Determinants of difficult laryngoscopy based on upper airway indicators: a prospective observational study.

BACKGROUND: The main cause of anesthesia-related deaths is the failure to manage difficult airways. Difficult laryngoscopic exposure is a major cause of unsuccessful management of difficult airways. Inadequate preoperative airway assessment hinders the clinical management of difficult airways cases, emphasizing the critical need for accurate identification of difficult airways. Currently, no definitive and reliable indicators are available to predict a difficult airway. Our study aims to predict laryngoscope exposure risk factors by combining ultrasonically measured upper airway anatomic parameters with physical examination indicators. METHODS: Patients aged 18 to 75 years, classified as American Standards Association (ASA) I-III, and scheduled for elective general anesthesia with endotracheal intubation were included. All patients received the upper airway and ultrasonographic measurements. After anesthesia induction, laryngoscope exposure was analyzed using the Cormack-Lehane grading system, with Grades III and IV as indicative of difficult laryngoscopy. Univariate and multivariate logistic regression analyses were performed to identify reliable indicators for predicting difficult laryngoscopy. Receiver Operating Characteristic (ROC) curve analysis was utilized to assess the predictive performance of each indicator. RESULTS: A total of 1120 patients finished the study, with 710 cases found in Grade I laryngoscopic exposure group, 360 cases in Grade II group, and 50 cases in Grade III group. There was no case observed in Grade IV group, thereby resulting in an incidence of difficult laryngoscopy of 4.46%. Univariate logistic regression analysis revealed that several parameters including age, Body Mass Index (BMI), neck circumference, neck mobility, snoring intensity, as well as ultrasound measurements of the pre-epiglottic space and thyromental distance were identified as significant risk factors for difficult laryngoscopy (P < 0.05). Among these, BMI, and neck circumference exhibited notable predictive value, with Area Under The Curve (AUC) values of 0.746 (95%CI 0.649-0.842) and 0.732 (95%CI 0.638-0.827), respectively. Neck mobility was also identified as an independent risk factor for predicting difficult laryngoscopy (P = 0.009) in multivariate logistic regression analysis, with an AUC of 0.672 (0.562-0.782) in the ROC curve. CONCLUSIONS: Our findings revealed a direct correlation between difficult laryngoscopy and age, BMI, neck circumference, neck mobility, snoring intensity, as well as ultrasound measurements of the pre-epiglottic space and thyromental distance. Furthermore, neck mobility was identified as an independent predictive factor. TRIAL REGISTRATION: The trial was registered prior to patient enrollment at clinicaltrials.gov (register no. ChiCTR2100053826, Date of registration: November 30, 2021).

Histone deacetylase OsHDA706 orchestrates rice broad-spectrum antiviral immunity and is impeded by a viral effector.

Lysine acetylation is a dynamic post-translational modification of proteins. Extensive studies have revealed that the acetylation modulated by histone acetyltransferases and histone deacetylases (HDACs) plays a crucial role in regulating protein function. However, there has been limited focus on how HDACs regulate jasmonic acid (JA) biosynthesis in plants. Here, we uncover that the protein stability of OsLOX14, a critical enzyme involved in JA biosynthesis, is regulated by a histone deacetylase, OsHDA706, and is hindered by a viral protein. Our results show that OsHDA706 deacetylates OsLOX14 and enhances the stability of OsLOX14, leading to JA accumulation and an improved broad-spectrum rice antiviral defense. Furthermore, we found that the viral protein P2, encoded by the destructive rice stripe virus, disrupts the association of OsHDA706-OsLOX14, promoting viral infection. Overall, our findings reveal how HDAC manipulates the interplay of deacetylation and protein stability of a JA biosynthetic enzyme to enhance plant antiviral responses.

Two different viral proteins suppress NUCLEAR FACTOR-YC-mediated antiviral immunity during infection in rice.

