bims-nocaut Biomed News
on Non-canonical autophagy
Issue of 2025–03–23
two papers selected by
Quentin Frenger, University of Strasbourg
  1. Adiponectin pathway activation dampens inflammation and enhances alveolar macrophage fungal killing via LC3-associated phagocytosis.
  2. Cold atmospheric plasma enhances immune clearance of Porphyromonas gingivalis via LC3-associated phagocytosis in mice with experimental periodontitis.
  1. PLoS Pathog. 2025 Mar 17. 21(3): e1012363
    Adiponectin pathway activation dampens inflammation and enhances alveolar macrophage fungal killing via LC3-associated phagocytosis.
    Sri Harshini Goli, Joo-Yeon Lim, Nese Basaran-Akgul, Steven P Templeton.
      Although innate immunity is critical for antifungal host defense against the human opportunistic fungal pathogen Aspergillus fumigatus, potentially damaging inflammation must be controlled. Adiponectin (APN) is an adipokine produced mainly in adipose tissue that exerts anti-inflammatory effects in adipose-distal tissues such as the lung. We observed increased mortality and increased fungal burden and inflammation in neutropenic mice with invasive aspergillosis (IA) that lack APN or the APN receptors AdipoR1 or AdipoR2. Alveolar macrophages (AMs), early immune sentinels that detect and respond to lung infection, express both receptors, and APN-deficient AMs exhibited an inflammatory phenotype that was associated with decreased fungal killing. Pharmacological stimulation of AMs with AdipoR agonist AdipoRon rescued deficient killing in APN-/- AMs and was dependent on the presence of either receptor. Finally, APN-enhanced fungal killing was associated with increased activation of the non-canonical LC3 pathway of autophagy. Thus, our study identifies a novel role for APN in LC3-mediated killing of A.fumigatus.
    DOI:  https://doi.org/10.1371/journal.ppat.1012363
  2. Int Immunopharmacol. 2025 Mar 20. pii: S1567-5769(25)00484-9. [Epub ahead of print]153 114494
    Cold atmospheric plasma enhances immune clearance of Porphyromonas gingivalis via LC3-associated phagocytosis in mice with experimental periodontitis.
    Wenqian Yu, Jialin Liu, Chang Yang, Yao Luo, Hailin Mu, Shuo Wang, Wei Dong, Meie Jia, Zhipeng Dong, Xinpei Lu, Jiawei Wang.
      Periodontitis is a microbe-driven infectious disease, in which Porphyromonas gingivalis (Pg) plays a keystone role. As the front line to eliminate dysbiotic microbiota, macrophages are critical for recognition, phagocytosis and digestion of bacteria. However, deficiencies in the antimicrobial function of periodontal macrophages lead to diminished Pg clearance and destructive periodontal inflammation. Cold atmospheric plasma (CAP) enables non-invasive treatment by producing reactive species including reactive oxygen species (ROS), reactive nitrogen species (RNS) and electro-magnetic field, and is of great interest for infectious diseases. These radicals have a significant influence on cellular biochemistry and are crucial components of the immune system. The CAP jet using helium gas was developed and driven by the bipolar pulse high voltage. The negative voltage was 5 kV and the positive voltage was 10 kV. The irradiation time was set to 120 s for in vivo experiments and 80 s for in vitro experiments. In vivo experiments demonstrated that CAP significantly alleviated periodontitis. In addition to the directly antimicrobial effects, in vitro experiments demonstrated that CAP enhanced intracellular killing of Pg by bone marrow-derived macrophages (BMMs) and murine macrophage cell line RAW 264.7 in a ROS-dependent manner. BMMs were collected from the tibias and femurs of healthy C57BL/6 mice aged 6-8 weeks old. Mechanistically, it is found that CAP promotes microtubule-associated protein 1A/1B-light chain 3 (MAP1LC3, LC3)-associated phagocytosis (LAP) in macrophages to defend against Pg. Therefore, CAP is proposed a potential therapy for effectively alleviating periodontitis through regulating the bactericidal activity of macrophages.
    Keywords:  Cold atmospheric plasma; LC3-associated phagocytosis; Macrophages; Periodontitis; Porphyromonas gingivalis
    DOI:  https://doi.org/10.1016/j.intimp.2025.114494
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