Aldehyde-Olefin Couplings Via Sulfoxylate-Mediated Oxidative Generation of Ketyl Radical Anions.

Ketyl radicals are valuable reactive intermediates because they allow carbonyl chemistry to be extended beyond traditional electrophilic reactivity through simple single-electron reduction to a nucleophilic radical. However, this pathway is challenging due to the large negative reduction potentials of carbonyls, thus requiring highly reducing conditions. Herein, we describe the development of an alternative strategy to access ketyl radicals from aldehydes, which avoids the reduction pathway by instead proceeding via single-electron oxidation and desulfination of α-hydroxy sulfinates. These redox-active aldehyde adducts are generated in situ through the addition of sulfoxylate (SO22-) to aldehydes and possess low oxidation potentials, thereby facilitating ketyl radical formation and circumventing the need for strongly reducing conditions. We demonstrate the application of this sulfoxylate-mediated ketyl radical formation in ketyl-olefin coupling reactions.

Preparation and anti-tumor activity of paclitaxel silk protein nanoparticles encapsulated by biofilm.

In order to overcome the poor bioavailability of paclitaxel (PTX), in this study, self-assembled paclitaxel silk fibronectin nanoparticles (PTX-SF-NPs) were encapsulated with outer membrane vesicles of Escherichia coli (E. coil), and biofilm-encapsulated paclitaxel silk fibronectin nanoparticles (OMV-PTX-SF-NPs) were prepared by high-pressure co-extrusion, the size and zeta potential of the OMV-PTX-SF-NPs were measured. The antitumor effects of OMV-PTX-SF-NPs were evaluated by cellular and pharmacodynamic assays, and pharmacokinetic experiments were performed. The results showed that hydrophobic forces and hydrogen bonding played a major role in the interaction between paclitaxel and filipin proteins, and the size of OMV-PTX-SF-NPs was 199.8 ± 2.8 nm, zeta potential was -17.8 ± 1.3 mv. The cellular and in vivo pharmacokinetic assays demonstrated that the OMV-PTX-SF-NPs possessed a promising antitumor effect. Pharmacokinetic experiments showed that the AUC0-∞ of OMV-PTX-SF-NPs was 5.314 ± 0.77, which was much larger than that of free PTX, which was 0.744 ± 0.14. Overall, we have successfully constructed a stable oral formulation of paclitaxel with a sustained-release effect, which is able to effectively increase the bioavailability of paclitaxel, improve the antitumor activity, and reduce the adverse effects.

Severe hypoxemia after radiofrequency ablation for atrial fibrillation in palliatively repaired tetralogy of Fallot: A case report.

BACKGROUND: Patients with tetralogy of Fallot (TOF) often have arrhythmias, commonly being atrial fibrillation (AF). Radiofrequency ablation is an effective treatment for AF and does not usually cause severe postoperative hypoxemia, but the risk of complications may increase in patients with conditions such as TOF. CASE SUMMARY: We report a young male patient with a history of TOF repair who developed severe hypoxemia after radiofrequency ablation for AF and was ultimately confirmed to have a new right-to-left shunt. The patient subsequently underwent atrial septal occlusion and eventually recovered. CONCLUSION: Radiofrequency ablation may cause iatrogenic atrial septal injury; thus possible complications should be predicted in order to ensure successful treatment and patient safety.

Overcoming neutrophil-induced immunosuppression in postoperative cancer therapy: Combined sialic acid-modified liposomes with scaffold-based vaccines.

Immunotherapy is a promising approach for preventing postoperative tumor recurrence and metastasis. However, inflammatory neutrophils, recruited to the postoperative tumor site, have been shown to exacerbate tumor regeneration and limit the efficacy of cancer vaccines. Consequently, addressing postoperative immunosuppression caused by neutrophils is crucial for improving treatment outcomes. This study presents a combined chemoimmunotherapeutic strategy that employs a biocompatible macroporous scaffold-based cancer vaccine (S-CV) and a sialic acid (SA)-modified, doxorubicin (DOX)-loaded liposomal platform (DOX@SAL). The S-CV contains whole tumor lysates as antigens and imiquimod (R837, Toll-like receptor 7 activator)-loaded PLGA nanoparticles as immune adjuvants for cancer, which enhance dendritic cell activation and cytotoxic T cell proliferation upon localized implantation. When administered intravenously, DOX@SAL specifically targets and delivers drugs to activated neutrophils in vivo, mitigating neutrophil infiltration and suppressing postoperative inflammatory responses. In vivo and vitro experiments have demonstrated that S-CV plus DOX@SAL, a combined chemo-immunotherapeutic strategy, has a remarkable potential to inhibit postoperative local tumor recurrence and distant tumor progression, with minimal systemic toxicity, providing a new concept for postoperative treatment of tumors.