Plant viruses have multiple strategies to counter and evade the host's antiviral immune response. However, limited research has been conducted on the antiviral defense mechanisms commonly targeted by distinct types of plant viruses. In this study, we discovered that NUCLEAR FACTOR-YC (NF-YC) and NUCLEAR FACTOR-YA (NF-YA), 2 essential components of the NF-Y complex, were commonly targeted by viral proteins encoded by 2 different rice (Oryza sativa L.) viruses, rice stripe virus (RSV, Tenuivirus) and southern rice black streaked dwarf virus (SRBSDV, Fijivirus). In vitro and in vivo experiments showed that OsNF-YCs associate with OsNF-YAs and inhibit their transcriptional activation activity, resulting in the suppression of OsNF-YA-mediated plant susceptibility to rice viruses. Different viral proteins RSV P2 and SRBSDV SP8 directly disrupted the association of OsNF-YCs with OsNF-YAs, thereby suppressing the antiviral defense mediated by OsNF-YCs. These findings suggest an approach for conferring broad-spectrum disease resistance in rice and reveal a common mechanism employed by viral proteins to evade the host's antiviral defense by hindering the antiviral capabilities of OsNF-YCs.

Hippocampal estrogens rescued the decline of synaptic plasticity after surgery and anesthesia by inhibiting microglia overactivation.

BACKGROUND: Elderly patients experience postoperative cognitive impairment frequently; therefore, effective interventions are urgently needed. Central nervous inflammation characterized by microglia may promote the progression of POCD by reducing synaptic plasticity. Notably, clinical studies revealed that the incidence of female patients was significantly lower than that of male patients. Besides, the brain estrogens have an anti-inflammatory effect and regulate the microglia at the same times. This study aimed to determine whether suppressing microglia overactivation by hippocampal estrogens can rescue the decrease of synaptic plasticity after surgery and anesthesia. METHODS: Exploratory laparotomy was used to establish the POCD model in 15-month-old male or female C57BL/6 J mice and animal behavioral tests were performed to test hippocampal-dependent memory capacity. Western blot and immunofluorescence were used to detect the microglial activation and plasticity related protein expressions. Elisa was used to detect the content of estrogens in the hippocampus. Estrogens and estrogen receptor inhibitor were used to replenish the estrogens in the brain and inhibit the effect of estrogens. RESULTS: Surgery and anesthesia did not cause POCD in female mice (P > 0.05), while the cognitive function decreased significantly after estrogen receptor inhibitor was given(P < 0.05). Male mice experienced cognitive dysfunction after surgery and anesthesia, and their cognitive function improved after estrogens supplementation (P < 0.05). Given estrogens and estrogen receptor inhibitors at the same time, the cognitive function of male mice could not be saved (P < 0.05). By correlation analysis, there was a negative correlation between the content of hippocampal estrogens and microglia (P < 0.05). The number or degree of activation of microglia affected the synaptic plasticity, which ultimately regulated the cognitive function of mice. CONCLUSION: Hippocampal estrogens rescued the decline of synaptic plasticity after surgery and anesthesia by inhibiting microglia overactivation.

Disinhibition of hippocampal parvalbumin interneurons on pyramidal neurons participates in LPS-induced cognitive dysfunction.

BACKGROUND: The vulnerability of hippocampal pyramidal (PY) neurons played a key role in the onset of cognitive impairment. Multiple researches revealed that neuroinflammation together with microglia activation and parvalbumin (PV) interneurons participated in the pathogenesis of cognitive dysfunction. However, the underlying mechanism was still unclear. This study aimed to determine whether microglia activation would induce PV interneurons impairment and PY neurons disinhibition, and as a result, promote cognitive dysfunction after lipopolysaccharide (LPS) challenge. METHODS: Male C57BL/6J mice were injected with LPS to establish systemic inflammation model, and animal behavioral tests were performed. For chemogenetics, the virus was injected bilaterally into the CA1 region. Clozapine N-Oxide (CNO) was used to activate the PV interneurons. Whole-cell patch clamp recording was applied to detect spontaneous inhibitory post synaptic current (sIPSC) and spontaneous excitatory post synaptic current (sEPSC) of PY neurons in the CA1 region. RESULTS: LPS induced hippocampal dependent memory impairment, which was accompanied with microglia activation. Meanwhile, PV protein level in hippocampus were decreased, and IPSCs of PY neurons in the CA1 were also suppressed. Minocycline reversed all the above changes. In addition, rescuing PV function with CNO improved memory impairment, sIPSCs of PY neurons and perisomatic PV boutons around PY neurons without affecting microglia activation. CONCLUSION: Disinhibition of hippocampal parvalbumin interneurons on pyramidal neurons participates in LPS-induced cognitive dysfunction.

Lactate Improves Long-term Cognitive Impairment Induced By Repeated Neonatal Sevoflurane Exposures Through SIRT1-mediated Regulation of Adult Hippocampal Neurogenesis and Synaptic Plasticity in Male Mice.

