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The RNA from Pseudomonas aeruginosa Reduces Neutrophil Responses Favoring Bacterial Survival. 铜绿假单胞菌的 RNA 可降低中性粒细胞的反应,有利于细菌存活。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-09-18 DOI: 10.1159/000541414
Jose R Pittaluga, Federico Birnberg-Weiss, Agustina Serafino, Joselyn E Castro, Luis A Castillo, Daiana Martire-Greco, Paula Barrionuevo, Gabriela C Fernández, Verónica I Landoni

Introduction: Epithelial and endothelial cells modulate innate immune responses in the lung, including the arrival of neutrophils (PMN), which are crucial cells for the antibacterial host defense. Cells are exposed to prokaryotic RNA (pRNA) during bacterial infections and different pRNA may promote or attenuate the inflammatory response on different immune cells. Pseudomonas aeruginosa (PAE) can cause severe pneumonia and has several immune-evading mechanisms. The aim of this study was to determine the effects of the RNA from PAE (RNAPAE) on lung epithelial, endothelial cells, and PMN, and its impact on bacterial elimination.

Methods: Purified total RNAPAE was used as a stimulus on a human lung epithelial cell line (Calu-6), human microvascular endothelial cell line HMEC-1 and isolated healthy human PMN. Activation and cytokine secretion were evaluated. In addition, PMN elimination of live ECO or PAE was determined in the presence of RNAPAE.

Results: We found that RNAPAE either induced a pro-inflammatory response on Calu-6 and HMEC-1 or PMN. Pre-stimulation of PMN with RNAPAE diminished activation and chemotaxis induced by live bacteria. Moreover, we found that RNAPAE reduced phagocytosis of live ECO. Finally, we also found that non-degraded fragments of small RNA (<200 bp) were responsible for the PMN microbicidal attenuation during PAE elimination.

Conclusion: Our results indicated that short fragments of RNAPAE diminished the immune response of PMN favoring bacterial survival.

导言上皮细胞和内皮细胞可调节肺部的先天性免疫反应,包括中性粒细胞(PMN)的到来,而中性粒细胞是抗菌宿主防御的关键细胞。在细菌感染过程中,细胞会接触到原核 RNA(pRNA),不同的 pRNA 可能会促进或减弱不同免疫细胞的炎症反应。铜绿假单胞菌(PAE)可导致重症肺炎,并具有多种免疫吞噬机制。本研究旨在确定来自 PAE 的 RNA(RNAPAE)对肺上皮细胞、内皮细胞和 PMN 的影响及其对细菌清除的影响:方法:用纯化的总 RNAPAE 刺激人肺上皮细胞系(Calu-6)、人微血管内皮细胞系 HMEC-1 和分离的健康人 PMN。对活化和细胞因子分泌进行了评估。此外,还测定了 PMN 在 RNAPAE 存在下消除活 ECO 或 PAE 的情况:结果:我们发现 RNAPAE 可诱导 Calu-6 和 HMEC-1 或 PMN 产生促炎反应。用 RNAPAE 预先刺激 PMN 可减少活细菌诱导的活化和趋化。此外,我们还发现 RNAPAE 减少了活 ECO 的吞噬作用。最后,我们还发现,在消除 PAE 的过程中,小 RNA 的非降解片段(<200 bp)是导致 PMN 杀微生物作用减弱的原因:我们的研究结果表明,RNAPAE 的短片段会降低 PMN 的免疫反应,有利于细菌存活。
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引用次数: 0
Metabolism Shapes Immune Responses to Staphylococcus aureus. 代谢影响对金黄色葡萄球菌的免疫反应。
IF 5.3 3区 医学 Q1 Medicine Pub Date : 2024-01-01 Epub Date: 2023-11-28 DOI: 10.1159/000535482
Prabhakar Arumugam, Tammy Kielian

Background: Staphylococcus aureus (S. aureus) is a common cause of hospital- and community-acquired infections that can result in various clinical manifestations ranging from mild to severe disease. The bacterium utilizes different combinations of virulence factors and biofilm formation to establish a successful infection, and the emergence of methicillin- and vancomycin-resistant strains introduces additional challenges for infection management and treatment.