Risk of atrial fibrillation in patients with multiple myeloma: what is known and directions for future study.

BACKGROUND: Multiple myeloma (MM) is a prevalent hematological tumor, and recent clinical data have highlighted the significance of atrial fibrillation (AF) as a crucial complication affecting the prognosis of MM. This review aims to consolidate findings from published clinical studies, focusing on the epidemiological characteristics of AF in MM patients and the associated risks arising from MM treatments such as autologous hematopoietic stem cell transplantation, proteasome inhibitors, and immunomodulatory agents. MAIN BODY: While existing data partially demonstrate a strong correlation between MM and AF, further clinical studies are necessary to comprehensively investigate their association. These studies should encompass various aspects, including the risk of AF resulting from MM treatment, the impact of AF-induced embolic events and heart failure on MM prognosis, as well as the influence of AF management methods like catheter ablation or left atrial appendage closure on MM prognosis. CONCLUSIONS: The supplementation of future data will provide more precise guidance for managing MM patients. By incorporating information regarding AF risk associated with MM treatment and examining the effects of AF management strategies on MM prognosis, healthcare professionals can enhance their decision-making process when caring for individuals with MM.

Repolarizing Tumor-Associated Macrophages and inducing immunogenic cell Death: A targeted liposomal strategy to boost cancer immunotherapy.

Cancer immunotherapy has shown promise in treating various malignancies. However, the presence of an immunosuppressive tumor microenvironment (TME) triggered by M2 tumor-associated macrophages (TAMs) and the limited tumor cell antigenicity have hindered its broader application. To address these challenges, we developed DOX/R837@ManL, a liposome loaded with imiquimod (R837) and doxorubicin (DOX), modified with mannose-polyethylene glycol (Man-PEG). DOX/R837@ManL employed a mannose receptor (MRC1)-mediated targeting strategy, allowing it to accumulate selectively at M2 Tumor associated macrophages (TAMs) and tumor sites. R837, an immune adjuvant, promoted the conversion of immunosuppressive M2 TAMs into immunostimulatory M1 TAMs, and reshaped the immunosuppressive TME. Simultaneously, DOX release induced immunogenic cell death (ICD) in tumor cells and enhanced tumor cell antigenicity by promoting dendritic cells (DCs) maturation. Through targeted delivery, the synergistic action of R837 and DOX activated innate immunity and coordinated adaptive immunity, enhancing immunotherapy efficacy. In vivo experiments have demonstrated that DOX/R837@ManL effectively eliminated primary tumors and lung metastases, while also preventing tumor recurrence post-surgery. These findings highlighted the potential of DOX/R837@ManL as a promising strategy for cancer immunotherapy.

Photoredox-Catalyzed Decarboxylative Bromination, Chlorination and Thiocyanation Using Inorganic Salts.

Decarboxylative halogenation reactions of alkyl carboxylic acids are highly valuable reactions for the synthesis of structurally diverse alkyl halides. However, many reported protocols rely on stoichiometric strong oxidants or highly electrophilic halogenating agents. Herein, we describe visible-light photoredox-catalyzed decarboxylative halogenation reactions of N-hydroxyphthalimide-activated carboxylic acids that avoid stoichiometric oxidants and use inexpensive inorganic halide salts as the halogenating agents. Bromination with lithium bromide proceeds under simple, transition-metal-free conditions using an organic photoredox catalyst and no other additives, whereas dual photoredox-copper catalysis is required for chlorination with lithium chloride. The mild conditions display excellent functional-group tolerance, which is demonstrated through the transformation of a diverse range of structurally complex carboxylic acid containing natural products into the corresponding alkyl bromides and chlorides. In addition, we show the generality of the dual photoredox-copper-catalyzed decarboxylative functionalization with inorganic salts by extension to thiocyanation with potassium thiocyanide, which was applied to the synthesis of complex alkyl thiocyanates.

