FoxO-promoted peroxiredoxin1 expression induced by Helicoverpa armigera single nucleopolyhedrovirus infection mediates host development and defensive responses

Tian, Zhiqiang; Zha, Meng; Cai, Limei; Michaud, J. P.; Cheng, Jie; Shen, Zhizhang; Liu, Xiaoming; Liu, Xiaoxia

doi:10.1016/j.ecoenv.2022.113414

Cited by 2 publications

(3 citation statements)

References 47 publications

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“…Similarly, larvae become more susceptible to HearNPV after knockdown of the HaTpx gene that protects against oxidative damage. 24,44 The microbial community of the gut may serve as a back-up defensive system in case of infection with ROS-resistant microbes. 45,46 When infected larvae were subjected to RNAi treatment with dsDuox, expression of the Duox gene was halved, and so was the midgut content of H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

“…Injection of infected larvae with H 2 O 2 diminished microbial abundance in the gut, promoted HearNPV infection, and accelerated larval death, mimicking the action of ROS generated via HearNPV‐induced expression of the Duox gene. Similarly, larvae become more susceptible to HearNPV after knockdown of the HaTpx gene that protects against oxidative damage 24,44 . The microbial community of the gut may serve as a back‐up defensive system in case of infection with ROS‐resistant microbes 45,46 .…”

Section: Discussionmentioning

confidence: 99%

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The gut microbiome of Helicoverpa armigera enhances immune response to baculovirus infection via suppression of Duox‐mediated reactive oxygen species

Tian

Guo

Michaud

et al. 2023

Pest Management Science

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BACKGROUNDBaculoviruses such as Helicoverpa armigera nucleopolyhedrovirus (HearNPV) infect their lepidopteran hosts via the larval midgut where they interact with host immune responses and gut microbiota. Here we demonstrate that gut microbiota proliferating in response to HearNPV infection promote larval immune responses which impede the infection process.RESULTSThe microbial load of the larval midgut increased following HearNPV infection, due primarily to increases in Enterococcus spp., whereas most other bacterial genera declined, with Firmicutes replacing Proteobacteria as the dominant phylum. Injection of abdominal prolegs of infected larvae with H2O2 promoted viral infection, diminished microbial abundance, and accelerated larval death, mimicking the effects of HearNPV infection, which up‐regulated dual oxidase (Duox) expression, increasing H2O2 levels in the midgut. Knockdown of Duox with RNAi reduced H2O2 production in the guts of infected larvae, increased bacterial loads, decreased viral replication, and improved larval survival. Germ‐free larvae were more susceptible to HearNPV than control larvae, exhibiting greater expression of Duox, higher levels of H2O2, and lower survival. Replenishment of gut bacteria in germ‐free larvae restored the base‐line immunity to HearNPV observed in normal larvae. Enterococcus spp., Levilactobacillus brevis, and Lactobacillus sp. bacteria were isolated and implicated in immunity restoration via replenishment in germ‐free larvae.CONCLUSIONThese findings illuminate how gut microbiota play important roles in larval defense against oral baculovirus infection, and suggest novel avenues of investigation to enhance the efficacy of baculoviruses and improve control of lepidopteran pests. © 2023 Society of Chemical Industry.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The gut microbiome of Helicoverpa armigera enhances immune response to baculovirus infection via suppression of Duox‐mediated reactive oxygen species

Tian

Guo

Michaud

et al. 2023

Pest Management Science

Self Cite

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“…Furthermore, our study did not address the cause of Prx1 increase by STZ treatment. It is known that many transcription factors are involved in the induction of Prx1, and it is very important to study the mechanism of Prx1 expression by STZ treatment in the hippocampus cell line 101 – 103 . The stability of Prx1 is also one of the factors to consider.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 1 inhibits streptozotocin-induced Alzheimer’s disease-like pathology in hippocampal neuronal cells via the blocking of Ca2+/Calpain/Cdk5-mediated mitochondrial fragmentation

Park,

Won,

Yang

et al. 2024

Sci Rep

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Oxidative stress plays an essential role in the progression of Alzheimer’s disease (AD), the most common age-related neurodegenerative disorder. Streptozotocin (STZ)-induced abnormal brain insulin signaling and oxidative stress play crucial roles in the progression of Alzheimer’s disease (AD)-like pathology. Peroxiredoxins (Prxs) are associated with protection from neuronal death induced by oxidative stress. However, the molecular mechanisms underlying Prxs on STZ-induced progression of AD in the hippocampal neurons are not yet fully understood. Here, we evaluated whether Peroxiredoxin 1 (Prx1) affects STZ-induced AD-like pathology and cellular toxicity. Prx1 expression was increased by STZ treatment in the hippocampus cell line, HT-22 cells. We evaluated whether Prx1 affects STZ-induced HT-22 cells using overexpression. Prx1 successfully protected the forms of STZ-induced AD-like pathology, such as neuronal apoptosis, synaptic loss, and tau phosphorylation. Moreover, Prx1 suppressed the STZ-induced increase of mitochondrial dysfunction and fragmentation by down-regulating Drp1 phosphorylation and mitochondrial location. Prx1 plays a role in an upstream signal pathway of Drp1 phosphorylation, cyclin-dependent kinase 5 (Cdk5) by inhibiting the STZ-induced conversion of p35 to p25. We found that STZ-induced of intracellular Ca2+ accumulation was an important modulator of AD-like pathology progression by regulating Ca2+-mediated Calpain activation, and Prx1 down-regulated STZ-induced intracellular Ca2+ accumulation and Ca2+-mediated Calpain activation. Finally, we identified that Prx1 antioxidant capacity affected Ca2+/Calpain/Cdk5-mediated AD-like pathology progress. Therefore, these findings demonstrated that Prx1 is a key factor in STZ-induced hippocampal neuronal death through inhibition of Ca2+/Calpain/Cdk5-mediated mitochondrial dysfunction by protecting against oxidative stress.

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FoxO-promoted peroxiredoxin1 expression induced by Helicoverpa armigera single nucleopolyhedrovirus infection mediates host development and defensive responses

Cited by 2 publications

References 47 publications

The gut microbiome of Helicoverpa armigera enhances immune response to baculovirus infection via suppression of Duox‐mediated reactive oxygen species

The gut microbiome of Helicoverpa armigera enhances immune response to baculovirus infection via suppression of Duox‐mediated reactive oxygen species

Peroxiredoxin 1 inhibits streptozotocin-induced Alzheimer’s disease-like pathology in hippocampal neuronal cells via the blocking of Ca2+/Calpain/Cdk5-mediated mitochondrial fragmentation

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