Microbes and Infection最新文献_第3页

Investigating the possible role of toxoplasmosis and Interleukin-1β variants on the immune response in Egyptian diabetic patients 研究弓形虫病和白细胞介素-1β变异对埃及糖尿病患者免疫反应的可能作用。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105559

Asmaa Ibrahim , Nancy O. kamel , Fatma Rageh , Rasha Elgamal , Mohamed A. Sakr , Eman M. Osman , Samar s. Ahmed , Hend A. Yassin , Yasmine N. Kamel , Reham F. Othman , Manar Ezzelarab Ramadan

The study assesses toxoplasmosis seroprevalence in Type 2 Diabetes Mellitus, identifies the potential risk factors, and examines IL-1β expression levels and polymorphisms in those infected with T. gondii.

One hundred healthy controls and 200 diabetic patients participated in the study. Diagnosis was made by Immunoassay to measure antibodies of T. gondii, IgM, and IgG, and molecular by targeting the 529 RE gene. Quantitative measurement of IL-1β levels was done, and genetic polymorphisms were assessed.

Among diabetic patients, 61.0 % were seropositive for T. gondii IgG, compared to 36.0 % in healthy controls. Significant associations were found with IgG and IgM (P = 0.0001, 0.022), respectively. Patients with diabetes and toxoplasmosis had significantly high levels of IL-1β (P = 0.0003). The +3954C/T variant showed a higher prevalence of CT and lower TT genotypes in T2DM patients, P = 0.017, 0.003, respectively. The CT genotype is considered a genetic risk factor for diabetic patients, and the TT genotype and T allele may increase susceptibility to infection with toxoplasmosis. The prevalence of toxoplasmosis in T2DM, levels of IL-1β, and +3954C/T polymorphism seem to be important factors for developing complications in diabetic patients infected with toxoplasmosis.

该研究评估了2型糖尿病患者弓形虫病的血清患病率，确定了潜在的危险因素，并检测了弓形虫感染者IL-1β的表达水平和多态性。100名健康对照者和200名糖尿病患者参与了这项研究。采用免疫分析法检测弓形虫抗体、IgM抗体和IgG抗体，并采用靶向529 RE基因的分子分析法进行诊断。定量测定IL-1β水平，并评估遗传多态性。糖尿病患者血清弓形虫IgG阳性率为61.0%，而健康对照组为36.0%。与IgG和IgM有显著相关性（P=0.0001, 0.022）。糖尿病和弓形虫病患者IL-1β水平显著升高（P=0.0003）。+3954C/T基因型在T2DM患者中CT患病率较高，TT基因型患病率较低，P=0.017, 0.003。CT基因型被认为是糖尿病患者的遗传危险因素，TT基因型和T等位基因可能增加弓形虫感染的易感性。T2DM患者弓形虫病患病率、IL-1β水平和+3954C/T多态性似乎是糖尿病感染弓形虫病患者发生并发症的重要因素。

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引用次数: 0

Lactococcus lactis and Bifidobacterium longum attenuate Clostridioides difficile- or Clostridium symbiosum-induced colitis and depression/anxiety-like behavior in male mice 乳酸乳球菌和长双歧杆菌可减弱艰难梭菌或共生梭菌诱导的雄性小鼠结肠炎和抑郁/焦虑样行为。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105560

Min-Kyung Joo , Xiaoyang Ma , Jung-Woo Shin , Yoon-Jung Shin , Dong-Hyun Kim

Clostridioides difficile causes severe colitis, which induces neuroinflammation and psychiatric disorder. In a preliminary study, we isolated Clostridium symbiosum from the stools of patients with ulcerative colitis. Therefore, we first examined whether oral infection with C. difficile or C. symbiosum could induce colitis and depression in male mice. Orally gavaged C. difficile or C. symbiosum caused diarrhea, bodyweight loss, depression/anxiety-like behavior, and tumor necrosis factor (TNF)-α and interleukin (IL)-6 overexpression in the colon and hippocampus in the pseudo-germ-free (PGF) and specific germ-free (SPF) mice. However, healthy volunteer microbiota-derived Lactococcus lactis P22 and/or Bifidobacterium longum P26 suppressed C. difficile or C. symbiosum growth and TNF-α expression in macrophage cells. They alleviated C. difficile- or C. symbiosum-induced bodyweight loss, diarrhea, and neurobehavioral changes in PGF and SPF mice, while reducing pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) levels in the colon and in the hippocampus. These findings suggest that C. difficile or C. symbiosum can cause colitis and depression/anxiety. Oral administration of P22 and/or P26 may alleviate gut bacteria-induced gut inflammation and depression/anxiety through the inhibition of their growth and inflammatory response.

