News Release

Immune cells halt fungal infection by triggering spore suicide

Peer-Reviewed Publication

American Association for the Advancement of Science (AAAS)

Immune Cells Halt Fungal Infection by Triggering Spore Suicide

video: Video depicting host induction of fungal programmed cell death and its role in lung immunity against ubiquitous inhaled fungal spores. This material relates to a paper that appeared in the Sept. 8, 2017, issue of <i>Science</i>, published by AAAS. The paper, by N. Shlezinger at Memorial Sloan Kettering Cancer Center in New York, NY, and colleagues was titled, "Sterilizing immunity in the lung relies on targeting fungal apoptosis-like programmed cell death." view more 

Credit: Generated by Terry Helms, Medical Illustrator, Department of Communications, Memorial Sloan Kettering Cancer Center

To protect the body from infection, immune cells in the lungs can exploit cell death programs in inhaled fungal pathogens, scientists have revealed, helping explain why most people aren't harmed by breathing in mold spores, and potentially offering new therapeutic strategies for people who do get infected. Humans inhale anywhere from 1,000 to 1010 mold spores daily. In order to prevent harmful fungal infection, neutrophils and other immune cells that "devour" cellular bodies help clear inhaled spores from the lungs. However, individuals with immune systems already weakened by tuberculosis, autoimmune disease, AIDS or chemotherapy, to name a few, can more easily contract disease from exposure to mold. To develop effective therapies for these individuals, a clearer picture of anti-fungal immunity is needed. In mice, Neta Shlezinger and colleagues studied how immune cells in the lungs combat Aspergillus fumigatus, the most common mold-related pneumonia worldwide. They discovered that lung neutrophils engulfed the spores and then triggered the fungi's own "programmed cell death" pathway, preventing fungal germination and host invasion. Importantly, the authors also found an A. fumigatus protein called AfBIR1, the fungal equivalent of the human Survivin protein known to suppress cell death and prolong tumor growth, resisted cell death. Mice exposed to spores overexpressing AfBIR1 readily developed fatal fungal infections. Pharmacologic inhibition of BIR1 encoding for AfBIR1 increased fungal cell death and clearance in infected airways, suggesting that blockade of AfBIR1 could be a viable therapeutic approach against invasive aspergillosis.

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