Summary: Metabolic programming of immune cells regulates the balance of energy requirements for activation and dictates pro- versus anti-inflammatory function. Recent investigations into metabolic adaptations of leukocytes and S. aureus during infection indicate that metabolic crosstalk plays a crucial role in pathogenesis. Furthermore, S. aureus can modify its metabolic profile to fit an array of niches for commensal or invasive growth.

Key messages: Here we focus on the current understanding of immunometabolism during S. aureus infection and explore how metabolic crosstalk between the host and S. aureus influences disease outcome. We also discuss how key metabolic pathways influence leukocyte responses to other bacterial pathogens when information for S. aureus is not available. A better understanding of how S. aureus and leukocytes adapt their metabolic profiles in distinct tissue niches may reveal novel therapeutic targets to prevent or control invasive infections.

金黄色葡萄球菌(金黄色葡萄球菌)是医院和社区获得性感染的常见原因,可导致从轻微到严重疾病的各种临床表现。细菌利用不同的毒力因子和生物膜形成组合来建立成功的感染,耐甲氧西林和万古霉素菌株的出现为感染管理和治疗带来了额外的挑战。免疫细胞的代谢程序调节了激活所需能量的平衡,并决定了促炎与抗炎功能。最近对白细胞和金黄色葡萄球菌在感染过程中的代谢适应的研究表明,代谢串扰在发病机制中起着至关重要的作用。此外,金黄色葡萄球菌可以修改其代谢谱,以适应共生或侵袭性生长的一系列生态位。在这里,我们着重于目前对金黄色葡萄球菌感染期间免疫代谢的理解,并探讨宿主和金黄色葡萄球菌之间的代谢串音如何影响疾病结局。我们还讨论了当金黄色葡萄球菌的信息不可用时,关键代谢途径如何影响白细胞对其他细菌病原体的反应。更好地了解金黄色葡萄球菌和白细胞如何在不同的组织龛中适应其代谢谱,可能会揭示新的治疗靶点,以预防或控制侵袭性感染。
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引用次数: 0
Mechanisms and Therapeutic Strategies for MAFLD Targeting TLR4 Signaling Pathways. 针对 TLR4 信号通路的 MAFLD 机制和治疗策略。
IF 5.3 3区 医学 Q1 Medicine Pub Date : 2024-01-01 Epub Date: 2023-12-21 DOI: 10.1159/000535524
Guanghui Ren, Changchuan Bai, Sitong Yi, Qingwei Cong, Ying Zhu

Background: Metabolic-associated fatty liver disease (MAFLD) is one of the most common chronic liver diseases. The underlying pathophysiological mechanisms are intricate and involve various factors. Unfortunately, there is currently a lack of available effective treatment options. Toll-like receptors (TLRs) are a group of pattern-recognition receptors that are responsible for activating the innate immune system. Research has demonstrated that TLR4 plays a pivotal role in the progression of MAFLD by facilitating the pathophysiological mechanisms.

Summary: Lipid peroxidation, pro-inflammatory factors, insulin resistance (IR), and dysbiosis of intestinal microbiota are considered as the pathogenic mechanisms of MAFLD. This review summarizes the impact of TLR4 signaling pathways on the progression of MAFLD, specifically in relation to lipid metabolic disorders, IR, oxidative stress, and gut microbiota disorders. Additionally, we emphasize the potential therapeutic approaches for MAFLD that target TLR4 signaling pathways, including the use of plant extracts, traditional Chinese medicines, probiotics, pharmaceuticals such as peroxisome proliferator-activated receptor antagonists and farnesol X agonists, and lifestyle modifications such as dietary changes and exercise also considered. Furthermore, TLR4 signaling pathways have also been linked to the lean MAFLD.

Key messages: TLR4 plays a crucial role in MAFLD by triggering IR, buildup of lipids, imbalance in gut microbiota, oxidative stress, and initiation of immune responses. The mitigation of MAFLD can be accomplished by suppressing the TLR4 signaling pathway. In the future, it could potentially emerge as a therapeutic target for the condition.