艰难梭菌引起严重的结肠炎，引起神经炎症和精神障碍。在一项初步研究中，我们从溃疡性结肠炎患者的粪便中分离出共生梭菌。因此，我们首先研究了口腔感染艰难梭菌或共生梭菌是否会导致雄性小鼠结肠炎和抑郁。在伪无菌（PGF）和特异性无菌（SPF）小鼠中，口服艰难梭菌或共生梭菌可引起腹泻、体重减轻、抑郁/焦虑样行为以及结肠和海马中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6的过表达。然而，健康志愿者微生物源性乳酸乳球菌P22和/或长双歧杆菌P26抑制艰难梭菌或共生梭菌的生长和巨噬细胞中TNF-α的表达。它们减轻了艰难梭菌或共生梭菌引起的PGF和SPF小鼠的体重减轻、腹泻和神经行为改变，同时降低了结肠和海马中的促炎细胞因子（IL-1β、IL-6和TNF-α）水平。这些发现表明艰难梭菌或共生梭菌可引起结肠炎和抑郁/焦虑。口服P22和/或P26可能通过抑制肠道细菌的生长和炎症反应来减轻肠道细菌诱导的肠道炎症和抑郁/焦虑。

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引用次数: 0

FOXP3 gene polymorphisms are associated with indeterminate clinical form of Chagas disease FOXP3基因多态性与恰加斯病不确定的临床形式有关。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105544

Nayara I. Medeiros , Daniela Silva Oliveira , Karine S. Ferreira , Tatjana S.L. Keesen , Luiz Paulo C. Rocha , Giovane R. Sousa , Marcos P.S. Damasio , Rafaelle C.G. Fares-Gusmao , Ana T. Chaves , Fernanda F. De Araújo , Walderez O. Dutra , Rodrigo Correa-Oliveira , Manoel O.C. Rocha , Juliana A.S. Gomes

The forkhead box protein 3 (FOXP3) transcription factor is the main marker of regulatory T-cell (Treg) development and activation, a subpopulation involved in immune system regulation, self-tolerance, and protection against infections. We previously showed that Treg cells control the exacerbated immune response and morbidity in chronic Chagas disease, by modulating the cytokine environment and killing effector cells. Although FOXP3 gene polymorphisms have already been studied in several diseases, their role in Chagas disease is underreported. This study investigated FOXP3 gene polymorphism (rs3761548) in patients with Chronic Chagas disease and the association between FOXP3 polymorphisms (−3279 C/T and −3499 G/T) with clinical forms of the disease. We show that the −3499 G/T polymorphism of the heterozygous genotype (GT) is twice as prevalent in women with indeterminate clinical form (IND). Other analyses showed that the polymorphic allele (T + −3499 G/T) is high in women with IND, suggesting a protective role for this polymorphism. This pattern is associated with high frequency of FOXP3 in Treg cells in individuals with the IND form. Our results suggest that −3499 G/T polymorphism in the FOXP3 gene may play an important role in T. cruzi infection, contributing to control and the development of the IND clinical form.

