Infection and Immunity最新文献

{"title":"<i>Edwardsiella ictaluri</i> type III secretion system effector EseG modulates cytoskeletal dynamics and immune response in macrophages.","authors":"Lidiya Dubytska, Ranjan Koirala, Matthew Rogge, Ronald Thune","doi":"10.1128/iai.00525-24","DOIUrl":"10.1128/iai.00525-24","url":null,"abstract":"<p><p><i>Edwardsiella ictaluri</i> is a gram-negative enteric pathogen responsible for enteric septicemia of catfish. One of the critical virulence factors identified in <i>E. ictaluri</i> is its type III secretion system (T3SS). In this study, we report that the T3SS effector protein EseG requires the small chaperone protein EscB for translocation. EseG shows partial homology to two <i>Salmonella</i> T3SS effectors, SseG and SseF, as well as to the <i>Edwardsiella piscicida</i> effector EseG, all of which also require chaperones for translocation. Functionally, EseG interacts with and inactivates Ras homolog family member A (RhoA), a small GTPase that regulates the dynamic organization of the microtubule and actin cytoskeleton. The cytoskeleton is vital for cell morphology, polarity, adhesion, exocytosis, endocytosis, cytokinesis, and transcriptional control. We demonstrate that inactivation of RhoA by EseG leads to the disassembly of both the microtubule and actin cytoskeleton. Moreover, EseG was found to modulate immune responses by altering the expression of several pro-inflammatory interleukins and transcription factors, as well as cyclooxygenase-2 (COX-2). Reduced expression of COX-2 leads to decreased production of prostaglandin E2, a key mediator of inflammation. Additionally, a Δ<i>eseG</i> mutant strain exhibited reduced virulence and persistence in channel catfish (<i>Ictalurus punctatus</i>), underscoring the importance of EseG in the disease process. Collectively, our data highlight EseG as a critical factor in <i>E. ictaluri</i> pathogenesis, particularly in its ability to modulate host immune responses. By elucidating the function of EseG, this study contributes to a deeper understanding of <i>E. ictaluri</i> pathogenesis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0052524"},"PeriodicalIF":2.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600296","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}

{"title":"Vaginal microbiome and recurrent pregnancy loss.","authors":"Xingxing Yuan, Jiawei Gao, Ousman Bajinka, Xiaoling Feng","doi":"10.1128/iai.00053-25","DOIUrl":"10.1128/iai.00053-25","url":null,"abstract":"<p><p>The joy of every mother is to survive a healthy pregnancy and give birth to a healthy baby. However, until today, many couples are finding it difficult to welcome a baby. Among the factors that cause infertility and recurrent pregnancy loss (RPL) is the microbiome composition that inhabits the vaginal space. These microbiomes occupying the vaginal space play a role in balancing acids, pH, and metabolites to ensure a healthy vaginal environment that can prevent pregnancy loss. What is even more evident is that these microbiomes, when dominated by <i>Lactobacillus</i> spp.<i>,</i> prevent the growth of vaginal pathogens and reduce the risk of developing drug resistance. Although there is compelling evidence centered on the vaginal microbiome in promoting a healthy vagina, RPL is attributed to their altered or reduced <i>Lactobacillus</i> spp. While there are discrepancies in the literature, this review aimed to summarize the recent findings on vaginal microbiome and RPL. In addition, this mini review further revealed vaginal microbiota as biomarkers that can predict a healthy vagina and the risk of vaginal microbiome causing RPL. In addition, the immune response and metabolite changes in vaginal microbiome-related RPL, as well as some limitations to this intervention and prospective studies, are summarized.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0005325"},"PeriodicalIF":2.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527773","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}