背景:代谢相关性脂肪肝(MAFLD)是最常见的慢性肝病之一:代谢相关性脂肪肝(MAFLD)是最常见的慢性肝病之一。其潜在的病理生理机制错综复杂,涉及多种因素。遗憾的是,目前缺乏有效的治疗方案。Toll 样受体(TLRs)是一组模式识别受体,负责激活先天性免疫系统。摘要:脂质过氧化、促炎、胰岛素抵抗(IR)和肠道微生物群失调被认为是 MAFLD 的致病机制。本综述总结了TLR4信号通路对MAFLD进展的影响,特别是与脂质代谢紊乱、IR、氧化应激和肠道微生物群紊乱的关系。此外,我们还强调了针对 TLR4 信号通路的 MAFLD 潜在治疗方法,包括使用植物提取物、传统中药、益生菌、PPAR 拮抗剂和 FXR 激动剂等药物,以及改变饮食和运动等生活方式。此外,TLR4 信号通路也与 MAFLD 瘦人症有关:TLR4通过引发胰岛素抵抗、脂质堆积、肠道微生物群失衡、氧化应激和免疫反应的启动,在MAFLD中发挥着至关重要的作用。可以通过抑制 TLR4 信号通路来缓解 MAFLD。未来,它有可能成为该疾病的治疗靶点。
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引用次数: 0
Impact of Extreme Prematurity, Chorioamnionitis, and Sepsis on Neonatal Monocyte Characteristics and Functions. 极度早产、绒毛膜羊膜炎和败血症对新生儿单核细胞特征和功能的影响。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-09-14 DOI: 10.1159/000541468
Khaleda Rahman Qazi, Dhanapal Govindaraj, Magalí Martí, Ymke de Jong, Georg Bach Jensen, Thomas Abrahamsson, Maria C Jenmalm, Eva Sverremark-Ekström

Introduction: The innate branch of the immune system is important in early life, in particular for infants born preterm.

Methods: We performed a longitudinal analysis of the peripheral monocyte compartment in extremely preterm children from a randomized, placebo-controlled study of probiotic supplementation. PBMCs and fecal samples were collected at several timepoints during the first months of life. Monocyte characteristics were analyzed by flow cytometry, and LPS-stimulated PBMC culture supernatants were analyzed by Luminex or ELISA. Plasma cytokines and gut microbiota composition were analyzed by ELISA and 16S rRNA-sequencing, respectively.

Results: The extremely preterm infants had persistent alterations in their monocyte characteristics that were further aggravated in chorioamnionitis cases. They showed a markedly reduced TLR4 expression and hampered LPS-stimulated cytokine responses 14 days after birth. Notably, at later timepoints, TLR4 expression and LPS responses no longer correlated. Sepsis during the first weeks of life strongly associated with increased pro-inflammatory, and reduced IL-10, responses also at postmenstrual week 36. Further, we report a correlation between gut microbiota features and monocyte phenotype and responses, but also that probiotic supplementation associated with distinct monocyte phenotypic characteristics, without significantly influencing their responsiveness.

Conclusion: Extremely preterm infants have monocyte characteristics and functional features that deviate from infants born full-term. Some of these differences persist until they reach an age corresponding to full-term, potentially making them more vulnerable to microbial exposures during the first months of life.

简介免疫系统的先天分支在生命早期非常重要,对于早产儿尤其如此:我们对一项补充益生菌的随机安慰剂对照研究中的极早产儿的外周单核细胞群进行了纵向分析。我们在婴儿出生后最初几个月的几个时间点收集了他们的白细胞和粪便样本。单核细胞特征通过流式细胞术进行分析,LPS 刺激的 PBMC 培养上清液通过 Luminex 或 ELISA 进行分析。血浆细胞因子和肠道微生物群组成分别通过 ELISA 和 16S rRNA 测序法进行分析:结果:极早产儿的单核细胞特征发生了持续性改变,在绒毛膜羊膜炎病例中进一步加剧。出生 14 天后,他们的 TLR4 表达明显减少,LPS 刺激的细胞因子反应受到阻碍。值得注意的是,在以后的时间点,TLR4 的表达和 LPS 的反应不再相关。在月经后第 36 周,生命最初几周的败血症与促炎症反应的增加和 IL-10 反应的减少密切相关。此外,我们还报告了肠道微生物群特征与单核细胞表型和反应之间的相关性,而且益生菌补充与不同的单核细胞表型特征相关,但不会显著影响其反应性:结论:极早产儿的单核细胞特性和功能特征与足月出生的婴儿不同。结论:极早产儿的单核细胞特征和功能特点与足月儿不同,其中一些差异会持续到足月儿,这可能会使他们在出生后的头几个月更容易受到微生物的影响。
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引用次数: 0
Immunometabolites Direct the Pathogenesis of Bacterial Infection. 免疫代谢物引导着细菌感染的发病机制。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-07-01 DOI: 10.1159/000540093
Alice Prince
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引用次数: 0
Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore. 模式识别受体与免疫代谢重编程:我们的认知与探索。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-05-13 DOI: 10.1159/000539278
Vijay Kumar, John H Stewart Iv