叉头盒蛋白3 （FOXP3）转录因子是调节性t细胞（Treg）发育和激活的主要标记物，Treg是一个参与免疫系统调节、自我耐受和抗感染保护的亚群。我们之前的研究表明，Treg细胞通过调节细胞因子环境和杀死效应细胞来控制慢性恰加斯病中加剧的免疫反应和发病率。虽然FOXP3基因多态性已经在几种疾病中得到了研究，但它们在恰加斯病中的作用被低估了。本研究探讨了慢性恰加斯病患者FOXP3基因多态性（rs3761548）以及FOXP3多态性（-3279 C/T和-3499 G/T）与该病临床形式的关系。我们发现杂合基因型（GT）的-3499 G/T多态性在不确定临床形式（IND）的女性中是其两倍。其他分析表明，多态等位基因（T+ -3499 G/T）在IND女性中较高，表明该多态性具有保护作用。这种模式与患有IND形式的Treg细胞中FOXP3的高频率有关。提示FOXP3基因的-3499 G/T多态性可能在克氏锥虫感染中发挥重要作用，有助于控制和发展IND临床形式。

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引用次数: 0

Averting collapse: Reimagining the NTDs ecosystem through G20 health diplomacy and science innovation 避免崩溃：通过G20卫生外交和科学创新重塑被忽视热带病生态系统。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105547

Maple Goh , Peter J. Hotez

The recent termination of the U.S. Government's neglected topical diseases (NTD) mass treatment program, following similar cuts by the UK, threatens decades of progress. Without a strategic reset, NTDs may re-emerge, exacerbating poverty across Africa and beyond. We call for a broadened donor base and reframing NTD control as a shared global interest, especially as NTDs rise in G20 nations due to climate change and urbanization. This moment demands investment in sustainable tools, like NextGen vaccines and biologics, and greater leadership from G20 countries. While USAID's exit is a setback, opportunities arise for decolonizing global health and fostering new partnerships.

继英国类似的削减之后，美国政府最近终止了被忽视的局部疾病（NTD）大规模治疗计划，威胁到数十年的进展。如果不重新调整战略，被忽视的热带病可能会再次出现，加剧非洲及其他地区的贫困。我们呼吁扩大捐助基础，将控制被忽视的传染性疾病重新定位为全球共同利益，特别是在气候变化和城市化导致被忽视的传染性疾病在20国集团国家中上升的情况下。这一时刻需要对可持续工具进行投资，如下一代疫苗和生物制剂，并需要G20国家发挥更大的领导作用。虽然美国国际开发署的退出是一个挫折，但为全球卫生非殖民化和培养新的伙伴关系带来了机会。

引用次数: 0

Cryptococcus neoformans and the EGFR Puzzle: Uncovering a Novel mechanism for blood-brain barrier crossing 新型隐球菌和EGFR之谜：揭示血脑屏障穿越的新机制。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105540

Jingyu Zhao , Wei Fang , Yangjie Gao , Zhenzong Fa , Guizhen Wang , Julin Gu

This study aims to investigate the molecular mechanisms by which Cryptococcus neoformans (C. neoformans) crosses the blood-brain barrier (BBB), focusing specifically on the role of the epidermal growth factor receptor (EGFR) and its ligand, HB-EGF. Cryptococcal meningitis, caused by C. neoformans, has a high mortality rate and poses a significant threat to global public health. Research indicates that C. neoformans employs various strategies to cross the BBB, with transcellular transport being particularly critical. We observed that C. neoformans infection significantly upregulates the expression and phosphorylation of EGFR in brain microvascular endothelial cells (BMECs). Silencing EGFR using siRNA technology resulted in a marked decrease in the ability of C. neoformans to traverse the BMEC monolayer. Furthermore, C. neoformans infection also upregulates EGFR ligands, such as HB-EGF, in BMECs, thereby activating the EGFR signaling pathway. This activation involves the engagement of ADAM family metalloproteinases and the metalloprotease Mpr1 from C. neoformans. The findings of this study underscore the critical role of the host EGFR signaling pathway in the ability of C. neoformans to cross the BBB and highlight potential targets for developing new therapies for infectious meningitis.

本研究旨在探讨新生隐球菌（C. neoformans）通过血脑屏障（BBB）的分子机制，特别关注表皮生长因子受体（EGFR）及其配体HB-EGF的作用。由新生隐球菌引起的隐球菌脑膜炎死亡率高，对全球公共卫生构成重大威胁。研究表明，新生C.采用多种策略穿越血脑屏障，其中跨细胞运输尤为关键。我们观察到新生C.感染显著上调脑微血管内皮细胞（BMECs）中EGFR的表达和磷酸化。使用siRNA技术沉默EGFR导致新生C.穿越BMEC单层的能力显著下降。此外，新生梭状芽胞杆菌感染还会上调bmec中的EGFR配体，如HB-EGF，从而激活EGFR信号通路。这种激活涉及ADAM家族金属蛋白酶和新生C.的金属蛋白酶Mpr1的参与。这项研究的发现强调了宿主EGFR信号通路在新生C.穿过血脑屏障的能力中的关键作用，并强调了开发感染性脑膜炎新疗法的潜在靶点。

