Noncanonical Fungal Autophagy Inhibits Inflammation in Response to IFN-γ via DAPK1
Open accessAbstract
Defects in a form of noncanonical autophagy, known as LC3-associated phagocytosis (LAP), lead to increased inflammatory pathology during fungal infection. Although LAP contributes to fungal degradation, the molecular mechanisms underlying LAP-mediated modulation of inflammation are unknown. We describe a mechanism by which inflammation is regulated during LAP through the death-associated protein kinase 1 (DAPK1). The ATF6/C/EBP-β/DAPK1 axis activated by IFN-γ not only mediates LAP to Aspergillus fumigatus but also concomitantly inhibits Nod-like receptor protein 3 (NLRP3) activation and restrains pathogenic inflammation. In mouse models and patient samples of chronic granulomatous disease, which exhibit defective autophagy and increased inflammasome activity, IFN-γ restores reduced DAPK1 activity and dampens fungal growth. Additionally, in a cohort of hematopoietic stem cell-transplanted patients, a genetic DAPK1 deficiency is associated with increased inflammation and heightened aspergillosis susceptibility. Thus, DAPK1 is a potential drugable player in regulating the inflammatory response during fungal clearance initiated by IFN-γ.
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The anti-inflammatory activity of IFN-γ in CGD occurs via induction of Ca+2/calmodulin-regulated serine-threonine kinase DAPK1 in macrophages, which subsequently activates LAP parallel with the proteosomal degradation of the NLRP3 inflammasome.
“Similarly, the anti-inflammatory activity of IFN-γ in CGD occurs via induction of the Ca+2/calmodulin-regulated serine-threonine kinase DAPK1 in macrophages, which subsequently activates LAP parallel with the proteosomal degradation of the NLRP3 inflammasome (259).”
From Aspergillus fumigatus and Aspergillosis in 2019 (2019) · cites this paper as [259]
Activation of LAP in macrophages also regulates inflammatory signaling pathways.
“Notably, activation of LAP in macrophages also regulates inflammatory signaling pathways (258, 259).”
From Aspergillus fumigatus and Aspergillosis in 2019 (2019) · cites this paper as [259]
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- Authors
- Oikonomou, V., Moretti, S., Renga, G., Galosi, C., Borghi, M., Pariano, M., Puccetti, M., Palmerini, C. A., Amico, L., Carotti, A., Prezioso, L., Spolzino, A., Finocchi, A., Rossi, P., Velardi, A., Aversa, F., Napolioni, V., & Romani, L.
- Affiliations
- University of Perugia (IT)
- University of Parma (IT)
- Bambino Gesù Children's Hospital (IT)
- Corresponding author
- Romani, Luigina
- ORCID
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2016-12
- Volume
- 20
- Issue
- 6
- Pages
- 744-757
- ISSN
- 1931-3128 (ISSN-L)
- PMC
- PMC5161749
- OpenAlex
- W2553424415
- Cited by
- 68
- References
- 67
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 7 · 2023: 6 · 2022: 9 · 2021: 7 · 2020: 8 · 2019: 8 · 2018: 8 · 2017: 10 · 2016: 1
- FWCI
- 8.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell Host & Microbe (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, cc-by-nc-nd)
- Unicam Scientific Publications (University of Camerino) (submittedVersion, other-oa)
- Funders
- Specific Targeted Research Project FunMeta (ERC-2011-AdG-293714)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Keywords
- non-canonical autophagy, LC3-associated phagocytosis, DAPK1, interferon-gamma, Aspergillus fumigatus, fungal infection, inflammation, NLRP3 inflammasome, chronic granulomatous disease, aspergillosis, hematopoietic stem cell transplantation
- MeSH terms
- RAW 264.7 Cells, NLR Proteins, Animals, Aspergillosis, Aspergillus fumigatus, Autophagy, Cell Line, Fungi, Granulomatous Disease, Chronic, Humans, Inflammation, Interferon-gamma, Lung, Macrophages, Mice, Inbred C57BL, Phagocytosis, Phagosomes, Spores, Fungal, Gene Expression Regulation, Fungal, Mice, Death-Associated Protein Kinases
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