Background: Evolutionarily, immune response is a complex mechanism that protects the host from internal and external threats. Pattern-recognition receptors (PRRs) recognize MAMPs, PAMPs, and DAMPs to initiate a protective pro-inflammatory immune response. PRRs are expressed on the cell membranes by TLR1, 2, 4, and 6 and in the cytosolic organelles by TLR3, 7, 8, and 9, NLRs, ALRs, and cGLRs. We know their downstream signaling pathways controlling immunoregulatory and pro-inflammatory immune response. However, the impact of PRRs on metabolic control of immune cells to control their pro- and anti-inflammatory activity has not been discussed extensively.

Summary: Immune cell metabolism or immunometabolism critically determines immune cells' pro-inflammatory phenotype and function. The current article discusses immunometabolic reprogramming (IR) upon activation of different PRRs, such as TLRs, NLRs, cGLRs, and RLRs. The duration and type of PRR activated, species studied, and location of immune cells to specific organ are critical factors to determine the IR-induced immune response.

Key message: The work herein describes IR upon TLR, NLR, cGLR, and RLR activation. Understanding IR upon activating different PRRs is critical for designing better immune cell-specific immunotherapeutics and immunomodulators targeting inflammation and inflammatory diseases.

背景:在进化过程中,免疫反应是一种保护宿主免受内外威胁的复杂机制。模式识别受体(PRRs)能识别 MAMPs、PAMPs 和 DAMPs,从而启动保护性促炎免疫反应。TLR1、2、4 和 6 在细胞膜上表达 PRRs,TLR3、7、8 和 9、NLRs、ALRs 和 cGLRs 则在细胞器中表达 PRRs。我们知道它们的下游信号通路控制着免疫调节和促炎免疫反应。摘要:免疫细胞代谢或免疫代谢决定着免疫细胞的促炎表型和功能。本文讨论了不同 PRRs(如 TLRs、NLRs、cGLRs 和 RLRs)激活时的免疫代谢重编程(IR)。激活 PRR 的持续时间和类型、研究的物种以及免疫细胞在特定器官的位置是决定 IR 诱导的免疫反应的关键因素:本文介绍了TLR、NLR、cGLR和RLR激活后的IR。了解激活不同 PRRs 时的 IR 对于设计更好的免疫细胞特异性免疫疗法和针对炎症和炎症性疾病的免疫调节剂至关重要。
{"title":"Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore.","authors":"Vijay Kumar, John H Stewart Iv","doi":"10.1159/000539278","DOIUrl":"10.1159/000539278","url":null,"abstract":"<p><strong>Background: </strong>Evolutionarily, immune response is a complex mechanism that protects the host from internal and external threats. Pattern-recognition receptors (PRRs) recognize MAMPs, PAMPs, and DAMPs to initiate a protective pro-inflammatory immune response. PRRs are expressed on the cell membranes by TLR1, 2, 4, and 6 and in the cytosolic organelles by TLR3, 7, 8, and 9, NLRs, ALRs, and cGLRs. We know their downstream signaling pathways controlling immunoregulatory and pro-inflammatory immune response. However, the impact of PRRs on metabolic control of immune cells to control their pro- and anti-inflammatory activity has not been discussed extensively.</p><p><strong>Summary: </strong>Immune cell metabolism or immunometabolism critically determines immune cells' pro-inflammatory phenotype and function. The current article discusses immunometabolic reprogramming (IR) upon activation of different PRRs, such as TLRs, NLRs, cGLRs, and RLRs. The duration and type of PRR activated, species studied, and location of immune cells to specific organ are critical factors to determine the IR-induced immune response.</p><p><strong>Key message: </strong>The work herein describes IR upon TLR, NLR, cGLR, and RLR activation. Understanding IR upon activating different PRRs is critical for designing better immune cell-specific immunotherapeutics and immunomodulators targeting inflammation and inflammatory diseases.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11250681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140916636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Development of a C3 Humanized Rat as a New Model for Evaluating Novel C3 Inhibitors. C3人源化大鼠作为评价新型C3抑制剂的新模型的建立。
IF 5.3 3区 医学 Q1 Medicine Pub Date : 2024-01-01 Epub Date: 2023-11-30 DOI: 10.1159/000534963
Jin Y Chen, Lingjun Zhang, Maojing Yang, Elizabeth D Hughes, Zachary T Freeman, Thomas L Saunders, Feng Lin