Association between circulating leukocytes and arrhythmias: Mendelian randomization analysis in immuno-cardiac electrophysiology.

Background: Cardiac arrhythmia is a common disease associated with high mortality and morbidity. Circulating leukocyte counts, which serve as a biomarker for assessing systemic immune status, have been linked to arrhythmias in observational studies. However, observational studies are plagued by confounding factors and reverse causality, whether alterations in circulating leukocyte components are causally associated with arrhythmias remains uncertain. The present study explored this question based on genetic evidence. Methods and findings: We performed Mendelian randomization (MR) analysis to evaluate whether alterations in leukocyte counts affect aggregated risk of all types of arrhythmia or risk of five specific types of arrhythmia. Single-nucleotide polymorphisms serving as proxies for leukocyte differential counts were retrieved from the Blood Cell Consortium, and statistical data on arrhythmias were obtained from the UK Biobank), FinnGenand a meta-analysis of genome-wide association studies for atrial fibrillation. We applied inverse variance-weighted method as the primary analysis, complemented by a series of sensitivity analyses. Bidirectional analyses were conducted to assess reverse causality. Finally, multivariable MR was performed to study the joint effects of multiple risk factors. We found that genetically predicted differential leukocyte counts were not significantly associated with aggregated occurrence of all types of arrhythmia. In contrast, each 1-standard deviation increase in lymphocyte count was associated with 46% higher risk of atrioventricular block (OR 1.46, 95% CI 1.11-1.93, p=0.0065). A similar effect size was observed across all MR sensitivity analyses, with no evidence of horizontal pleiotropy. Reverse MR analysis suggested that atrioventricular block was unlikely to cause changes in lymphocyte count. Primary MR analysis based on the inverse-variance weighted method suggested that changes in neutrophil count alter risk of right bundle branch block, and changes in basophil count alter risk of atrial fibrillation. However, these causal relationships were not robust in sensitivity analyses. We found no compelling evidence that neutrophil or lymphocyte counts cause atrial fibrillation. Conclusion: Our data support higher lymphocyte count as a causal risk factor for atrioventricular block. These results highlight the importance of immune cells in the pathogenesis of specific cardiac conduction disorders.

Self-Assembled L-DNA Linkers for Rapid Construction of Multi-Specific Antibody-Drug Conjugates Library.

One of the key challenges of improving clinical outcomes of antibody drug conjugates (ADCs) is overcoming cancer resistance to the antibody and/or drug components of ADCs, and hence the need for ADC platforms with high combinatory flexibility. Here, we introduce the use of self-assembled left-handed DNA (L-DNA) oligonucleotides to link combinatory single-domain antibodies and toxin payloads for tunable and adaptive delivery of ADCs. We demonstrate that the method allows convenient construction of a library of ADCs with multi-specific targeting, multi-specific payloads, and exact drug-antibody ratio. The newly constructed ADCs with L-DNA scaffold showed favorable properties of in vitro cell cytotoxicity and in vivo suppression and eradication of solid tumors. Collectively, our data suggest that the L-DNA based modular ADC (MADC) platform is a viable option for generating therapeutic ADCs and for potentially expanding ADC therapeutic window via multi-specificity.

Deep Reinforcement Learning on Autonomous Driving Policy With Auxiliary Critic Network.

Deep reinforcement learning (DRL) is a machine learning method based on rewards, which can be extended to solve some complex and realistic decision-making problems. Autonomous driving needs to deal with a variety of complex and changeable traffic scenarios, so the application of DRL in autonomous driving presents a broad application prospect. In this article, an end-to-end autonomous driving policy learning method based on DRL is proposed. On the basis of proximal policy optimization (PPO), we combine a curiosity-driven method called recurrent neural network (RNN) to generate an intrinsic reward signal to encounter the agent to explore its environment, which improves the efficiency of exploration. We introduce an auxiliary critic network on the original actor-critic framework and choose the lower estimate which is predicted by the dual critic network when the network update to avoid the overestimation bias. We test our method on the lane- keeping task and overtaking task in the open racing car simulator (TORCS) driving simulator and compare with other DRL methods, experimental results show that our proposed method can improve the training efficiency and control performance in driving tasks.

AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model.

Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney.

The kidney-expressed transcription factor ZKSCAN3 is dispensable for autophagy transcriptional regulation and AKI progression in mouse.

