ArticleCell death discovery2015
Caspase-independent apoptosis in infected macrophages triggered by sulforaphane via Nrf2/p38 signaling pathways.
Article in Cell death discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Cell Death Mechanisms inPathogens (Basel, Switzerland) · 2025Review
- Phytochemical-mediated efferocytosis and autophagy in inflammation control.Cell death discovery · 2024Review
- The Role of the Nrf2 Pathway in Airway Tissue Damage Due to Viral Respiratory Infections.International journal of molecular sciences · 2024Review
- High-Frequency Repetitive Magnetic Stimulation Activates Bactericidal Activity of Macrophages via Modulation of p62/Keap1/Nrf2 and p38 MAPK Pathways.Antioxidants (Basel, Switzerland) · 2023Article
- Druggable redox pathways against Mycobacterium abscessus in cystic fibrosis patient-derived airway organoids.PLoS pathogens · 2023Article
- Article
- Sulforaphane kills Mycobacterium tuberculosis H37Ra and Mycobacterium smegmatis mcJournal of microbiology (Seoul, Korea) · 2022Article
- Streptococcus pneumoniae exerts oxidative stress, subverts antioxidant signaling and autophagy in human corneal epithelial cells that is alleviated by tert-Butylhydroquinone.Medical microbiology and immunology · 2022Article
- Modulating macrophage function to reinforce host innate resistance againstFrontiers in immunology · 2022Review
- The Role of NRF2 in Mycobacterial Infection.Antioxidants (Basel, Switzerland) · 2021Review
- Sulforaphane induces S-phase arrest and apoptosis via p53-dependent manner in gastric cancer cells.Scientific reports · 2021Article
- Type I Interferons Are Involved in the Intracellular Growth Control ofFrontiers in immunology · 2021Article
- Sulforaphane reduces intracellular survival of Staphylococcus aureus in macrophages through inhibition of JNK and p38 MAPK‑induced inflammation.International journal of molecular medicine · 2020Article
- Real-Ambient Particulate Matter Exposure-Induced Cardiotoxicity in C57/B6 Mice.Frontiers in pharmacology · 2020Article
- Article
- A small molecule targeting glutathione activates Nrf2 and inhibits cancer cell growth through promoting Keap-1RSC advances · 2018Article
- Imaging flow cytometry analysis of intracellular pathogens.Methods (San Diego, Calif.) · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium abscessus (Mabs), a non-tuberculous mycobacterium, is an emerging and rapidly growing opportunistic pathogen that is frequently found in patients with cystic fibrosis and in immunosuppressed patients. Its high tolerance to antibiotics is of great concern for public health. In this study, our results showed that human THP-1-derived macrophages infected with M. abscessus presented an increase in ROS production and cell necrosis. In addition, M. abscessus infection triggered activation of the Nuclear factor E2-related factor 2 (Nrf2) signaling pathway, and the induction of HO-1 and NQO1 expression levels. Interestingly, pretreatment of macrophages with sulforaphane (SFN), an activator of the antioxidant key regulator Nrf2, followed by M. abscessus infection significantly decreased mycobacterial burden. We demonstrated that this reduction in mycobacterial growth was due to an activation in cell apoptosis in SFN-pretreated and M. abscessus-infected macrophages. Pretreatment with specific MAPK inhibitors, PD98059, SP600125, and SB203580 to ERK, JNK, and p38 respectively, failed to inhibit induction of Nrf2 expression, suggesting that Nrf2 signaling pathway was upstream of MAPK signaling. Activation of cell apoptosis was caspase 3/7 independent but p38 MAPK dependent. Moreover, p38 MAPK induction was abolished in macrophages transfected with Nrf2 siRNA. In addition, p38 inhibitor abolished Nrf2-dependent apoptosis in infected macrophages. Taken together, our results indicate that modulation of the Nrf2 signaling using Nrf2 activators may help potentiate the actual drug therapies used to treat mycobacterial infection.
Identifiers
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Registered trials
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.