ArticlePloS one2016
Brucella Melitensis 16M Regulates the Effect of AIR Domain on Inflammatory Factors, Autophagy, and Apoptosis in Mouse Macrophage through the ROS Signaling Pathway.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- SIRT2 inhibition enhances mitochondrial apoptosis in Brucella-infected bovine placental trophoblast cells.Veterinary research · 2025Article
- Analysis and validation of serum biomarkers in brucellosis patients through proteomics and bioinformatics.Frontiers in cellular and infection microbiology · 2024Article
- Review
- Exosomes released by Brucella-infected macrophages inhibit the intracellular survival of Brucella by promoting the polarization of M1 macrophages.Microbial biotechnology · 2023Article
- The mechanism of chronic intracellular infection withFrontiers in cellular and infection microbiology · 2023Review
- Small ubiquitin-related modifier 2 affects the intracellular survival ofInnate immunity · 2021Article
- Deletion of the Type IV Secretion System Effector VceA Promotes Autophagy and Inhibits Apoptosis in Brucella-Infected Human Trophoblast Cells.Current microbiology · 2019Article
- Bacteria Exploit Autophagy For Their Own Benefit.Infection and drug resistance · 2019Review
- The relationship between caspase-1 related inflammasome expression and serum inflammatory cytokine levels during acute brucellosis.Northern clinics of Istanbul · 2019Article
- Guanylate-binding protein 5 licenses caspase-11 for Gasdermin-D mediated host resistance to Brucella abortus infection.PLoS pathogens · 2018Article
- Mitochondrial fragmentation affects neither the sensitivity to TNFα-induced apoptosis of Brucella-infected cells nor the intracellular replication of the bacteria.Scientific reports · 2018Article
- Brucella abortus Induces a Warburg Shift in Host Metabolism That Is Linked to Enhanced Intracellular Survival of the Pathogen.Journal of bacteriology · 2017Article
- Selection and characterization of specific nanobody against bovine virus diarrhea virus (BVDV) E2 protein.PloS one · 2017Article
- The effects of hyperbaric oxygen therapy on neuropathic pain via mitophagy in microglia.Molecular painArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brucellosis is a highly contagious zoonosis caused by Brucella. Brucella can invade and persist inside host cells, which results in chronic infection. We constructed AIR interference and overexpression lentiviruses to acquire AIR interference, overexpression, and rescue stable expression cell lines. We also established a Brucella melitensis 16M-infected macrophage model, which was treated with either the vehicle control or NAC (ROS scavenger N-acetylcysteine (NAC) for 0, 3, 6, 12, and 24 h. Confocal laser microscopy, transmission electron microscopy, fluorescence quantitative PCR, flow cytometry, ELISA, and Western blot were used to detect inflammation, cell autophagy and apoptosis-related protein expression levels, ROS levels, and the distribution of mitochondria. It was found that after interference and overexpression of AIR, ROS release was significantly changed, and mitochondria became abnormally aggregated. B. melitensis 16M activated the NLRP3/AIM2 inflammatory complex, and induced RAW264.7 cells to secrete IL-1β and IL-18 through the ROS pathway. B. melitensis 16M also altered autophagy-related gene expression, increased autophagy activity, and induced cell apoptosis through the ROS pathway. The results showed that after B. melitensis 16M infection, ROS induced apoptosis, inflammation, and autophagy while AIR inhibited autophagosome maturation and autophagy initiation. Autophagy negatively regulated the activation of inflammasomes and prevented inflammation from occurring. In addition, mitophagy could promote cell apoptosis.
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