Introduction: C3 is central for all complement activation pathways, thus making it an attractive therapeutic target. Many C3-targeted agents are under extensive development with one already approved for clinical use. However, most, if not all, C3 inhibitors are human or nonhuman primate C3-specific, making evaluating their efficacies in vivo before a clinical trial extremely difficult and costly.

Methods: We first studied the compatibility of human C3 in the rat complement system, then developed a C3 humanized rat using the CRISPR/Cas9 technology. We thoroughly characterized the resultant human C3 humanized rats and tested the treatment efficacy of an established primate-specific C3 inhibitor in a model of complement-mediated hemolysis in the C3 humanized rats.

Results: We found that supplementing human C3 protein into the C3-deficient rat blood restored its complement activity, which was inhibited by rat factor H or compstatin, suggesting that human C3 is compatible to the rat complement system. The newly developed C3 humanized rats appeared healthy and expressed human but not rat C3 without detectable spontaneous C3 activation. More importantly, complement-mediated hemolysis in the C3 humanized rats was also inhibited by compstatin both in vitro and in vivo.

Conclusion: The successfully developed C3 humanized rats provided a much-desired rodent model to evaluate novel C3 inhibitors in vivo as potential drugs.

C3是所有补体激活途径的中枢,因此是一个有吸引力的治疗靶点。许多靶向c3的药物正在广泛开发中,其中一种已经被批准用于临床。然而,大多数(如果不是全部的话)C3抑制剂是人类或非人类灵长类动物C3特异性的,这使得在临床试验之前评估其体内疗效极其困难和昂贵。方法:首先研究人C3在大鼠补体系统中的相容性,然后利用CRISPR/Cas9技术培养C3人源化大鼠。我们彻底表征了由此产生的人C3人源化大鼠,并在补体介导的C3人源化大鼠溶血模型中测试了一种已建立的灵长类特异性C3抑制剂的治疗效果。结果:我们发现,在缺乏C3的大鼠血液中补充人C3蛋白可以恢复其补体活性,而补体活性被大鼠因子H或压缩抑素抑制,这表明人C3与大鼠补体系统兼容。新发育的C3人源化大鼠表现健康,表达人C3而非大鼠C3,没有可检测到的自发C3激活。更重要的是,补体介导的溶血在C3人源化大鼠体内和体外均被压缩抑素抑制。结论:成功培育的C3人源化大鼠为体内评价新型C3抑制剂作为潜在药物提供了理想的啮齿类动物模型。
{"title":"Development of a C3 Humanized Rat as a New Model for Evaluating Novel C3 Inhibitors.","authors":"Jin Y Chen, Lingjun Zhang, Maojing Yang, Elizabeth D Hughes, Zachary T Freeman, Thomas L Saunders, Feng Lin","doi":"10.1159/000534963","DOIUrl":"10.1159/000534963","url":null,"abstract":"<p><strong>Introduction: </strong>C3 is central for all complement activation pathways, thus making it an attractive therapeutic target. Many C3-targeted agents are under extensive development with one already approved for clinical use. However, most, if not all, C3 inhibitors are human or nonhuman primate C3-specific, making evaluating their efficacies in vivo before a clinical trial extremely difficult and costly.</p><p><strong>Methods: </strong>We first studied the compatibility of human C3 in the rat complement system, then developed a C3 humanized rat using the CRISPR/Cas9 technology. We thoroughly characterized the resultant human C3 humanized rats and tested the treatment efficacy of an established primate-specific C3 inhibitor in a model of complement-mediated hemolysis in the C3 humanized rats.</p><p><strong>Results: </strong>We found that supplementing human C3 protein into the C3-deficient rat blood restored its complement activity, which was inhibited by rat factor H or compstatin, suggesting that human C3 is compatible to the rat complement system. The newly developed C3 humanized rats appeared healthy and expressed human but not rat C3 without detectable spontaneous C3 activation. More importantly, complement-mediated hemolysis in the C3 humanized rats was also inhibited by compstatin both in vitro and in vivo.</p><p><strong>Conclusion: </strong>The successfully developed C3 humanized rats provided a much-desired rodent model to evaluate novel C3 inhibitors in vivo as potential drugs.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10786584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138460291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Murine Ribonuclease 6 Limits Bacterial Dissemination during Experimental Urinary Tract Infection. 小鼠核糖核酸酶 6 限制了实验性尿路感染过程中的细菌扩散
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-05-14 DOI: 10.1159/000539177
Hanna Cortado, Macie Kercsmar, Birong Li, Gabriela Vasquez-Martinez, Sudipti Gupta, Christina Ching, Gregory Ballash, Israel Cotzomi-Ortega, Yuriko I Sanchez-Zamora, Ester Boix, Diana Zepeda-Orozco, Ashley R Jackson, John David Spencer, Juan de Dios Ruiz-Rosado, Brian Becknell