Acute kidney injury (AKI) is a common clinical disease that can cause serious harm to the kidneys, but it has no effective treatment till now. The modulation of autophagy pathway regulation is considered a potentially effective therapeutic approach in AKI prevention and treatment. ZKSCAN3 has been shown to be an important transcription factor that negatively regulates autophagy activity in cancer tissues. In order to determine whether autophagy could be activated by knocking out ZKSCAN3 to exert the renal protective effect of autophagy, we constructed AKI models with Zkscan3 knockout (KO) mice and detected renal pathological changes and renal function changes as well as autophagy-related indicators. We found that Zkscan3 KO had no significant effect on kidney development. Besides, no significant changes in autophagy activity were observed under normal physiological or AKI conditions. In non-tumor tissues, ZKSCAN3 did not mediate transcriptional regulation of autophagy-related genes. These findings suggest that because ZKSCAN3 may not function in the transcriptional regulation of autophagy-related genes in non-tumor tissues, it may not be used as a therapeutic target for AKI.

The Role of Parietal Epithelial Cells in the Pathogenesis of Podocytopathy.

Podocytopathy is the most common feature of glomerular disorder characterized by podocyte injury- or dysfunction-induced excessive proteinuria, which ultimately develops into glomerulosclerosis and results in persistent loss of renal function. Due to the lack of self-renewal ability of podocytes, mild podocyte depletion triggers replacement and repair processes mostly driven by stem cells or resident parietal epithelial cells (PECs). In contrast, when podocyte recovery fails, activated PECs contribute to the establishment of glomerular lesions. Increasing evidence suggests that PECs, more than just bystanders, have a crucial role in various podocytopathies, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy, IgA nephropathy, and lupus podocytopathy. In this review, we attempt to dissect the diverse role of PECs in the pathogenesis of podocytopathy based on currently available information.

Pore Evolution in Refractory Gold Ore Formed by Oxidation Roasting and the Effect on the Cyanide Leaching Process.

Refractory gold ore is usually affected by the associated carbonaceous matter through the preg-robbing effect, which is eliminated by oxidation roasting, followed by leaching, to achieve a satisfactory gold leaching efficiency. Roasting-leaching experiments, pore structure measurements, scanning electron microscopy (SEM), and X-ray diffraction are used to explore the structural evolution of pores on the surface and its effect on the leaching performance. Pores with optimal sizes were obtained by roasting at 650 °C for 2.0 h with a ventilation of 0.6 m3/h; approximately 92.55% gold could be recovered under these conditions. A porous structure observed by SEM became more compact as the temperature further increased to 850 °C. The formation of CaSiO3 and CaSO4 in pores led to pore shrinkage. The mechanism of oxidation roasting, followed by cyanide leaching, was schematically analyzed and revealed the effects of pore structural evolution and phase transformation on the leaching efficiency.

Hydroxychloroquine administration exacerbates acute kidney injury complicated by lupus nephritis.

BACKGROUND: Hydroxychloroquine (HCQ) has been recommended as a basic treatment for lupus nephritis (LN) during this decade based on its ability to improve LN-related renal immune-mediated inflammatory lesions. As a classical lysosomal inhibitor, HCQ may inhibit lysosomal degradation and disrupt protective autophagy in proximal tubular epithelial cells (PTECs). Therefore, the final renal effects of HCQ on LN need to be clarified. METHOD: HCQ was administered on spontaneous female MRL/lpr LN mice with severe proteinuria daily for 4 weeks. Moreover, the MRL/lpr mice with proteinuric LN were subjected to cisplatin-induced or unilateral ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) after 2 weeks of HCQ preadministration. RESULTS: As expected, HCQ treatment increased the survival ratio and downregulated the levels of serum creatinine in the mice with LN, ameliorated renal lesions, and inhibited renal interstitial inflammation. Unexpectedly, HCQ preadministration significantly increased susceptibility to and delayed the recovery of AKI complicated by LN, as demonstrated by an increase in PTEC apoptosis and expression of the tubular injury marker KIM-1 as well as the retardation of PTEC replenishment. HCQ preadministration suppressed the proliferation of PTECs by arresting cells in G1/S phase and upregulated the expression of cell cycle inhibitors. Furthermore, HCQ preadministration disrupted the PTEC autophagy-lysosomal pathway and accelerated PTEC senescence. CONCLUSION: HCQ treatment may increase susceptibility and delay the recovery of AKI complicated by LN despite its ability to improve LN-related renal immune-mediated inflammatory lesions. The probable mechanism involves accelerated apoptosis and inhibited proliferation of PTECs via autophagy-lysosomal pathway disruption and senescence promotion.

