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<p>Porcine reproductive and respiratory syndrome virus (PRRSV) modulates host immune responses, including apoptotic pathways, during infection. This study examined the role of TNF-α and IL-10 in regulating apoptosis during PRRSV-1 infection of bone marrow-derived dendritic cells (BMDCs), using four isolates with distinct cytokine profiles: 3262 (TNF-α<sup>+</sup>/IL-10<sup>+</sup>), 3249 (TNF-α<sup>+</sup>/IL-10<sup>-</sup>), 2988 (TNF-α<sup>-</sup>/IL-10<sup>+</sup>), and 3267 (TNF-α<sup>-</sup>/IL-10<sup>-</sup>). Early after infection (≤ 24 hpi), infected cells were predominantly non-apoptotic; by 48 hpi, apoptotic bystander cells increased markedly, consistent with a bystander apoptotic process. Neutralizing TNF-α in TNF-α-inducing isolates (3262, 3249) increased the proportion of infected cells and reduced bystander apoptosis, suggesting an antiviral role for TNF-α at the cellular level. In contrast, IL-10 blockade in IL-10-inducing isolates (3262, 2988) increased non-apoptotic infected cells without altering overall infection frequency, suggesting IL-10 modulates apoptotic progression in infected cells. Collectively, these data indicate that TNF-α and IL-10 differentially modulate apoptotic outcomes during PRRSV-1 infection in an isolate-dependent manner.</p>

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TNF-α and IL-10 differentially modulate apoptosis during PRRSV-1 infection of bone marrow-derived dendritic cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月1日

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  • Yanli Li,
  • Enric Mateu

摘要

Porcine reproductive and respiratory syndrome virus (PRRSV) modulates host immune responses, including apoptotic pathways, during infection. This study examined the role of TNF-α and IL-10 in regulating apoptosis during PRRSV-1 infection of bone marrow-derived dendritic cells (BMDCs), using four isolates with distinct cytokine profiles: 3262 (TNF-α+/IL-10+), 3249 (TNF-α+/IL-10-), 2988 (TNF-α-/IL-10+), and 3267 (TNF-α-/IL-10-). Early after infection (≤ 24 hpi), infected cells were predominantly non-apoptotic; by 48 hpi, apoptotic bystander cells increased markedly, consistent with a bystander apoptotic process. Neutralizing TNF-α in TNF-α-inducing isolates (3262, 3249) increased the proportion of infected cells and reduced bystander apoptosis, suggesting an antiviral role for TNF-α at the cellular level. In contrast, IL-10 blockade in IL-10-inducing isolates (3262, 2988) increased non-apoptotic infected cells without altering overall infection frequency, suggesting IL-10 modulates apoptotic progression in infected cells. Collectively, these data indicate that TNF-α and IL-10 differentially modulate apoptotic outcomes during PRRSV-1 infection in an isolate-dependent manner.