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引用次数: 0

Neutrophils display antibacterial defense via non-canonical LC3 decoration of extracellular bacteria 中性粒细胞通过胞外细菌的非规范LC3装饰显示抗菌防御。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105545

Jurate Skerniskyte , Marina Valente Barroso , Johana Chicher , Philippe Hammann , Valerie Demais , Kathryn Wright , Serge Mostowy , Benoit S. Marteyn

Neutrophils play a pivotal role in the innate immune response to bacterial infection, being one of the first immune cells to reach infectious sites. Bacterial infection may induce neutrophil degranulation, production of neutrophil extracellular traps (NETs), or pathogen phagocytosis. While LC3 is typically linked to autophagy, here we observed a non-canonical role of LC3 when peripheral neutrophils interact with bacteria both in vivo and in vitro, using Shigella spp. as a model. Upon incubation with neutrophils, extracellular bacteria became labelled by LC3 (LC3+) along with granules-localised antimicrobial components, such as lactotransferrin, defensin, elastase, and myeloperoxidase, as demonstrated by mass spectrometry. Co-localisation of LC3 and plasma membrane-specific dyes indicated that neutrophil plasma membrane-derived elongated structures covering bacteria were responsible for the labelling. This phenomenon was associated with bacterial growth restriction and bacterial cell-death induction. Testing with specific inhibitors demonstrated that this labelling was dependent on functional V-type ATP synthase. Covering bacteria with membrane-derived elongated structures enhanced the subsequent phagocytosis of bacteria by neutrophils. Finally, the LC3 labelling rate increased with higher bacterial burden. In conclusion, we propose that this defense mechanism is beneficial when the burden of bacterial infection overwhelms neutrophils' capacity for phagocytosis.

中性粒细胞是最早到达感染部位的免疫细胞之一，在对细菌感染的先天免疫反应中起着关键作用。细菌感染可诱导中性粒细胞脱颗粒，产生中性粒细胞胞外陷阱（NETs），或病原体吞噬。虽然LC3通常与自噬有关，但在这里，我们以志贺氏菌为模型，观察到当外周中性粒细胞在体内和体外与细菌相互作用时，LC3的非规范作用。在与中性粒细胞孵卵后，胞外细菌被LC3 （LC3+）和颗粒局部抗菌成分标记，如乳转铁蛋白、防御素、弹性酶和髓过氧化物酶，如质谱证实。LC3和质膜特异性染料的共定位表明，覆盖细菌的中性粒细胞质膜衍生的细长结构负责标记。这种现象与细菌生长限制和细菌细胞死亡诱导有关。特异性抑制剂的测试表明，这种标记依赖于功能性v型ATP合酶。用膜衍生的细长结构覆盖细菌增强了中性粒细胞随后对细菌的吞噬作用。最后，LC3标记率随着细菌负荷的增加而增加。总之，我们认为当细菌感染的负担超过中性粒细胞的吞噬能力时，这种防御机制是有益的。

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引用次数: 0

The impact of DeoRF on Listeria monocytogenes stress tolerance and survival DeoRF对单核增生李斯特菌耐受性及存活的影响。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105549