Introduction: The ribonuclease (RNase) A superfamily encodes cationic antimicrobial proteins with potent microbicidal activity toward uropathogenic bacteria. Ribonuclease 6 (RNase6) is an evolutionarily conserved, leukocyte-derived antimicrobial peptide with potent microbicidal activity toward uropathogenic Escherichia coli (UPEC), the most common cause of bacterial urinary tract infections (UTIs). In this study, we generated Rnase6-deficient mice to investigate the hypothesis that endogenous RNase 6 limits host susceptibility to UTI.

Methods: We generated a Rnase6EGFP knock-in allele to identify cellular sources of Rnase6 and determine the consequences of homozygous Rnase6 deletion on antimicrobial activity and UTI susceptibility.

Results: We identified monocytes and macrophages as the primary cellular sources of Rnase6 in bladders and kidneys of Rnase6EGFP/+ mice. Rnase6 deficiency (i.e., Rnase6EGFP/EGFP) resulted in increased upper urinary tract UPEC burden during experimental UTI, compared to Rnase6+/+ controls. UPEC displayed increased intracellular survival in Rnase6-deficient macrophages.

Conclusion: Our findings establish that RNase6 prevents pyelonephritis by promoting intracellular UPEC killing in monocytes and macrophages and reinforce the overarching contributions of endogenous antimicrobial RNase A proteins to host UTI defense.

