ArticleInfection and immunity2006
The SecA2 secretion factor of Mycobacterium tuberculosis promotes growth in macrophages and inhibits the host immune response.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 106 citations in OpenAlex.
- Epigenetic Reprogramming byAntibiotics (Basel, Switzerland) · 2026Review
- Mycobacterium tuberculosis bacteriology and immunity necessitate a multi-pronged immune strategy for vaccination.NPJ vaccines · 2026Review
- Live Attenuated Vaccines against Tuberculosis: Targeting the Disruption of Genes Encoding the Secretory Proteins of Mycobacteria.Vaccines · 2024Review
- Mycobacterium tuberculosis SecA2-dependent activation of host Rig-I/MAVs signaling is not conserved in Mycobacterium marinum.PloS one · 2024Article
- Mycobacterium tuberculosis and its clever approaches to escape the deadly macrophage.World journal of microbiology & biotechnology · 2023Review
- Comprehensive essentiality analysis of themBio · 2023Article
- Mycobacterium smegmatis: The Vanguard of Mycobacterial Research.Journal of bacteriology · 2023Review
- The functional response of human monocyte-derived macrophages to serum amyloid A andFrontiers in immunology · 2023Article
- E3 Ligase FBXW7 FacilitatesFrontiers in cellular and infection microbiology · 2022Article
- Virulence-Associated Secretion inFrontiers in immunology · 2022Review
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- The Macrophage Response toFrontiers in cellular and infection microbiology · 2020Review
- Global Assessment of Mycobacterium avium subsp.mSystems · 2019Article
- Immunology ofMicrobiology spectrum · 2019Review
- Screening Mycobacterium tuberculosis Secreted Proteins Identifies Mpt64 as a Eukaryotic Membrane-Binding Bacterial Effector.mSphere · 2019Article
- The Two Distinct Types of SecA2-Dependent Export Systems.Microbiology spectrum · 2019Review
- Article
- Article
- The SecA2 pathway of Mycobacterium tuberculosis exports effectors that work in concert to arrest phagosome and autophagosome maturation.PLoS pathogens · 2018Article
- c-Abl-TWIST1 Epigenetically Dysregulate Inflammatory Responses during Mycobacterial Infection by Co-Regulating Bone Morphogenesis Protein and miR27a.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The SecA protein is present in all bacteria, and it is a central component of the general Sec-dependent protein export pathway. An unusual property of Mycobacterium tuberculosis is the presence of two SecA proteins: SecA1, the essential "housekeeping" SecA, and SecA2, the accessory secretion factor. Here, we report that a DeltasecA2 mutant of M. tuberculosis was defective for growth in the early stages of low-dose aerosol infection of C57BL/6 mice, a time during which the bacillus is primarily replicating in macrophages. Consistent with this in vivo phenotype, we found that the DeltasecA2 mutant was defective for growth in macrophages from C57BL/6 mice. The DeltasecA2 mutant was also attenuated for growth in macrophages from phox(-/-) mice and from NOS2(-/-) mice. These mice are defective in the reactive oxygen intermediate (ROI)-generating phagocyte oxidase and the reactive nitrogen intermediate (RNI)-generating inducible nitric oxide synthase, respectively. This indicated a role for SecA2 in the intracellular growth of M. tuberculosis that is independent of protecting against these ROIs or RNIs. Macrophages infected with the DeltasecA2 mutant produced higher levels of tumor necrosis factor alpha, interleukin-6, RNI, and gamma interferon-induced major histocompatibility complex class II. This demonstrated a function for M. tuberculosis SecA2 in suppressing macrophage immune responses, which could explain the role of SecA2 in intracellular growth. Our results provide another example of a relationship between M. tuberculosis virulence and inhibition of the host immune response.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.