{"title":"Targeting anemia-induced CD71⁺ reticulocytes protects mice from <i>Plasmodium</i> infection.","authors":"Sareh Zeydabadinejad, Jong Sung Anthony Kim, Anna Zheng, Mrunmayee Rajendra Kandalgaonkar, Prince Boakye Ababio, Amira Gohara, Matam Vijay-Kumar, Beng San Yeoh, Piu Saha","doi":"10.1128/iai.00093-25","DOIUrl":"10.1128/iai.00093-25","url":null,"abstract":"<p><p>Malaria, caused by <i>Plasmodium</i> spp., is a global health concern linked to anemia and increased mortality. Compensatory erythropoiesis seen during acute anemia results in an increased circulating reticulocyte count (i.e., immature RBC), a key factor in understanding the relationship between pre-existing anemia and <i>Plasmodium</i> burden. Reticulocytes in mice are marked by transferrin receptor (CD71⁺) and glycophorin A-associated protein (Ter119⁺). To model acute anemia with increased reticulocytes, C57BL/6J mice were either bled (i.e., phlebotomized) or administered phenylhydrazine before being infected with <i>Plasmodium yoelii</i> (<i>P. yoelii</i>), a mouse-specific strain with a preference for reticulocytes. In <i>P. yoelii</i>-infected anemic mice, we observed heightened parasitemia and significant body weight loss compared with non-anemic <i>P. yoelii</i>-infected mice. Additionally, serum inflammatory cytokines, erythropoietin, and liver injury markers, along with hemozoin deposition, significantly increased in anemic <i>P. yoelii</i>-infected mice. Blood transfusion from healthy normal donors to <i>P. yoelii</i>-infected anemic recipient mice ameliorated anemia by reducing overall reticulocyte count and increasing mature RBC count. Blood transfusion rescued body weight loss, decreased parasitemia, and reduced serum erythropoietin levels. Finally, to confirm the role of reticulocytes in <i>P. yoelii</i> infection, reticulocytes were depleted using anti-CD71 monoclonal antibody in <i>P. yoelii</i>-infected mice. We observed improvement in hematologic parameters and stark reduction in parasitemia in both pre-existing anemic and non-anemic <i>P. yoelii</i>-infected mice. Collectively, our results suggest that pre-existing anemia may increase the risk of <i>Plasmodium</i> infection due to the greater reticulocyte population. Anti-CD71 treatment in <i>Plasmodium</i> infection may offer a novel therapeutic strategy to combat <i>Plasmodium</i> infection and malaria.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0009325"},"PeriodicalIF":2.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540005","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}

{"title":"<i>Clostridioides difficile</i> toxins alter host metabolic pathway and bile acid homeostasis gene expression in colonic epithelium.","authors":"Stephanie A Thomas, Colleen M Pike, Cypress E Perkins, Sean T Brown, Xochilt M Espinoza Jaen, Arthur S McMillan, Casey M Theriot","doi":"10.1128/iai.00150-25","DOIUrl":"10.1128/iai.00150-25","url":null,"abstract":"<p><p>A major risk factor for acquiring <i>Clostridioides difficile</i> is antibiotic usage that disrupts a healthy microbial gut community, facilitating the establishment of infection. Once established, <i>C. difficile</i> secretes exotoxins (TcdA and TcdB) that are internalized into host colonic epithelial cells where they disrupt gut barrier function and induce hyperinflammation resulting in severe diarrhea and possibly leading to death. We employed three different platforms to explore gene expression of cells in the gut when exposed to <i>C. difficile</i> or its toxins, TcdA and TcdB. An antibiotic-treated mouse model of <i>Clostridioides difficile</i> infection (CDI) was used to identify differential gene expression with a NanoString Technologies mouse inflammatory gene panel consisting of 770 genes, including a subset of bile acid (BA) homeostasis and nuclear receptor genes. In the cecal tissue of mice with CDI, reduced expression was observed for genes involved in peroxisome proliferator-activated receptor (PPAR) signaling and cholesterol and glucose metabolism, while a significant increase in expression was observed for IL-17 related inflammatory genes. Similarly, Caco-2 cell culture and primary human colonic epithelial cells (hCE) exposed to toxins for 24 h showed altered expression in several PPAR-regulated and cholesterol metabolic genes similar to those found in mice. These cell culture experiments also revealed significant alterations in gene expression of the Farnesoid X receptor BA regulatory pathway. Together, these data suggest that exposure to <i>C. difficile</i> and its toxins may alter host cholesterol metabolic processes, including BA transport and synthesis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0015025"},"PeriodicalIF":2.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527770","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}

{"title":"Live fast, die young: neutrophils streamline their metabolism to maximize inflammation.","authors":"Bailey E Holder, Callista P Reber, Andrew J Monteith","doi":"10.1128/iai.00498-24","DOIUrl":"10.1128/iai.00498-24","url":null,"abstract":"<p><p>Neutrophils are the most abundant leukocytes at sites of inflammation and form the front line of the innate immune response. Neutrophils have a relatively short lifespan compared to other cell types, as they have streamlined their metabolic processes to support an arsenal of antimicrobial functions to combat invading pathogens at the cost of maximizing ATP output. To elicit antimicrobial stress, neutrophils rewire their glycolytic pathways to sustain phagocytosis and the oxidative burst and modify their mitochondrial metabolism to dictate degranulation or release of neutrophil extracellular traps. While many of these effector functions are sufficient to protect the \"healthy\" host from infection, chronic diseases disrupting metabolic and inflammatory homeostasis render the host susceptible to more frequent and severe bacterial infections. With the growing incidence of many metabolic and autoimmune diseases, a clearer understanding of the mechanisms regulating or disrupting neutrophil antimicrobial processes is required. This review focuses on the relationship between neutrophil function and metabolism and what is known about how this impacts autoimmune and metabolic diseases and/or disorders in the case of bacterial infection.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0049824"},"PeriodicalIF":2.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527772","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}