Repeated neonatal exposures to sevoflurane induce long-term cognitive impairment that has been reported to have sex-dependent differences. Exercise promotes learning and memory by releasing lactate from the muscle. The study tested the hypothesis that lactate may improve long-term cognitive impairment induced by repeated neonatal exposures to sevoflurane through SIRT1-mediated regulation of adult hippocampal neurogenesis and synaptic plasticity. C57BL/6 mice of both genders were exposed to 3% sevoflurane for 2 h daily from postnatal day 6 (P6) to P8. In the intervention experiments, mice received lactate at 1 g/kg intraperitoneally once daily from P21 to P41. Behavioral tests including open field (OF), object location (OL), novel object recognition (NOR), and fear conditioning (FC) tests were performed to assess cognitive function. The number of 5-Bromo-2'- deoxyuridine positive (BrdU+) cells and BrdU+/DCX+ (doublecortin) co-labeled cells, expressions of brain-derived neurotrophic factor (BDNF), activity-regulated cytoskeletal-associated protein (Arc), early growth response 1 (Egr-1), SIRT1, PGC-1α and FNDC5, and long-term potentiation (LTP) were evaluated in the hippocampus. Repeated exposures to sevoflurane induced deficits in OL, NOR and contextual FC tests in male but not female mice. Similarly, adult hippocampal neurogenesis, synaptic plasticity-related proteins and hippocampal LTP were impaired after repeated exposures to sevoflurane in male but not female mice, which could rescue by lactate treatment. Our study suggests that repeated neonatal exposures to sevoflurane inhibit adult hippocampal neurogenesis and induce defects of synaptic plasticity in male but not female mice, which may contribute to long-term cognitive impairment. Lactate treatment rescues these abnormalities through activation of SIRT1.

Different viral effectors suppress hormone-mediated antiviral immunity of rice coordinated by OsNPR1.

Salicylic acid (SA) and jasmonic acid (JA) are plant hormones that typically act antagonistically in dicotyledonous plants and SA and JA signaling is often manipulated by pathogens. However, in monocotyledonous plants, the detailed SA-JA interplay in response to pathogen invasion remains elusive. Here, we show that different types of viral pathogen can disrupt synergistic antiviral immunity mediated by SA and JA via OsNPR1 in the monocot rice. The P2 protein of rice stripe virus, a negative-stranded RNA virus in the genus Tenuivirus, promotes OsNPR1 degradation by enhancing the association of OsNPR1 and OsCUL3a. OsNPR1 activates JA signaling by disrupting the OsJAZ-OsMYC complex and boosting the transcriptional activation activity of OsMYC2 to cooperatively modulate rice antiviral immunity. Unrelated viral proteins from different rice viruses also interfere with the OsNPR1-mediated SA-JA interplay to facilitate viral pathogenicity, suggesting that this may be a more general strategy in monocot plants. Overall, our findings highlight that distinct viral proteins convergently obstruct JA-SA crosstalk to facilitate viral infection in monocot rice.

Microglia participate in postoperative cognitive dysfunction by mediating the loss of inhibitory synapse through the complement pathway.

BACKGROUND: Elderly patients after surgery are prone to cognitive decline known as postoperative cognitive dysfunction (POCD). Several studies have shown that the microglial activation and the increase of complement protein expression in hippocampus induced by surgery may be related to the pathogenesis of POCD. The purpose of this study was to determine whether microglia and complement system were involved in cognitive dysfunction in aged mice. METHODS: The POCD model was established by exploratory laparotomy in 15-month-old male C57BL/6J mice and animal behavioral tests were performed to test hippocampal-dependent memory capacity. Minocycline was used to suppress the activation of microglia, and complement 3 receptor inhibitor was used to suppress the association between microglia and complement 3. Western blot and immunofluorescence were used to detect the microglial activation, complement protein, and synaptic protein expressions. RESULTS: Operation induced hippocampal-dependent memory impairment (P < 0.01), which was accompanied by microglial activation (P < 0.01). There was also a significant reduction in inhibitory synaptic protein expression in the hippocampus of mice in the surgery group (P < 0.01). However, minocycline, a microglia inhibitor, rescued all the above changes. In addition, C3RI intervention inhibited the phagocytosis of inhibitory synapses by microglia (P < 0.05) and improved the cognitive function of mice (P < 0.01). CONCLUSION: Microglia participate in postoperative cognitive dysfunction by mediating inhibitory synaptic loss through the complement pathway.

