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Paralytic peptide activates insect humoral immune response via epidermal growth factor receptor
Liang Song1, Fei Wang1, Shifeng Dong1
1State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, China.
Abstract:
Paralytic peptide (PP) activates innate immunity of silkworm Bombyx mori, inducing production of anti-microbial peptides (AMPs) and phagocytosis-related proteins; however the signal pathways of PP-dependent immune responses are not clear. In present study, we characterized BmE cells as a PP-responsive cell line by examining the expression of AMP genes and activation of p38 mitogen-activated protein kinase (p38 MAPK) under PP stimulation, and we also found PP directly binds to BmE cell membrane. Then we found that PP-dependent expression of AMP genes is suppressed by tyrosine kinase inhibitor (genistein) both in BmE cells and in fat body of silkworm larvae. Moreover, the specific tyrosine kinase epidermal growth factor receptor (EGFR) inhibitor (AG1478) attenuates PP-induced expression of AMP genes in BmE cells and fat body of silkworm and RNA interference (RNAi) to BmEGFR also suppresses PP-induced expression of AMP genes. Furthermore, the PP-induced p38 MAPK phosphorylation is inhibited by AG1478. Our results suggest that BmE cells can be used as a cell model to investigate the signal pathway of PP-dependent humoral immune response and receptor tyrosine kinase EGFR/p38 MAPK pathway is involved in the production of AMPs induced by PP.
Insights
Paralytic peptide (PP) activates silkworm immunity by inducing antimicrobial peptides (AMPs). The epidermal growth factor receptor (EGFR)/p38 MAPK pathway is crucial for this PP-induced immune response.
Area of Science:
- Immunology
- Molecular Biology
- Entomology
Background:
- Silkworm immunity involves antimicrobial peptides (AMPs) and phagocytosis.
- The signaling pathways for paralytic peptide (PP)-induced immune responses remain unclear.
Purpose of the Study:
- To characterize silkworm BmE cells as a model for studying PP-induced immune responses.
- To elucidate the signaling pathway involved in PP-mediated activation of innate immunity.
Main Methods:
- Stimulation of BmE cells and silkworm fat body with PP.
- Inhibition of tyrosine kinases and epidermal growth factor receptor (EGFR) using specific inhibitors (genistein, AG1478).
- Gene expression analysis of AMPs and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) via RNA interference (RNAi).
Main Results:
- BmE cells were confirmed as PP-responsive, showing increased AMP gene expression and p38 MAPK activation.
- PP was found to bind directly to the BmE cell membrane.
- Inhibition of tyrosine kinases and specifically EGFR significantly suppressed PP-induced AMP gene expression.
- EGFR inhibition also reduced PP-induced p38 MAPK phosphorylation.
- RNA interference targeting BmEGFR confirmed its role in the PP-induced immune response.
Conclusions:
- BmE cells serve as a valuable model for investigating PP-dependent humoral immunity.
- The receptor tyrosine kinase EGFR/p38 MAPK pathway is essential for PP-induced production of antimicrobial peptides in silkworms.
