Plants have evolved complex phytochemical and immune defense mechanisms in response to pathogen invasion. Plants deploy phytochemical defense system—signaling molecules, secondary metabolites, antimicrobial proteins and peptides—to mitigate the pathogens they encounter. Pathogens have developed strategies—effector proteins, efflux pumps and detoxification mechanisms—to manipulate or overcome plant defenses. This review offers insights into how these bioactive compounds are biosynthesized and activated following pathogen recognition. We provide an overview of the dynamic crosstalk between PTI and ETI and their role in optimizing plant defense. Additionally, we discuss the potential of advanced genetic engineering approaches, nanocarrier-mediated elicitor delivery, and microbiome engineering to enhance these natural defenses. Finally, we address the technical bottlenecks of engineering plant immunity and provide a roadmap for future research directions. This review provides a stronger mechanistic foundation for breeding crops with durable, broad-spectrum resilience for sustainable crop protection.
Fish exhibit a high degree of susceptibility to shifts in thermal conditions within the water. The liver is central to metabolic homeostasis and immune defense, and its physiological stability is critical for fish health. The present study evaluated the hepatic physiological responses of Trachinotus ovatus following a 7-day exposure to high-temperature (HT) stress, including alterations in histology, oxidative stress, iron homeostasis, inflammation, immunity, apoptosis, and bile acid (BA) metabolism. HT stress induced alterations in liver histology and disrupted redox homeostasis, accompanied by enhanced Nrf2-mediated antioxidant signaling and changes in antioxidant defense enzyme activities and peroxide levels. Iron homeostasis and lipid peroxide defense exhibited complex alterations, including Fe levels and NCOA4 expression were increased, accompanied by compensatory upregulation of iron-homeostasis genes (FTH1, FPN1, and NFS1) and antioxidant defense genes (GPx4, SLC7A11, and p53). However, reduced lipid peroxidation products (LPO and MDA) suggested that these changes reflected regulatory adaptation rather than the execution of ferroptosis. HT stress induced hepatic inflammatory and immune responses, characterized by activation of pro-inflammatory signaling, dysregulated anti-inflammatory regulation, downregulation of IL-8 expression, and downregulation of the immunoglobulin genes IgM and IgT. Apoptosis-related genes showed divergent expression patterns, with CHOP, Casp-9, and Casp-3 being upregulated, whereas CytC was downregulated. Furthermore, BA metabolism was affected, as shown by reductions in total BA pool size and free BA levels, along with the upregulated expression of BA metabolism-related genes (FXR, SULT1, and UGT8). Three metabolites, cholic acid, chenodeoxycholic acid, and 7-ketolithocholic acid were identified as potential biomarkers. Collectively, these findings suggest that HT stress impaired hepatic physiological homeostasis in T. ovatus, accompanied by tissue architecture disruption, redox imbalance, inflammatory responses, immune suppression, BA metabolic remodeling, and coordinated changes in iron homeostasis and apoptosis-related regulatory pathways.
Plants encounter various abiotic stress during their growth, making it essential to understand their responses to such challenges. Though function of OsHMA3 in cadmium (Cd) sequestration into rice root vacuoles has been well characterized, little is known about how different OsHMA3 alleles influence plant responses to high Cd exposure. In this study, we utilized rice cultivars carrying a functional OsHMA3 allele (9311) and a loss-of-function OsHMA3 allele (W4) to investigate their differences in Cd detoxification responses. Morphological, physiological and subcellular changes, as well as Cd species were analyzed. The results indicated that Cd was more extensively transported to shoots in W4 than 9311 as expected. However, W4 exhibited a more pronounced growth inhibition with reductions in shoot and root length, more severe leaf chlorosis with chlorophyll a, b, and carotenoid levels decreased by 31
T-2 toxin is a trichothecene mycotoxin produced by Fusarium species and can cause disease after contaminated food or feed ingestion. This study aimed to investigate the impact of lycopene (Ly) on systemic inflammation, oxidative stress, and dysbiosis in mice exposed to T-2 toxin. A total of 20 male BALB/c mice (6 weeks old, weighing 23.5 ± 0.32 g) randomly divided into four groups (n = 5): Control (Cont), Ly, T-2, and T-2 + Ly groups. Findings revealed that Ly enhanced the body weight, feedd, and water intake that have been reduced by T-2. Ly increased the villus height (VH) and VH: crypt depth (CD) and decreased CD and villus width (VW) in ileum compared to the T-2 group. In alpha diversity, Staphylococcus and Corynebacterium were the most prevalent in Cont group; Staphylococcus, and Lactobacillus, were the most prevalent in T-2 group; Candidatus-Arthromitus and Staphylococcus were the most prevalent in T-2 + Ly group. Moreover, T-2 mice had significantly (p < 0.05) greater levels of interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), Interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α) than Cont, while the Ly significantly (p < 0.05) lowered their concentration. The T-2 mice had significantly (p < 0.05) higher levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while their catalase (CAT),, glutathione (GSH), adenosine triphosphate (ATP), and superoxide dismutase 1(SOD1) activities were significantly (p < 0.05) lower than Cont. Ly significantly (p < 0.05) restored their concentration. Moreover, there was a significant reduction (p < 0.05) of hexanoic, butyric, acetic, pentanoic, and Heptanoic acids in the T-2 mice compared to Cont. In contrast, treatment with Ly was found to significantly restore their levels compared to T-2 group. We conclude that Ly administration in the context of T-2–induced toxicity may help attenuate systemic oxidative stress and inflammation, possibly through modulation of gut microbiota and fecal short-chain fatty acids (SCFAs).
