AQUACULTURE
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2025
·
IF 3.9
Li-Peng Shan,Mao-Mao Wang,Yang Hu,Lei Liu,Bin Zhu,Jiong Chen
Hepatopancreatic microsporidiosis (HPM), caused by Enterocytozoon hepatopenaei (EHP), has emerged as a major threat to the shrimp aquaculture industry. However, no effective strategies have yet been developed to control the spread of this disease. In this study, we assessed the anti-EHP activity of ten monomeric compounds in Penaeus vannamei . The results showed that tetrahydropalmatine reduced the EHP copy number by 73.8 % at a concentration of 20 mg/L. In a therapeutic experiment, feeding EHP-infected shrimp a diet containing 0.1 % tetrahydropalmatine significantly lowered the EHP load. Additionally, the growth-related gene juvenile hormone esterase-like carboxylesterase 1 was significantly upregulated, while ecdysteroid-regulated protein and farnesoic acid O-methyltransferase were significantly downregulated, suggesting that tetrahydropalmatine may enhance the growth potential of EHP-infected shrimp. After 30 days of feeding, the EHP-infected shrimp's body weight in the groups fed with tetrahydropalmatine increased by 19.9 % compared to those fed with the normal diet. In a prevention experiment, healthy shrimp fed a diet containing tetrahydropalmatine and subsequently infected with EHP showed an increase in body weight by day 30 post-infection, compared to the control group, although this difference was not statistically significant. Tetrahydropalmatine can inhibit spore germination and electron dense disc formation, which may be an important reason for its suppression of EHP infection. Moreover, tetrahydropalmatine effectively inhibited the horizontal transmission of EHP, suggesting its potential to limit HPM outbreaks. These findings indicate that tetrahydropalmatine may serve as a feed additive for the treatment of HPM caused by EHP.
研究领域:
水产养殖学
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寄生虫学
·
分子生物学
✓ 已验证
DOI
高影响因子
ANALYTICAL CHEMISTRY
·
2025
·
IF 6.7
Songkuan Zhuang,Xiaojun Huang,Muyan Diao,Ruiling Dong,Yueyu Dong,Jun Liu,Yizhen Liu
Current one-pot CRISPR diagnostics necessitate meticulous control of nucleic acid hybridization parameters or extensive modification of CRISPR components to achieve complete enzymatic silencing, a fundamental bottleneck limiting their robustness and generalizability. Here, we resolve this challenge through dynamic crRNA reconfiguration, a paradigm-shifting strategy that exploits the intrinsic structural duality of CRISPR RNA. We present CONVERT (CRISPR One-Pot Nucleic acid detection Via Engineered crRNA Reconfiguration Technology), a universal platform where nontarget intact crRNA acts as a universal suppressor, achieving complete Cas12a inhibition during RPA (recombinase polymerase amplification) by irreversible enzyme sequestration. Target detection is initiated through programmable conversion to split crRNA activators, bypassing sequence-specific design constraints entirely. This crRNA conformational switching mechanism is implemented via photocleavable linker cleavage and subsequent assembly with presupplied truncated crRNA (tcrRNA), activating trans-cleavage signal amplification. Three transformative advances emerge: First, the endogenous crRNA engineering eliminates dependency on exogenous nucleic acid blockers or chemical modifications, reducing optimization costs and time. Second, near-total enzymatic suppression ensures zero cross-talk between amplification and detection phases. Third, the unified workflow enables contamination-resistant operation through spatiotemporal control, requiring no physical partitioning. Validated for Enterocytozoon bieneusi detection, the system demonstrates attomolar sensitivity of 1 aM, 100% diagnostic concordance with qPCR, and absolute specificity against related pathogens. By effectively decoupling CRISPR regulation from sequence-context constraints through rational crRNA structural plasticity, this work establishes a generalized framework for next-generation molecular diagnostics.
研究领域:
分子生物学
·
生物工程
·
诊断技术
·
合成生物学
·
核酸扩增
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产品关联
DOI
PubMed
高影响因子
Life Science Alliance
·
2024
·Vol. 7
·期 4
·e202302375
·
IF 3.3
Jialing Bao,Yunlin Tang,Yebo Chen,Jiangyan Jin,Xue Wang,Guozhen An,Lu Cao,Huarui Zhang,Gong Cheng,Guoqing Pan,Zeyang Zhou
Microsporidia are difficult to be completely eliminated once infected, and the persistence disrupts host cell functions. Here in this study, we aimed to elucidate the impairing effects and consequences of microsporidia on host DCs. Enterocytozoon hellem, one of the most commonly diagnosed zoonotic microsporidia species, was applied. In vivo models demonstrated that E. hellem-infected mice were more susceptible to further pathogenic challenges, and DCs were identified as the most affected groups of cells. In vitro assays revealed that E. hellem infection impaired DCs’ immune functions, reflected by down-regulated cytokine expressions, lower extent of maturation, phagocytosis ability, and antigen presentations. E. hellem infection also detained DCs’ potencies to prime and stimulate T cells; therefore, host immunities were disrupted. We found that E. hellem Ser/Thr protein phosphatase PP1 directly interacts with host p38α (MAPK14) to manipulate the p38α(MAPK14)/NFAT5 axis of the MAPK pathway. Our study is the first to elucidate the molecular mechanisms of the impairing effects of microsporidia on host DCs’ immune functions. The emergence of microsporidiosis may be of great threat to public health.
研究领域:
免疫学
·
微生物学
·
病理学
✓ 已验证
DOI
PubMed
高影响因子
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