treatment.
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