简介:核糖核酸酶(RNase)A超家族编码的阳离子抗菌蛋白对尿路病原菌具有强大的杀微生物活性。核糖核酸酶 6(RNase6)是一种进化保守的白细胞衍生抗菌肽,对尿路感染(UTI)中最常见的细菌--尿路致病性大肠杆菌(UPEC)具有强大的杀菌活性。在这项研究中,我们产生了 Rnase6 缺乏小鼠,以研究内源性 RNase 6 限制宿主对 UTI 易感性的假设:我们产生了一个 Rnase6EGFP 基因敲入等位基因,以确定 Rnase6 的细胞来源,并确定同源 Rnase6 缺失对抗菌活性和 UTI 易感性的影响:结果:我们确定单核细胞和巨噬细胞是 Rnase6EGFP/+ 小鼠膀胱和肾脏中 Rnase6 的主要细胞来源。与 Rnase6+/+ 对照组相比,Rnase6 缺乏(即 Rnase6EGFP/EGFP)导致实验性 UTI 期间上尿路 UPEC 负担增加。UPEC 在缺乏 Rnase6 的巨噬细胞中的细胞内存活率增加:我们的研究结果证实,RNase6 可通过促进单核细胞和巨噬细胞杀死细胞内的 UPEC 来预防肾盂肾炎,并加强了内源性抗微生物 RNase A 蛋白对宿主 UTI 防御的重要贡献。
{"title":"Murine Ribonuclease 6 Limits Bacterial Dissemination during Experimental Urinary Tract Infection.","authors":"Hanna Cortado, Macie Kercsmar, Birong Li, Gabriela Vasquez-Martinez, Sudipti Gupta, Christina Ching, Gregory Ballash, Israel Cotzomi-Ortega, Yuriko I Sanchez-Zamora, Ester Boix, Diana Zepeda-Orozco, Ashley R Jackson, John David Spencer, Juan de Dios Ruiz-Rosado, Brian Becknell","doi":"10.1159/000539177","DOIUrl":"10.1159/000539177","url":null,"abstract":"<p><strong>Introduction: </strong>The ribonuclease (RNase) A superfamily encodes cationic antimicrobial proteins with potent microbicidal activity toward uropathogenic bacteria. Ribonuclease 6 (RNase6) is an evolutionarily conserved, leukocyte-derived antimicrobial peptide with potent microbicidal activity toward uropathogenic Escherichia coli (UPEC), the most common cause of bacterial urinary tract infections (UTIs). In this study, we generated Rnase6-deficient mice to investigate the hypothesis that endogenous RNase 6 limits host susceptibility to UTI.</p><p><strong>Methods: </strong>We generated a Rnase6EGFP knock-in allele to identify cellular sources of Rnase6 and determine the consequences of homozygous Rnase6 deletion on antimicrobial activity and UTI susceptibility.</p><p><strong>Results: </strong>We identified monocytes and macrophages as the primary cellular sources of Rnase6 in bladders and kidneys of Rnase6EGFP/+ mice. Rnase6 deficiency (i.e., Rnase6EGFP/EGFP) resulted in increased upper urinary tract UPEC burden during experimental UTI, compared to Rnase6+/+ controls. UPEC displayed increased intracellular survival in Rnase6-deficient macrophages.</p><p><strong>Conclusion: </strong>Our findings establish that RNase6 prevents pyelonephritis by promoting intracellular UPEC killing in monocytes and macrophages and reinforce the overarching contributions of endogenous antimicrobial RNase A proteins to host UTI defense.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11250601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140922428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Obituary of Prof. Uli Theopold, 1957-2023. 乌利-西奥波德教授的讣告,1957-2023。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-01-08 DOI: 10.1159/000535642
Ylva Engström, Bruno Lemaitre, Dan Hultmark
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引用次数: 0
Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy. 揭开错综复杂的网络:补体激活决定败血症诱发凝血病的发病机制
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-05-31 DOI: 10.1159/000539502
Xin Wei, Ye Tu, Shuhong Bu, Guimei Guo, Hongbin Wang, Zhibin Wang

Background: Sepsis-associated coagulopathy specifically refers to widespread systemic coagulation activation accompanied by a high risk of hemorrhage and organ damage, which in severe cases manifests as disseminated intravascular coagulation (DIC), or even develops into multiple organ dysfunction syndrome (MODS). The complement system and the coagulation system as the main columns of innate immunity and hemostasis, respectively, undergo substantial activation after sepsis.

Summary: Dysfunction of the complement, coagulation/fibrinolytic cascades caused by sepsis leads to "thromboinflammation," which ultimately amplifies the systemic inflammatory response and accelerates the development of MODS. Recent studies have revealed that massive activation of the complement system exacerbates sepsis-induced coagulation and even results in DIC, which suggests that inhibition of complement activation may have therapeutic potential in the treatment of septic coagulopathy.

Key messages: Sepsis-associated thrombosis involves the upregulation or activation of procoagulant factors, down-regulation or inactivation of anticoagulant factors, and impairment of the fibrinolytic mechanism. This review aims to summarize the latest literature and analyze the underlying molecular mechanisms of the activation of the complement system on the abnormal coagulation cascades in sepsis.

脓毒症相关凝血病特指广泛的全身性凝血活化,伴随着出血和器官损伤的高风险,严重者表现为弥散性血管内凝血(DIC),甚至发展为多器官功能障碍综合征(MODS)。补体系统和凝血系统分别作为先天免疫和止血的主要支柱,在败血症后会被大量激活。脓毒症引起的补体、凝血和纤维蛋白溶解级联功能失调会导致 "血栓炎",最终扩大全身炎症反应,加速 MODS 的发展。最近的研究表明,补体系统的大量激活会加剧脓毒症引起的凝血,甚至导致 DIC,这表明抑制补体激活可能具有治疗脓毒症凝血病的潜力。脓毒症相关血栓形成涉及促凝因子的上调或激活、抗凝因子的下调或失活以及纤溶机制的损害。本综述旨在总结最新文献,分析脓毒症中补体系统激活导致凝血级联异常的潜在分子机制。
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引用次数: 0
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Journal of Innate Immunity
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