Plants have evolved sophisticated immune systems to defend against diverse pathogens, whereas pathogens deploy effectors to manipulate host cellular processes for successful infection. Recent studies have revealed that pathogen effectors can target host RNA processing, particularly pre-mRNA alternative splicing (AS), to reshape transcript isoform profiles and modulate plant immunity. However, the common principles and specific differences among pathogen effector-mediated regulation of host AS and their impacts on plant immunity have not been systematically summarized. In this review, we summarize recent advances in pathogen effector-mediated regulation of plant AS, focusing on three major mechanisms: targeting host splicing factors, altering RNA regulatory elements, and interfering with RNA-processing pathways. We discuss how effector-induced AS reprogramming affects immune-related gene expression and contributes to pathogen virulence. Furthermore, we highlight the emerging potential of AS regulation in disease resistance and disease-resistant crop breeding, and propose future directions for dissecting effector-specific splicing targets and translating AS-based regulatory mechanisms into crop improvement strategies. This review emphasizes host RNA splicing as an important regulatory layer in plant-pathogen interactions and provides new perspectives for understanding pathogen manipulation of plant immunity.

Background/Objectives: This study is the first to investigate the potential mechanism of star anise extract (SAE) in protecting against cold stress-aggravated acute lung injury (CSALI) in rats. Methods: A rat CSALI model was induced via combined lipopolysaccharide challenge and cold stress exposure. The preventive effects of SAE were evaluated using cytotoxicity assays, quantification of biochemical indices and inflammatory factors, and histopathological examination. Ultra-performance liquid chromatography coupled with high-resolution mass spectrometry (UPLC–HRMS)-based serum metabolomics was employed to systematically profile CSALI-associated metabolic alterations and decipher the potential mechanism underlying the preventive effects of SAE. Results: SAE alleviated pathological progression of CSALI, suppressed inflammatory cell migration, markedly reduced pulmonary inflammatory cell infiltration, and ameliorated lung tissue injury in CSALI rats. SAE also improved abnormal liver function indicators and lowered the levels of pro-inflammatory factors in both serum and bronchoalveolar lavage fluid (BALF). Serum metabolomics analysis identified and annotated 24 disease-altered differential metabolites and evaluated the protective effects of SAE on them. These metabolites were significantly enriched in two key metabolic pathways related to the pathogenesis of CSALI, including arachidonic acid metabolism and glycerophospholipid metabolism. Furthermore, based on metabolite changes, phospholipase A2 was hypothesized as a potential key regulatory factor that may cooperate with arachidonic metabolism to suppress the inflammatory cascade. Conclusions: These findings demonstrated that SAE exerted prominent anti-inflammatory activity and effectively protected against lung injury in CSALI rats.