Selected article for: "impaired NOX signaling and inflammasome activation"
Author: Yen, Wei-Chen; Wu, Yi-Hsuan; Wu, Chih-Ching; Lin, Hsin-Ru; Stern, Arnold; Chen, Shih-Hsiang; Shu, Jwu-Ching; Tsun-Yee Chiu, Daniel
Title: Impaired inflammasome activation and bacterial clearance in G6PD deficiency due to defective NOX/p38 MAPK/AP-1 redox signaling
  • Document date: 2019_11_2
    • ID: 6fw4thkq_58
    Snippet: In conclusion, impaired inflammasome activation by G6PD deficiency can present a phenomenon of increased susceptibility to bacterial infections. Mechanistically, defective bacterial clearance found in G6PD-kd THP-1 cells is due to impaired NOX/p38 MAPK/AP-1 signaling and may appear in patients with G6PD deficiency. The change in G6PD status contributes to an imbalance in cellular redox homeostasis that affects inflammatory-associated signal trans.....
    Document: In conclusion, impaired inflammasome activation by G6PD deficiency can present a phenomenon of increased susceptibility to bacterial infections. Mechanistically, defective bacterial clearance found in G6PD-kd THP-1 cells is due to impaired NOX/p38 MAPK/AP-1 signaling and may appear in patients with G6PD deficiency. The change in G6PD status contributes to an imbalance in cellular redox homeostasis that affects inflammatory-associated signal transduction to influence cellular infectivity. The care of patients with G6PD deficiency to prevent infection might include appropriate antibiotic prophylaxis and the modulation of inflammasome activity. G6PD knockdown results in the reduced generation of pro-IL-1β and an impairment of the LPS-induced p38/MAPK-AP-1 pathway. IL-1β secretion is also reduced in G6PD-knockdown cells.

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