Insights Into the Effect of Rice Stripe Virus P2 on Rice Defense by Comparative Proteomic Analysis.

Rice stripe virus (RSV) has a serious effect on rice production. Our previous research had shown that RSV P2 plays important roles in RSV infection, so in order to further understand the effect of P2 on rice, we used Tandem Mass Tag (TMT) quantitative proteomics experimental system to analyze the changes of protein in transgenic rice expressing P2 for the first time. The results of proteomics showed that a total of 4,767 proteins were identified, including 198 up-regulated proteins and 120 down-regulated proteins. Functional classification results showed that differentially expressed proteins (DEPs) were mainly localized in chloroplasts and mainly involved in the metabolic pathways. Functional enrichment results showed that DEPs are mainly involved in RNA processing and splicing. We also verified the expression of several DEPs at the mRNA level and the interaction of a transcription factor (B7EPB8) with RSV P2. This research is the first time to use proteomics technology to explore the mechanism of RSV infection in rice with the RSV P2 as breakthrough point. Our findings provide valuable information for the study of RSV P2 and RSV infection mechanism.

NF-YA transcription factors suppress jasmonic acid-mediated antiviral defense and facilitate viral infection in rice.

NF-Y transcription factors are known to play many diverse roles in the development and physiological responses of plants but little is known about their role in plant defense. Here, we demonstrate the negative roles of rice NF-YA family genes in antiviral defense against two different plant viruses, Rice stripe virus (RSV, Tenuivirus) and Southern rice black-streaked dwarf virus (SRBSDV, Fijivirus). RSV and SRBSDV both induced the expression of OsNF-YA family genes. Overexpression of OsNF-YAs enhanced rice susceptibility to virus infection, while OsNF-YAs RNAi mutants were more resistant. Transcriptome sequencing showed that the expression of jasmonic acid (JA)-related genes was significantly decreased in plants overexpressing OsNF-YA when they were infected by viruses. qRT-PCR and JA sensitivity assays confirmed that OsNF-YAs play negative roles in regulating the JA pathway. Further experiments showed that OsNF-YAs physically interact with JA signaling transcription factors OsMYC2/3 and interfere with JA signaling by dissociating the OsMYC2/3-OsMED25 complex, which inhibits the transcriptional activation activity of OsMYC2/3. Together, our results reveal that OsNF-YAs broadly inhibit plant antiviral defense by repressing JA signaling pathways, and provide new insight into how OsNF-YAs are directly associated with the JA pathway.

Genome-Wide Identification and Gene Expression Analysis of the OTU DUB Family in Oryza sativa.

Ovarian tumor domain (OTU)-containing deubiquitinating enzymes (DUBs) are an essential DUB to maintain protein stability in plants and play important roles in plant growth development and stress response. However, there is little genome-wide identification and analysis of the OTU gene family in rice. In this study, we identified 20 genes of the OTU family in rice genome, which were classified into four groups based on the phylogenetic analysis. Their gene structures, conserved motifs and domains, chromosomal distribution, and cis elements in promoters were further studied. In addition, OTU gene expression patterns in response to plant hormone treatments, including SA, MeJA, NAA, BL, and ABA, were investigated by RT-qPCR analysis. The results showed that the expression profile of OsOTU genes exhibited plant hormone-specific expression. Expression levels of most of the rice OTU genes were significantly changed in response to rice stripe virus (RSV), rice black-streaked dwarf virus (RBSDV), Southern rice black-streaked dwarf virus (SRBSDV), and Rice stripe mosaic virus (RSMV). These results suggest that the rice OTU genes are involved in diverse hormone signaling pathways and in varied responses to virus infection, providing new insights for further functional study of OsOTU genes.

Research Progress on the Role of Inflammatory Mechanisms in the Development of Postoperative Cognitive Dysfunction.

Postoperative cognitive dysfunction (POCD), as one of the common postoperative complications, mainly occurs after surgery and anesthesia, especially in the elderly. It refers to cognitive function changes such as decreased learning and memory ability and inability to concentrate. In severe cases, there could be personality changes and a decline in social behavior. At present, a great deal of research had been carried out on POCD, but its specific mechanism remains unclear. The release of peripheral inflammation-related factors, the degradation and destruction of the blood-brain barrier, the occurrence of central inflammation, and the neuronal apoptosis and synaptic loss could be promoted by neuroinflammation indicating that inflammatory mechanisms may play key roles in the occurrence of POCD.