Rice starch multi-level structure and functional relationships.

Starch from 15 different rice genotypes with amylose content (AC) ranging 1.5%-30.6% were investigated for relationships between structures and properties. For parameters related to the granular level, the most important relationships were found for AC, average chain lengths (ACL) of the amylopectin (AP) fb1 chains having a length of DP 13-24, crystallinity, and the thickness of the crystalline (dc) and the amorphous lamellae (da) of the starch granule. AC and dc were negatively correlated with the peak gelatinization temperature (Tp), thermal enthalpy (ΔH), and peak viscosity (PV), but positively correlated with swelling power. ACLfb1 and da, as compared to AC and dc, had the opposite effects on these parameters, demonstrating important roles of specific molecular and lamellar structures on the starch granular stability. For the gelatinized systems, increasing ACLfb1 decreased retrogradation, while AC increased retrogradation by increasing the resistant starch (RS) content, storage modulus (G'), and setback (SB).

High-Stability Silver Nanowire-Al2O3 Composite Flexible Transparent Electrodes Prepared by Electrodeposition.

Silver nanowire (AgNW) conductive film fabricated by solution processing was investigated as an alternative to indium tin oxide (ITO) in flexible transparent electrodes. In this paper, we studied a facile and effective method by electrodepositing Al2O3 on the surface of AgNWs. As a result, flexible transparent electrodes with improved stability could be obtained by electrodepositing Al2O3. It was found that, as the annealing temperature rises, the Al2O3 coating layer can be transformed from Al2O3·H2O into a denser amorphous state at 150 °C. By studying the increase of electrodeposition temperature, it was observed that the transmittance of the AgNW-Al2O3 composite films first rose to the maximum at 70 °C and then decreased. With the increase of the electrodeposition time, the figure of merit (FoM) of the composite films increased and reached the maximum when the time was 40 s. Through optimizing the experimental parameters, a high-stability AgNW flexible transparent electrode using polyimide (PI) as a substrate was prepared without sacrificing optical and electrical performance by electrodepositing at -1.1 V and 70 °C for 40 s with 0.1 mol/L Al(NO3)3 as the electrolyte, which can withstand a high temperature of 250 °C or 250,000 bending cycles with a bending radius of 4 mm.

Lysosome Depletion-Triggered Autophagy Impairment in Progressive Kidney Injury.

BACKGROUND: Macroautophagy (autophagy) is a cellular recycling process involving the destruction of damaged organelles and proteins in intracellular lysosomes for efficient nutrient reuse. SUMMARY: Impairment of the autophagy-lysosome pathway is tightly associated with multiple kidney diseases, such as diabetic nephropathy, proteinuric kidney disease, acute kidney injury, crystalline nephropathy, and drug- and heavy metal-induced renal injury. The impairment in the process of autophagic clearance may induce injury in renal intrinsic cells by activating the inflammasome, inducing cell cycle arrest, and cell death. The lysosome depletion may be a key mechanism triggering this process. In this review, we discuss this pathway and summarize the protective mechanisms for restoration of lysosome function and autophagic flux via the endosomal sorting complex required for transport (ESCRT) machinery, lysophagy, and transcription factor EB-mediated lysosome biogenesis. KEY MESSAGE: Further exploring mechanisms of ESCRT, lysophagy, and lysosome biogenesis may provide novel therapy strategies for the management of kidney diseases.

Cyclosporine A blocks autophagic flux in tubular epithelial cells by impairing TFEB-mediated lysosomal function.

Cyclosporine A (CsA) is an immunosuppressor widely used for the prevention of acute rejection during solid organ transplantation. However, severe nephrotoxicity has substantially limited its long-term usage. Recently, an impaired autophagy pathway was suggested to be involved in the pathogenesis of chronic CsA nephrotoxicity. However, the underlying mechanisms of CsA-induced autophagy blockade in tubular cells remain unclear. In the present study, we observed that CsA suppressed the activation and expression of transcription factor EB (TFEB) by increasing the activation of mTOR, in turn promoting lysosomal dysfunction and autophagy flux blockade in tubular epithelial cells (TECs) in vivo and in vitro. Restoration of TFEB activation by Torin1-mediated mTOR inhibition significantly improved lysosomal function and rescued autophagy pathway activity, suppressing TEC injury. In summary, targeting TFEB-mediated autophagy flux represents a potential therapeutic strategy for CsA-induced nephrotoxicity.