{"title":"<i>Rickettsia heilongjiangensis</i> suppresses RIPK1 kinase-mediated host cell death during the infection.","authors":"Maozhang He, Qingyin Shi, Yu Xin, Shurui Zheng, Yan Liu, Kehan Xu","doi":"10.1128/iai.00158-25","DOIUrl":"10.1128/iai.00158-25","url":null,"abstract":"<p><p>Spotted fever group <i>Rickettsia</i> (SFGR) poses a significant challenge in the field of tick-borne diseases, characterized by its obligate intracellular lifestyle and its ability to disrupt various host cellular pathways. A deeper understanding of <i>Rickettsia</i>'s interactions with immune signaling is crucial for the development of novel therapeutic strategies. While previous research has shown that SFGR infection manipulates host cell death responses, the specific effects on receptor-interacting protein kinase 1 (RIPK1)-mediated multiple cell death pathways-collectively referred to as PANoptosis-remain poorly understood. In this study, we reveal that infection with <i>Rickettsia heilongjiangensis</i> suppresses RIPK1 kinase-dependent apoptosis and necroptosis in human microvascular endothelial cells (HMEC-1). However, mitochondria-dependent apoptosis during the late stages of infection is essential for bacterial replication. Interestingly, inhibition of caspase-8 does not sensitize <i>Rickettsia</i>-infected host cells to necroptosis. Transcriptomic analysis further reveals that <i>Rickettsia</i> infection upregulates the host tumor necrosis factor (TNF) and NF-κB signaling pathways, which subsequently suppress RIPK1 kinase activity and contribute to the inhibition of host cell death. These findings provide new insights into the molecular mechanisms by which <i>Rickettsia</i> evades host defenses.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0015825"},"PeriodicalIF":2.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553419","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}

{"title":"Ficolin-1 in pediatric <i>Plasmodium falciparum</i> malaria and its possible role in parasite clearance and anemia.","authors":"Di Zheng, Natalie Ferrington, Dilini Rathnayake, Wina Hasang, Agersew Alemu, Visopo Harawa, Amalia Karahalios, Phoebe Fitzpatrick, Evelyne Gout, Nicole M Thielens, Karl Seydel, Terrie E Taylor, Wilson Mandala, Stephen J Rogerson, Elizabeth H Aitken, Louise M Randall","doi":"10.1128/iai.00194-25","DOIUrl":"10.1128/iai.00194-25","url":null,"abstract":"<p><p><i>Plasmodium falciparum</i> malaria causes significant disease, especially in young children. A successful immune response to <i>P. falciparum</i> is a major determinant of clinical outcome. The ficolins are a family of lectins that act as pattern recognition molecules and can activate the lectin complement pathway and may promote inflammation and facilitate opsonization and lysis of pathogens. Here, we have investigated the potential roles of ficolin-1 and ficolin-2 in the context of <i>P. falciparum</i> infection. We measured ficolin-1 and ficolin-2 concentrations in plasma from Malawian children presenting with uncomplicated or severe malaria or healthy controls (HCs) by ELISA. Using flow cytometry, we assessed whether ficolin-1 could bind to infected red blood cells (iRBCs) and whether it binds sialic acid on the iRBCs. Ficolin-1 and ficolin-2 plasma levels were measured in children from all clinical groups. Compared to HCs (reference), Ficolin-1 concentrations in plasma were higher in children with uncomplicated (geometric mean ratio: 1.88; 95% confidence interval [CI]: 1.25-2.82) and severe malaria (1.65; 95% CI: 1.10-2.46). Ficolin-1 levels were positively associated with peripheral blood monocyte (1.30; 1.02-1.67) and neutrophil counts (1.06; 1.00-1.13). Ficolin-2 was not associated with malaria. Hemoglobin levels were negatively associated with ficolin-1 (-0.38; -0.68 to -0.09) and ficolin-2 (-0.36; -0.68 to -0.04). Ficolin-1 bound more to iRBCs compared to uninfected RBCs, and binding was reduced in a ficolin-1 mutant that did not bind to sialic acid. These results highlight a largely overlooked role for ficolin-1 in the immune response to <i>P. falciparum</i> infection and point to a potential role for lectins contributing to parasite clearance and anaemia.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0019425"},"PeriodicalIF":2.9,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150379","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}