Seto C. Ogunleye, Minna Hassan, Mark L. Lawrence, Hossam Abdelhamed

Listeria monocytogenes, a significant foodborne pathogen, is known for its remarkable adaptability to diverse environments through a genomic regulatory network that coordinates metabolic activities and stress responses. However, many of these genomic elements remain poorly understood. This study investigates the role of deoRF, a previously understudied member of the DeoR-family, in oxidative tolerance, intracellular infection, and virulence. Interestingly, the F2365ΔdeoRF strain showed no significant growth defects in minimal media with glucose, fructose, or sucrose, suggesting that DeoRF does not play a critical role in the uptake or metabolism of these sugars. Results showed that DeoRF plays a significant role in the ability of L. monocytogenes to adapt to oxidative stress. Additionally, DeoRF contributed significantly to cell-to-cell spread in L2 fibroblast cells, intracellular replication in macrophage cells, and virulence in mice following both intravenous and oral infection models. Transcriptomic analysis further revealed that deletion of deoRF caused downregulation of propanediol utilization, transcription regulators, phosphotransferase systems (PTS), complex networks of transcriptional regulators, and proteases genes. Conversely, sigma B regulator genes were upregulated in the ΔdeoRF strain. This study demonstrates that L. monocytogenes DeoRF contributes to pathogenicity and stress adaptation, and it is an important contributor to the complex listerial regulatory network.

单核细胞增生李斯特菌是一种重要的食源性病原体，它通过一个协调代谢活动和应激反应的基因组调控网络，对不同环境具有显著的适应性。然而，许多这些基因组元素仍然知之甚少。本研究调查了deoRF在氧化耐受性、细胞内感染和毒力中的作用，deoRF是deor家族中一个先前未被充分研究的成员。有趣的是，F2365ΔdeoRF菌株在含有葡萄糖、果糖或蔗糖的最小培养基中没有表现出明显的生长缺陷，这表明DeoRF在这些糖的摄取或代谢中没有发挥关键作用。结果表明，DeoRF在单核增生乳杆菌适应氧化应激的能力中起着重要作用。此外，DeoRF显著促进L2成纤维细胞的细胞间扩散、巨噬细胞的细胞内复制以及静脉和口腔感染模型小鼠的毒力。转录组学分析进一步表明，deoRF的缺失导致丙二醇利用、转录调节因子、磷酸转移酶系统（PTS）、转录调节因子复杂网络和蛋白酶基因的下调。相反，在ΔdeoRF菌株中，sigma B调节基因上调。本研究表明，单核增生乳杆菌DeoRF参与致病性和胁迫适应，是复杂菌体调控网络的重要组成部分。

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引用次数: 0

Effects of sequential administration of phage cocktail, ciprofloxacin, and caspofungin on Staphylococcus aureus and Candida albicans dual-species biofilms 噬菌体鸡尾酒、环丙沙星和卡泊芬金序贯给药对金黄色葡萄球菌和白色念珠菌双种生物膜的影响。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105531

Marta Gliźniewicz , Barbara Dołęgowska , Adrian Augustyniak , Rafał Rakoczy , Tomasz Kędzierski , Ewa Mijowska , Bartłomiej Grygorcewicz

Polymicrobial biofilms, including inter-kingdom ones, represent another threat in the post-antibiotic era. Therefore, many alternative solutions are being investigated, including phage-antibiotic synergy (PAS), which may be more effective due to the differing mechanisms of action of drugs and phages. In this study, we evaluated how different sequences of administering a bacteriophage cocktail, ciprofloxacin, and caspofungin affect the eradication of S. aureus and C. albicans in vitro (planktonic culture and in biofilms). In liquid culture, the phage → caspofungin → ciprofloxacin treatment completely eradicated both organisms. In biofilms, the most effective regimens were either the simultaneous application of all three agents or phages + ciprofloxacin followed by caspofungin. Therefore, the sequence of administration of drugs and phages is a key factor in achieving effective therapy and revealing the most synergistic combinations.

多微生物生物膜，包括跨界生物膜，是后抗生素时代的另一个威胁。因此，许多替代方案正在研究中，包括噬菌体-抗生素协同作用（PAS），由于药物和噬菌体的作用机制不同，它可能更有效。在这项研究中，我们评估了噬菌体混合物、环丙沙星和卡泊芬金不同的给药顺序对体外（浮游培养和生物膜）根除金黄色葡萄球菌和白色念珠菌的影响。在液体培养中，噬菌体→卡泊真菌素→环丙沙星处理完全根除这两种微生物。在生物膜中，最有效的方案是同时应用所有三种药物或噬菌体+环丙沙星再加卡泊芬金。因此，药物和噬菌体的给药顺序是实现有效治疗和揭示最协同的组合的关键因素。

