Immunopharmacology and immunotoxicology · 2026
Diethylcarbamazine reduces the viral titer of influenza A (H1N1)pdm09 virus and regulates IFN-β and IL-8 in infected epithelial cells.
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Ruelas-Ruiz Luis C, Medina-De la Garza Carlos E, Martinez-Castilla Azalia M, Salinas-Carmona Mario C, Rosas-Taraco Adrian G
Аннотация
CONTEXT: Influenza is a viral infection with pandemic potential that affects individuals of all ages. The immune response is key to resolving the disease; however, immune deregulation, such as cytokine storm, can cause tissue damage and death. Diethylcarbamazine (DEC), a drug with immunomodulatory effects, has demonstrated anti-inflammatory and antifibrotic properties. However, DEC's activity in viral respiratory infections remains unknown.
OBJECTIVE: This study aimed to analyze the effect of DEC in a model of respiratory epithelial cells infected with Influenza A (H1N1)pdm09 virus (IAV) to evaluate its action on antiviral immune effectors and viral titer.
MATERIALS AND METHODS: A549 cells were cultured, infected with IAV, and treated with DEC. Viral load was quantified at 24 h and 48 h. Subsequently, Cytokine levels (IL-1β, IL-6, IL-8, IL-10, IL-15, and RANTES) were analyzed from supernatants at both timepoints using a Bio-Plex Pro-Human Proinflammatory Cytokine kit. RNA was obtained from cells, and RT-qPCR was performed to evaluate the expression of genes encoding MYD88, NLRP3, NF-κB, IFN-β, and IFN-λ.
RESULTS AND DISCUSSION: Results showed that IFN-λ1 expression was consistent across all groups (p > .05). IFN-β expression increased at 24 h in DEC-treated infected groups (p < .05) but returned to baseline at 48h (p > .05). IL-8 secretion was significantly higher in the IAV + DEC20 group at 24h compared to the MOCK (p ≤ .05), but no differences were found at 48 h (p > .05). Infected cells treated with the lowest DEC dose showed a lower viral titer compared to IAV-infected (p ≤ .05).
CONCLUSION: DEC maintained IFN-λ1 expression, regulated levels of IFN-β and IL-8, and reduced viral load in IAV-infected epithelial cells.
OBJECTIVE: This study aimed to analyze the effect of DEC in a model of respiratory epithelial cells infected with Influenza A (H1N1)pdm09 virus (IAV) to evaluate its action on antiviral immune effectors and viral titer.
MATERIALS AND METHODS: A549 cells were cultured, infected with IAV, and treated with DEC. Viral load was quantified at 24 h and 48 h. Subsequently, Cytokine levels (IL-1β, IL-6, IL-8, IL-10, IL-15, and RANTES) were analyzed from supernatants at both timepoints using a Bio-Plex Pro-Human Proinflammatory Cytokine kit. RNA was obtained from cells, and RT-qPCR was performed to evaluate the expression of genes encoding MYD88, NLRP3, NF-κB, IFN-β, and IFN-λ.
RESULTS AND DISCUSSION: Results showed that IFN-λ1 expression was consistent across all groups (p > .05). IFN-β expression increased at 24 h in DEC-treated infected groups (p < .05) but returned to baseline at 48h (p > .05). IL-8 secretion was significantly higher in the IAV + DEC20 group at 24h compared to the MOCK (p ≤ .05), but no differences were found at 48 h (p > .05). Infected cells treated with the lowest DEC dose showed a lower viral titer compared to IAV-infected (p ≤ .05).
CONCLUSION: DEC maintained IFN-λ1 expression, regulated levels of IFN-β and IL-8, and reduced viral load in IAV-infected epithelial cells.