iScience · 2026
Mycobacterium tuberculosis subverts macrophage-mediated defense through exploitation of the Zn transporter ZIP8.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Arnett Eusondia, Lumbreras Miranda, Hernandez Elizabeth, Campos Daniela, Leopold Wager Chrissy M, Pahari Susanta, Matouba Dahlia, Determann Brenden F, Renshaw Charles, Longstreet Brandon, Gonzalez Olga, Shivanna Vinay, Dick Edward J, Azad Abul, Pyle Charlie, Smith Deandra, Tomar Vartika, Guirado Evelyn, Ojha Anil K, Melia Joanna, Knoell Daren, Schlesinger Larry S
Аннотация
Zinc (Zn) is an essential micronutrient whose concentration and location are tightly regulated by Zn transporters. Mycobacterium tuberculosis (M.tb) resides in macrophage phagosomes, where it requires access to micronutrients, including Zn. Our data show that ZIP8 is the only Zn transporter in human macrophages highly induced by M.tb and is enriched at the M.tb phagosome. Using human and murine macrophages and mice deficient in ZIP8, we found that M.tb exploits ZIP8 to enhance its growth. ZIP8 imports Zn into the cytosol and out of the phagosome to subvert Zn poisoning. Cytosolic Zn dampens NF-κB activation and pro-inflammatory cytokine production while enhancing matrix metalloproteinase (MMP) production. Understanding the Zn- and ZIP8-dependent host response to M.tb infection is critical since dietary Zn deficiency and polymorphic ZIP8 variants are associated with increased susceptibility to tuberculosis and other infectious diseases.