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Background <p>Molting is a critical yet vulnerable stage in insect development, during which the peritrophic matrix is temporarily disrupted. This transient loss of gut barrier integrity can allow gut bacteria to escape into the hemocoel, where they may proliferate in the nutrient-rich hemolymph, leading to developmental impairments or septicemia. Despite this threat, insects typically complete molting successfully, suggesting the involvement of robust immune mechanisms that control hemolymph bacterial load.</p> Results <p>This study identifies the <i>Spätzle</i> gene cluster (<i>HaSpz3–6</i>) in the cotton bollworm (<i>Helicoverpa armigera</i>) as essential for limiting hemolymph bacterial proliferation during molting. Knockdown of <i>HaSpz3–6</i> suppresses antimicrobial peptide expression, leading to <i>Bacillus</i> spp. overgrowth and delayed molting. The ensuing bacterial proliferation triggers tryptophan catabolism, elevating serotonin and N-acetylserotonin (NAS) levels. Serotonin enhances phagocytosis, which cooperates with reactive oxygen species (ROS) to reduce bacterial burden. NAS subsequently mitigates oxidative stress by scavenging excess ROS.</p> Conclusions <p>These findings reveal that <i>Spätzle</i>-mediated immunity is crucial for bacterial regulation during molting. When this pathway is impaired, tryptophan catabolism provides a compensatory defense, albeit with developmental trade-offs. Overall, this study underscores the plasticity of insect immune responses and highlights the critical role of <i>Spätzle</i> in safeguarding developmental transitions.</p>

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Tryptophan catabolism reprograms immunity to prevent hemolymph bacterial dysbiosis and support molting in Spätzle-deficient Helicoverpa armigera larvae

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月17日

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  • Pei Xiong,
  • Ling-Ling Luo,
  • Bing-Yan Kang,
  • Jing-Jing Yao,
  • Xu-Sheng Liu,
  • Jia-Lin Wang

摘要

Background

Molting is a critical yet vulnerable stage in insect development, during which the peritrophic matrix is temporarily disrupted. This transient loss of gut barrier integrity can allow gut bacteria to escape into the hemocoel, where they may proliferate in the nutrient-rich hemolymph, leading to developmental impairments or septicemia. Despite this threat, insects typically complete molting successfully, suggesting the involvement of robust immune mechanisms that control hemolymph bacterial load.

Results

This study identifies the Spätzle gene cluster (HaSpz3–6) in the cotton bollworm (Helicoverpa armigera) as essential for limiting hemolymph bacterial proliferation during molting. Knockdown of HaSpz3–6 suppresses antimicrobial peptide expression, leading to Bacillus spp. overgrowth and delayed molting. The ensuing bacterial proliferation triggers tryptophan catabolism, elevating serotonin and N-acetylserotonin (NAS) levels. Serotonin enhances phagocytosis, which cooperates with reactive oxygen species (ROS) to reduce bacterial burden. NAS subsequently mitigates oxidative stress by scavenging excess ROS.

Conclusions

These findings reveal that Spätzle-mediated immunity is crucial for bacterial regulation during molting. When this pathway is impaired, tryptophan catabolism provides a compensatory defense, albeit with developmental trade-offs. Overall, this study underscores the plasticity of insect immune responses and highlights the critical role of Spätzle in safeguarding developmental transitions.