A rice LRR receptor-like protein associates with its adaptor kinase OsSOBIR1 to mediate plant immunity against viral infection.

Plants sense pathogen attacks using a variety of receptors at the cell surface. The LRR receptor-like proteins (RLP) and receptor-like kinases (RLK) are widely reported to participate in plant defence against bacterial and fungal pathogen invasion. However, the role of RLP and RLK in plant antiviral defence has rarely been reported. We employed a high-throughput-sequencing approach, transgenic rice plants and viral inoculation assays to investigate the role of OsRLP1 and OsSOBIR1 proteins in rice immunity against virus infection. The transcript of a rice LRR receptor-like protein, OsRLP1, was markedly up-regulated following infection by RBSDV, a devastating pathogen of rice and maize. Viral inoculation on various OsRLP1 mutants demonstrated that OsRLP1 modulates rice resistance against RBSDV infection. It was also shown that OsRLP1 is involved in the RBSDV-induced defence response by positively regulating the activation of MAPKs and PTI-related gene expression. OsRLP1 interacted with a receptor-like kinase OsSOBIR1, which was shown to regulate the PTI response and rice antiviral defence. Our results offer a novel insight into how a virus-induced receptor-like protein and its adaptor kinase activate the PTI response and antiviral defence in rice.

A class of independently evolved transcriptional repressors in plant RNA viruses facilitates viral infection and vector feeding.

Plant viruses employ diverse virulence strategies to achieve successful infection, but there are few known general strategies of viral pathogenicity and transmission used by widely different plant viruses. Here, we report a class of independently evolved virulence factors in different plant RNA viruses which possess active transcriptional repressor activity. Rice viruses in the genera Fijivirus, Tenuivirus, and Cytorhabdovirus all have transcriptional repressors that interact in plants with the key components of jasmonic acid (JA) signaling, namely mediator subunit OsMED25, OsJAZ proteins, and OsMYC transcription factors. These transcriptional repressors can directly disassociate the OsMED25-OsMYC complex, inhibit the transcriptional activation of OsMYC, and then combine with OsJAZ proteins to cooperatively attenuate the JA pathway in a way that benefits viral infection. At the same time, these transcriptional repressors efficiently enhanced feeding by the virus insect vectors by repressing JA signaling. Our findings reveal a common strategy in unrelated plant viruses in which viral transcriptional repressors hijack and repress the JA pathway in favor of both viral pathogenicity and vector transmission.

The OsGSK2 Kinase Integrates Brassinosteroid and Jasmonic Acid Signaling by Interacting with OsJAZ4.

The crosstalk between brassinosteroid (BR) and jasmonic acid (JA) signaling is crucial for plant growth and defense responses. However, the detailed interplay between BRs and JA remains obscure. Here, we found that the rice (Oryza sativa) Glycogen synthase kinase3 (GSK3)-like kinase OsGSK2, a conserved kinase serving as a key suppressor of BR signaling, enhanced antiviral defense and the JA response. We identified a member of the JASMONATE ZIM-domain (JAZ) family, OsJAZ4, as a OsGSK2 substrate and confirmed that OsGSK2 interacted with and phosphorylated OsJAZ4. We demonstrated that OsGSK2 disrupted the OsJAZ4-OsNINJA complex and OsJAZ4-OsJAZ11 dimerization by competitively binding to the ZIM domain, perhaps helping to facilitate the degradation of OsJAZ4 via the 26S proteasome pathway. We also showed that OsJAZ4 negatively modulated JA signaling and antiviral defense and that the BR pathway was involved in modulating the stability of OsJAZ4 protein in an OsCORONATINE INSENSITIVE1-dependent manner. Collectively, these results suggest that OsGSK2 enhances plant antiviral defenses by activating JA signaling as it directly interacts with, phosphorylates, and destabilizes OsJAZ4. Thus, our findings provide a clear link between BR and JA signaling.

Distinct modes of manipulation of rice auxin response factor OsARF17 by different plant RNA viruses for infection.

