Cited by 74Immune Response and InflammationInflammasome and immune disordersNF-κB Signaling Pathways

Surfactin inducing mitochondria-dependent ROS to activate MAPKs, NF-κB and inflammasomes in macrophages for adjuvant activity

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Gan, Ping, Gao, Zhenqiu, Zhao, Xiuyun, Qi, Gaofu·2016·Scientific Reports

Abstract

Surfactin, a natural lipopeptide, can be used both as parenteral and non-parenteral adjuvant for eliciting immune response. However, the mechanisms that confer its adjuvant properties have not been fully explored. By staining with NHS-Rhodamine B labeled surfactin and Mito-Tracker Green, we found surfactin could penetrate into macrophages to bind with mitochondria, following induce ROS that could be inhibited by mitochondria-dependent ROS inhibitor. ROS enhanced p38 MAPK and JNK expression, as well their phorsphorylation, following activated NF-κB nuclear translocation in macrophages that was obviously inhibited by mitochondria-dependent ROS inhibitor. However, inhibition of ROS production only weakened p38 MAPK and JNK expression, but not their phosphorylation in macrophages. As a result, surfaction could activate NF-κB to release TNF-α by the mitochondria-dependent ROS signalling pathway. ROS also induced macrophages apoptosis to release endogenous danger signals, following activated inflammasomes of NLRP1, NLRP3, IPAF and AIM2 in vitro and only NLRP1 in vivo , as well caspase-1 and IL-1 in macrophages, which were significantly inhibited by pre-treatment with ROS inhibitors. Collectively, surfactin as a kind of non-pathogen-associated molecular patterns, modulates host innate immunity by multiple signalling pathways, including induction of mitochondria-dependent ROS, activating MAPKs and NF-κB, and inducing cell apoptosis to realease endogenous danger signals for activation of inflammasomes.

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  • Mitochondrial ROS have been implicated in pathways leading to cell proliferation and senescence and in activation of JNK and NF-κB.

    “Additionally, mitochondrial ROS have been implicated in pathways leading to cell proliferation and senescence (233, 1046) as well as in the activation of other major cell signaling molecules such as the MAP kinase JNK and NF-κB (330, 689).”

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Authors
Gan, P., Gao, Z., Zhao, X., & Qi, G.
Affiliations
  • Guilin Medical University (CN)
  • Yancheng Teachers University (CN)
  • Huazhong Agricultural University (CN)
Corresponding author
Qi, Gaofu
Venue
Scientific Reports
Published
2016-12-14
Volume
6
Issue
1
Pages
39303-39303
ISSN
2045-2322 (ISSN-L)
OpenAlex
W2562514953
Cited by
74
References
35
Citations by year
2026: 9 · 2025: 15 · 2024: 4 · 2023: 7 · 2022: 7 · 2021: 8 · 2020: 8 · 2019: 5 · 2018: 6 · 2017: 5
FWCI
3.23
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
surfactin, macrophages, p38 MAPK, JNK, NF-κB, inflammasome, NLRP1, NLRP3, caspase-1, IL-1β, TNF-α, macrophage apoptosis, endogenous danger signals, innate immunity
MeSH terms
RAW 264.7 Cells, Adjuvants, Immunologic, Animals, Macrophages, Mitochondria, Peptides, Cyclic, NF-kappa B, Reactive Oxygen Species, Mitogen-Activated Protein Kinases, Mice, Lipopeptides, Inflammasomes

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