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Model of a novel ULK1-mediated LAP-like pathway in airway cells during A. fumigatus conidial internalization. During the interaction between A. fumigatus conidia and airway cells, several changes occur: intracellular LC3-II levels, phosphorylation of AMPK and ULK1, and reactive oxygen species (ROS) content all increase. Additionally, the release of cytokines—including IL-6, IL-8, and MCP-1—also rises. Inhibiting ULK1 activity or silencing its expression can suppress the increase in LC3-II levels and cytokine release triggered by A. fumigatus . Notably, common fungal polysaccharides <t>and</t> <t>Dectin-1</t> did not impact this process, but the loss of complement receptor 3 elevated both basal and conidia-induced autophagy, correlating with increased AMPK expression. Dashed lines indicate signal pathway interactions hypothesized to occur in airway cells.
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Model of a novel ULK1-mediated LAP-like pathway in airway cells during A. fumigatus conidial internalization. During the interaction between A. fumigatus conidia and airway cells, several changes occur: intracellular LC3-II levels, phosphorylation of AMPK and ULK1, and reactive oxygen species (ROS) content all increase. Additionally, the release of cytokines—including IL-6, IL-8, and MCP-1—also rises. Inhibiting ULK1 activity or silencing its expression can suppress the increase in LC3-II levels and cytokine release triggered by A. fumigatus . Notably, common fungal polysaccharides and Dectin-1 did not impact this process, but the loss of complement receptor 3 elevated both basal and conidia-induced autophagy, correlating with increased AMPK expression. Dashed lines indicate signal pathway interactions hypothesized to occur in airway cells.

Journal: Frontiers in Microbiology

Article Title: ULK1 mediated autophagy in airway cells during Aspergillus infection

doi: 10.3389/fmicb.2026.1756294

Figure Lengend Snippet: Model of a novel ULK1-mediated LAP-like pathway in airway cells during A. fumigatus conidial internalization. During the interaction between A. fumigatus conidia and airway cells, several changes occur: intracellular LC3-II levels, phosphorylation of AMPK and ULK1, and reactive oxygen species (ROS) content all increase. Additionally, the release of cytokines—including IL-6, IL-8, and MCP-1—also rises. Inhibiting ULK1 activity or silencing its expression can suppress the increase in LC3-II levels and cytokine release triggered by A. fumigatus . Notably, common fungal polysaccharides and Dectin-1 did not impact this process, but the loss of complement receptor 3 elevated both basal and conidia-induced autophagy, correlating with increased AMPK expression. Dashed lines indicate signal pathway interactions hypothesized to occur in airway cells.

Article Snippet: LC3 Rabbit Polyclonal antibody(#14600-1-AP, 1:1000), Rubicon Rabbit Polyclonal Antibody (#21444-1-AP, 1:1000), GAPDH Polyclonal antibody(#10494-1-AP, 1:2000) were purchased from proteintech, Phospho-UKL1(Ser555) Rabbit monoclonal antibody (#5869, 1:500), Phospho-UKL1(Ser757) Rabbit monoclonal antibody (#6888, 1:500), ULK1 rabbit monoclonal antibody (#8054, 1:1000), SQSTM1/p62 antibody (#5114, 1:1000), Atg5 Rabbit monoclonal antibody (#12994, 1:1000), Dectin-1 Rabbit monoclonal antibody (#60128, 1:1000), AMPKalpha Antibody (#2532, 1:1000), Phospho-AMPKalpha (Thr172) Rabbit monoclonal antibody(#50081, 1:1000), β -tubulin Rabbit monoclonal antibody(#2128, 1:2000) were purchased from Cell Signaling Technology (USA).

Techniques: Phospho-proteomics, Activity Assay, Expressing