Frontiers in microbiology · 2025
Effect of periostin (OSF-2) on phagocytosis of Plasmodium-infected erythrocytes.
СтатьяНазвание и аннотация: Перевод в очереди
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Chin Joo-Yie, Mohammed-Syafiei Muhammed-Nur-Iman, Lim Yi-Jun, Chong Gordon Xue-Zhen, Suhaimi Muhammad-Nasreen, Phong Zhi-Ying, Ng Yee Ling, Lau Yee-Ling, Sam I-Ching, Rénia Laurent, Lee Wenn-Chyau
Аннотация
INTRODUCTION: Phagocytosis is a pivotal component of the human innate immune defense against malaria. This essential defense mechanism is often modulated by various host-derived soluble factors. We investigated the phagocytosis of Plasmodium falciparum- and P. knowlesi-infected erythrocytes (IRBC) by human monocytic THP-1 cells in the presence of periostin (OSF-2), a human secretory protein involved in inflammation and tissue repair. This focus was prompted by the fact that OSF-2 is a potent stimulator of Plasmodium IRBC rosette formation, a parasite-derived cytoadherence phenomenon known to impede phagocytosis.
METHODS: Culturable parasite isolates were recruited, and tested with the THP-1 cells and recombinant human OSF-2 protein. The role of OSF-2 in IRBC phagocytosis by the phagocytes was evaluated in the presence and absence of uninfected erythrocytes (URBC), and the receptor involved was investigated with antibody blocking assay.
RESULTS: OSF-2 exerted a dual role. When rosetting was prevented via IRBC purification, OSF-2 increased IRBC phagocytosis. This stimulatory effect was also seen when THP-1 cells were primed with OSF-2 before IRBC exposure. This OSF-2-mediated phagocytosis was CD36-dependent and rapidly reversible upon OSF-2 removal. However, when rosetting was induced by the addition of URBC, the presence of OSF-2 reduced the rate of IRBC phagocytosis.
DISCUSSION: These findings highlight the complex parasite-host interactions influencing the infection pathogenesis.
METHODS: Culturable parasite isolates were recruited, and tested with the THP-1 cells and recombinant human OSF-2 protein. The role of OSF-2 in IRBC phagocytosis by the phagocytes was evaluated in the presence and absence of uninfected erythrocytes (URBC), and the receptor involved was investigated with antibody blocking assay.
RESULTS: OSF-2 exerted a dual role. When rosetting was prevented via IRBC purification, OSF-2 increased IRBC phagocytosis. This stimulatory effect was also seen when THP-1 cells were primed with OSF-2 before IRBC exposure. This OSF-2-mediated phagocytosis was CD36-dependent and rapidly reversible upon OSF-2 removal. However, when rosetting was induced by the addition of URBC, the presence of OSF-2 reduced the rate of IRBC phagocytosis.
DISCUSSION: These findings highlight the complex parasite-host interactions influencing the infection pathogenesis.