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引用次数: 0

TLR3 regulation and cytokine response during BoAHV-1 and BoAHV-5 infection of neuronal-like cells 神经元样细胞感染BoAHV-1和BoAHV-5时TLR3的调控和细胞因子反应。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105558

María Belén Brunner , Juan José Rosales , Marla Ladera , María Victoria Nieto Farías , Andrea Verna , Sandra Pérez

Varicellovirus bovinealpha (BoAHV) 1 and 5 are alphaherpesviruses that differ in their neuropathogenic potential. While BoAHV-5 causes necrotizing meningoencephalitis in calves, neurological cases associated with BoAHV-1 are less frequent. In this study we used differentiated the human neuroblastoma cell line (SH-SY5Y) to evaluate the mRNA expression of Toll-like receptor 3 (TLR3), its adaptor molecule TRIF and the production of interferons and pro-inflammatory cytokines during infection with both alphaherpesviruses. TLR3 was activated with polyinosinic acid: polycytidylic acid (Poly I:C) and it was genetically silenced using TLR3-targeted siRNA. BoAHV infection induced an initial upregulation of TLR3, followed by a notable decrease, particularly in BoAHV-5-infected cells. TLR3 knockdown was effective for 72 h in uninfected cells although it was reversed shortly after BoAHV infection. In the presence of activated TLR3, virus titers remained high, indicating limited antiviral activity of TLR3 signaling. TRIF was downregulated early after infection, implying viral interference with the innate immune response. In contrast, Poly I:C upregulated TLR3 and TRIF. IFN-β was upregulated following infection and IFN-α/β, TNF-α and IL-6 were induced even in TLR3-silenced cells, implicating the involvement of alternative signaling pathways. These findings demonstrate how bovine alphaherpesviruses modulate the innate immune mechanisms, highlighting differential viral strategies to evade the immune response which may contribute to neuropathogenesis.

牛α水痘病毒（BoAHV） 1和5是具有不同神经致病性的α疱疹病毒。虽然BoAHV-5引起小牛坏死性脑膜脑炎，但与BoAHV-1相关的神经系统病例较少。在这项研究中，我们使用分化的人神经母细胞瘤细胞系（SH-SY5Y）来评估toll样受体3 （TLR3）及其接头分子TRIF的mRNA表达以及干扰素和促炎细胞因子在两种α疱疹病毒感染期间的产生。TLR3被多肌苷酸：多胞苷酸（Poly I:C）激活，并被TLR3靶向siRNA基因沉默。BoAHV感染诱导TLR3的初始上调，随后显著降低，特别是在BoAHV-5感染的细胞中。TLR3敲除在未感染的细胞中有效72小时，但在BoAHV感染后不久就会逆转。在激活的TLR3存在的情况下，病毒滴度仍然很高，表明TLR3信号的抗病毒活性有限。TRIF在感染后早期下调，暗示病毒干扰了先天免疫反应。相反，Poly I:C上调TLR3和TRIF。感染后IFN-β表达上调，即使在tlr3沉默的细胞中，IFN-α/β、TNF-α和IL-6也被诱导，这暗示了其他信号通路的参与。这些发现证明了牛甲疱疹病毒如何调节先天免疫机制，突出了不同的病毒策略来逃避免疫反应，这可能有助于神经发病机制。

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引用次数: 0

Therapeutic strategies to combat Staphylococcus aureus infections in cystic fibrosis 抗囊性纤维化金黄色葡萄球菌感染的治疗策略。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Microbes and Infection

Pub Date : 2025-09-01 DOI: 10.1016/j.micinf.2025.105546

Aygun Israyilova , Gabriele Trespidi , Viola Camilla Scoffone , Silvia Buroni

Staphylococcus aureus infections remain a great concern in people with cystic fibrosis also after the introduction of modulator therapy. Here we describe the state of the art of traditional and novel therapeutic strategies to fight both acute and chronic infections caused by sensitive and drug resistant strains.

在引入调节剂治疗后，金黄色葡萄球菌感染仍然是囊性纤维化患者非常关注的问题。在这里，我们描述了对抗敏感和耐药菌株引起的急性和慢性感染的传统和新型治疗策略的最新进展。

引用次数: 0