Gut microbial community research has garnered considerable attention due to its pivotal role in shaping diverse insect hosts’ life-history traits, with key studies confirming that insect gut microbiota is vital for core physiological processes including growth, nutrient metabolism, nitrogen fixation, pheromone biosynthesis, and environmental adaptation. Findings highlight that integrating insect ecology understanding with gut microbial community characterization is indispensable for innovative pest management strategies. Notably, S. frugiperda, a globally destructive agricultural pest causing substantial annual economic losses, has been extensively investigated. Its host range is extremely wide, from staple food crops such as corn and rice to various cash crops. This review systematically synthesizes the prevalent diversity of its gut’s dominant microbes, clarifies the important mechanism of gut microbiota in host stress adaptation (providing direct evidence for explaining the pest’s stress resistance formation), draws the key conclusion that host–microbe interaction mechanisms can serve as key pest management targets to guide more targeted control technologies. We also discuss current limitations such as inadequate microbial function verification and unclear host–microbe molecular mechanisms while outlining future directions including focusing on microbial community dynamic changes under multiple environmental stresses and functional microbe screening and application.

Chironomids are abundant aquatic macroinvertebrates with known pollutant tolerance, but the molecular effects of chlorantraniliprole (CAP) remain unclear. In this study, we exposed Propsilocerus akamusi larvae to LC₁₀ and LC₅₀ of CAP, sampled at 48 h and 144 h, and integrated biochemical assays, metabolomics, and transcriptomics to profile stress responses. Our results showed that CAP elevated antioxidant enzymes and protein carbonyls, indicating severe oxidation, especially at LC₅₀. At 48 h, LC₁₀ activated JNK-mediated antioxidative and drug metabolism pathways, whereas LC₅₀ altered glycolysis, cofactor biosynthesis, and fatty acid metabolism. At 144 h, LC₁₀ enriched proteasome and oxidative phosphorylation pathways; chaperones PaHsp70 and PaHsp90 were upregulated by 4.14- and 2.08-fold, respectively, and were negatively correlated with lipid and carbohydrate metabolites, indicating a metabolic shift toward protein repair. In contrast, LC₅₀ CAP triggered protein processing in the endoplasmic reticulum (ER) and TCA cycle dysregulation, with upregulation of PaCalreticulin linked to energy crisis markers, reflecting severe energy collapse. After knockdown of PaHsp70, the survival rates of chironomid larvae exposed to LC₁₀ and LC₅₀ CAP significantly decreased from 80.8% to 65.8% and from 43.3% to 28.3%, respectively. Collectively, our results revealed that low CAP concentrations triggered early detoxification followed by proteasome- and Hsp-mediated strategies to sustain protein homeostasis whereas high concentrations directly disrupted core metabolism and ultimately caused energy collapse and lethal ER stress in chironomid larvae. These findings provide mechanistic insights into the chronic effects of CAP on aquatic insects.