Molecular characterization and protective efficacy of a new conserved hypothetical protein of Eimeria tenella.

Eimeria tenella is an obligate intracellular parasite that actively invades cecal epithelial cells of chickens. This parasite encodes a genome of more than 8000 genes. However, more than 70% of the gene models for this species are currently annotated as hypothetical proteins. In this study, a conserved hypothetical protein gene of E. tenella, designated EtCHP18905, was cloned and identified, and its immune protective effects were evaluated. The open reading frame of EtCHP18905 was 1053bp and encoded a protein of 350 amino acids with a molecular weight of 38.7kDa. The recombinant EtCHP18905 protein (rEtCHP18905) was expressed in E. coli. Using western blot, the recombinant protein was successfully recognized by anti GST-Tag monoclonal antibody and anti-sporozoites protein rabbit serum. Real-time quantitative PCR analysis revealed that the EtCHP18905 mRNA levels were higher in sporozoites than in unsporulated oocysts, sporulated oocysts and second-generation merozoites. Western blot analysis showed that EtCHP18905 protein expression levels were lower in sporozoites than in other stages. Immunofluorescence analysis indicated that the EtCHP18905 protein was located on the surface of sporozoites and second-generation merozoites. Inhibition experiments showed that the ability of sporozoites to invade host cells was significantly decreased after treatment with the anti-rEtCHP18905 polyclonal antibody. Vaccination with rEtCHP18905 protein was able to significantly decrease mean lesion scores and oocyst outputs as compared to non-vaccinated controls. The results suggest that the rEtCHP18905 protein can induce partial immune protection against infection with E. tenella and could be an effective candidate for the development of new vaccines.

TITLE: Caractérisation moléculaire et efficacité protectrice d'une nouvelle protéine hypothétique conservée d'Eimeria tenella. ABSTRACT: Eimeria tenella est un parasite intracellulaire obligatoire qui envahit activement les cellules épithéliales du caecum des poulets. Ce parasite code un génome de plus de 8000gènes. Cependant, plus de 70% des modèles de gènes de cette espèce sont actuellement annotés en tant que protéines hypothétiques. Dans cette étude, un gène de protéine hypothétique conservé d'E. tenella, désigné par EtCHP18905, a été cloné et identifié, et ses effets immuno-protecteurs ont été évalués. Le cadre de lecture ouvert d'EtCHP18905 était de 1053 pb et codait pour une protéine de 350 acides aminés avec un poids moléculaire de 38,7kDa. La protéine recombinante EtCHP18905 (rEtCHP18905) a été exprimée dans E. coli. En utilisant le Western blot, la protéine recombinante a été reconnue avec succès par un anticorps monoclonal anti-GST-Tag et un sérum de lapin anti-protéines de sporozoïtes. Une analyse PCR quantitative en temps réel a révélé que les niveaux d'ARNm d'EtCHP18905 étaient plus élevés dans les sporozoïtes que dans les oocystes non sporulés, les oocystes sporulés et les mérozoïtes de deuxième génération. L'analyse par Western blot a montré que les niveaux d'expression de la protéine EtCHP18905 étaient plus faibles dans les sporozoïtes que dans les autres stades. L'analyse par immunofluorescence a indiqué que la protéine EtCHP18905 était localisée à la surface des sporozoïtes et des mérozoïtes de deuxième génération. Des expériences d'inhibition ont montré que la capacité des sporozoïtes à envahir les cellules hôtes était significativement diminuée après le traitement par l'anticorps polyclonal anti-rEtCHP18905. La vaccination avec la protéine rEtCHP18905 a permis de réduire significativement les scores moyens des lésions et les sorties d'oocystes par rapport aux témoins non vaccinés. Les résultats suggèrent que la protéine rEtCHP18905 peut induire une protection immunitaire partielle contre l'infection par E. tenella et pourrait être un candidat efficace pour le développement de nouveaux vaccins.