Plant auxin response factor (ARF) transcription factors are an important class of key transcriptional modulators in auxin signaling. Despite the well-studied roles of ARF transcription factors in plant growth and development, it is largely unknown whether, and how, ARF transcription factors may be involved in plant resistance to pathogens. We show here that two fijiviruses (double-stranded RNA viruses) utilize their proteins to disturb the dimerization of OsARF17 and repress its transcriptional activation ability, while a tenuivirus (negative-sense single-stranded RNA virus) directly interferes with the DNA binding activity of OsARF17. These interactions impair OsARF17-mediated antiviral defense. OsARF17 also confers resistance to a cytorhabdovirus and was directly targeted by one of the viral proteins. Thus, OsARF17 is the common target of several very different viruses. This suggests that OsARF17 plays a crucial role in plant defense against different types of plant viruses, and that these viruses use independently evolved viral proteins to target this key component of auxin signaling and facilitate infection.

Suppression of auxin signalling promotes rice susceptibility to Rice black streaked dwarf virus infection.

Auxin plays a fundamental role in plant growth and development, and also influences plant defence against various pathogens. Previous studies have examined the different roles of the auxin pathway during infection by biotrophic bacteria and necrotrophic fungi. We now show that the auxin signalling pathway was markedly down-regulated following infection of rice by Rice black streaked dwarf virus (RBSDV), a dsRNA virus. Repression of the auxin receptor TIR1 by a mutant overexpressing miR393 increased rice susceptibility to RBSDV. Mutants overexpressing the auxin signalling repressors OsIAA20 and OsIAA31 were also more susceptible to RBSDV. The induction of jasmonic acid (JA) pathway genes in response to RBSDV was supressed in auxin signalling mutants, suggesting that activation of the JA pathway may be part of the auxin signalling-mediated rice defence against RBSDV. More importantly, our results also revealed that OsRboh-mediated reactive oxygen species levels played important roles in this defence. The results offer novel insights into the regulatory mechanisms of auxin signalling in the rice-RBSDV interaction.

Rice black-streaked dwarf virus P10 acts as either a synergistic or antagonistic determinant during superinfection with related or unrelated virus.

Rice black-streaked dwarf virus (RBSDV), a member of the genus Fijivirus, is a devastating pathogen of crop plants. RBSDV S10 encodes a capsid protein (P10) that is an important component of the double-layered particle. However, little information is available on the roles of RBSDV P10 in viral infection or in interactions with other viruses. Here, we demonstrate that the expression of P10 in plants alleviates the symptoms of both RBSDV and the closely related Southern rice black-streaked dwarf virus (SRBSDV), and reduces the disease incidence, but renders the plants more susceptible to the unrelated Rice stripe virus (RSV). Further experiments suggest that P10-mediated resistance to RBSDV and SRBSDV operates at the protein level, rather than the RNA level, and is not a result of post-transcriptional gene silencing. Transcriptomic data reveal that the expression of P10 in plants significantly suppresses the expression of rice defence-related genes, which may play important roles in resistance to RSV infection. After infection with RBSDV, plants are more resistant to subsequent challenge by SRBSDV, but more susceptible to RSV. Overall, these results indicate that P10 acts as an important effector in virus interactions.

The Dual Effect of the Brassinosteroid Pathway on Rice Black-Streaked Dwarf Virus Infection by Modulating the Peroxidase-Mediated Oxidative Burst and Plant Defense.

The phytohormone brassinosteroid (BR) not only plays key roles in regulating plant growth and development but is also involved in modulating the plant defense system in response to pathogens. We previously found that BR application made rice plants more susceptible to the devastating pathogen rice black-streaked dwarf virus (RBSDV), but the mechanism of BR-mediated susceptibility remains unclear. We now show that both BR-deficient and -insensitive mutants are resistant to RBSDV infection. High-throughput sequencing showed that the defense hormone salicylic acid and jasmonic acid pathways were activated in the RBSDV-infected BR mutant. Meanwhile, a number of class III peroxidases (OsPrx) were significantly changed and basal reactive oxygen species (ROS) accumulated in BR mutants. Treatment with exogenous hormones and other chemicals demonstrated that the BR pathway could suppress the levels of OsPrx and the ROS burst by directly binding the promoters of OsPrx genes. Together, our findings indicate that BR-mediated susceptibility is at least partly caused by inhibition of the action of defense hormones, preventing the accumulation of the peroxidase-mediated oxidative burst.