{"title":"Characterization of the <i>Listeria monocytogenes</i> PieRS regulon distinguishes the function of the critical secretion chaperone PrsA2 from other regulon members.","authors":"Xiomarie Alejandro-Navarreto, Laty A Cahoon, Nancy E Freitag","doi":"10.1128/iai.00357-24","DOIUrl":"10.1128/iai.00357-24","url":null,"abstract":"<p><p><i>Listeria monocytogenes</i> (<i>Lm</i>) is a gram-positive pathogen that is widespread throughout the environment and known for its ability to infect mammalian hosts following the ingestion of contaminated food. <i>Lm</i> uses a variety of mechanisms to survive challenging conditions experienced both during life in the outside environment and inside of the infected host. We recently described a novel two-component signaling system known as PieRS that regulates the secretion of the chaperone PrsA2, which is essential for bacterial virulence, as well as its related homolog PrsA1 and a variety of gene products of unknown function. Here, we examine the roles of the less characterized PieRS-regulated gene products and contrast their functions with PrsA2 in terms of bacterial survival under stress conditions and virulence in mice. Characterization of targeted in-frame deletion mutants of PieRS regulon members indicates-in contrast to <i>prsA2</i> mutants-minimal contributions to stress survival and bacterial virulence. Modest contributions of select regulon members were associated with <i>Lm</i> colonization of the gastrointestinal tract. The PieRS regulon thus consists of gene products that contribute to <i>Lm</i> physiology in ways that are clearly distinct from PrsA2 and the chaperone's essential function for both stress survival and bacterial virulence.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0035724"},"PeriodicalIF":2.9,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150377","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}

{"title":"Trimming the fat: a brief review of lipids at the host-pathogen interface.","authors":"Filiz T Korkmaz","doi":"10.1128/iai.00506-24","DOIUrl":"10.1128/iai.00506-24","url":null,"abstract":"<p><p>Microbial-derived lipids and the host receptors that bind them are collectively critical for immune regulation on the host side and for a multitude of biological functions on the microbial side, including membrane structure, energy generation, resistance to stress, and, importantly, virulence. Bacteria, viruses, fungi, and eukaryotic microorganisms comprise common and unique lipid species that can be modified to avoid immune detection and aid in antimicrobial resistance. Moreover, the host receptors that interact with lipids are equally diverse in their structure and function, driving both beneficial and pathogenic responses depending on the location, strength, and duration of signaling. The following review will discuss all the aforementioned aspects of lipids at the host-pathogen interface, which should be expanded upon in future studies to develop novel therapeutics that consider lipids as distinct immune modulators.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0050624"},"PeriodicalIF":2.9,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283817","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}

{"title":"Working together: gut microbe-microbe interactions shape host inflammation.","authors":"Ally Lawing, Rachel Bleich","doi":"10.1128/iai.00512-24","DOIUrl":"10.1128/iai.00512-24","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a debilitating disorder characterized by chronic intestinal inflammation that currently has no cure. Alterations to the composition of the gut microbiota, including reduced microbial diversity and expansion of pathobionts like Enterobacteriaceae, are implicated in IBD. While this dysbiosis has been well-documented, our understanding of the function of these microbes in the development and progression of IBD is more limited. As part of the gut microbiota, these microbes undergo complex interactions with many other microorganisms that impact the structure and function of the microbial community and the health of the host. These include competitive interactions for nutrients and space and cooperative interactions that help optimize resource utilization and microbial fitness. In this minireview, we discuss the microbe-microbe interactions that can impact host inflammation and IBD progression and treatment. Due to their association with IBD, we put special emphasis on interactions between Enterobacteriaceae and other members of the microbiota that are competitive, commensal, and mutualistic. To better understand these interactions, the signals that mediate microbial interactions are highlighted, including contact-dependent and contact-independent mechanisms. Finally, mucosal biofilms involving pathobionts are examined due to their proximity to the host and ability to influence inflammation.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0051224"},"PeriodicalIF":2.9,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283818","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}