Infection and Immunity最新文献

{"title":"DksA-dependent stringent stress response drives virulence and gastrointestinal persistence of <i>Klebsiella pneumoniae</i>.","authors":"Md Maidul Islam, Robert L Beckman, Noah A Nutter, Juan D Valencia-Bacca, Giovanna E Hernandez, Renee M Fleeman, Karen M Haas, M Ammar Zafar","doi":"10.1128/iai.00194-26","DOIUrl":"https://doi.org/10.1128/iai.00194-26","url":null,"abstract":"<p><p>Successful gastrointestinal (GI) colonization by bacterial pathogens requires adaptation to nutrient competition and host-derived stresses in the gut, with adaptation via the bacterial stringent stress response playing a critical role. Epidemiological data suggest that the GI tract serves as a reservoir from which <i>K. pneumoniae</i> can spread and cause invasive disease or transmit to another host. DksA is a conserved stringent response transcriptional regulator that was identified in an <i>in vivo</i> transposon mutagenesis screen as an important <i>K. pneumoniae</i> gut determinant. However, its role in <i>K. pneumoniae</i> pathogenesis and gut colonization remain uncharacterized. Here, we demonstrate that DksA is required for survival against membrane-targeting antibiotics, consistent with a role in cell envelope stress tolerance. In addition, DksA positively influences capsule biosynthesis gene expression and hypermucoviscosity, and is essential for robust biofilm formation. Using a murine model, we establish that DksA functions as a determinant of GI colonization, despite disruption of the resident gut microbiota. Furthermore, we demonstrate that DksA is important for environmental survival and transmission by regulating RpoS, thereby providing a mechanistic link between the stringent stress response, environmental survival, and subsequent transmission. Together, these findings establish DksA as a central integrator of the stringent response, coordinating membrane stress resistance, virulence traits, and gastrointestinal colonization in <i>K. pneumoniae</i>.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0019426"},"PeriodicalIF":3.4,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging two kingdoms: binding interactions between enteric viruses and intestinal bacteria.","authors":"Rachel P Tat, Christopher M Robinson","doi":"10.1128/iai.00291-26","DOIUrl":"https://doi.org/10.1128/iai.00291-26","url":null,"abstract":"<p><p>Enteric viruses are major causes of gastrointestinal disease worldwide and are primarily transmitted through the fecal-oral route. Upon entering the gastrointestinal tract, these viruses encounter the dense and diverse population of intestinal microbiota, leading to frequent interactions with commensal bacteria. Over the past decade, numerous studies have demonstrated that bacteria can enhance enteric viral replication, stability, and overall pathogenesis. Although direct binding interactions between enteric viruses and bacteria have been observed, the molecular determinants governing these interactions remain poorly understood. Defining the viral and bacterial factors that mediate binding is, therefore, critical for understanding how bacteria can influence viral infection, transmission, and disease. Here, in this minireview, we summarize the current findings on enteric viral-bacterial interactions, with a focus on the mechanisms of viral binding to bacteria and the implications of these interactions on enteric virus pathogenesis and transmission.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0029126"},"PeriodicalIF":3.4,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A plasmid-encoded T3SS underlies the virulence of enteropathogenic <i>Providencia alcalifaciens</i> strains isolated from a large foodborne outbreak in Japan.","authors":"Jayedul Hassan, Shigeaki Matsuda, Eiji Ishii, Takayuki Uda, Daisuke Motooka, Tetsuya Iida","doi":"10.1128/iai.00151-26","DOIUrl":"https://doi.org/10.1128/iai.00151-26","url":null,"abstract":"<p><p><i>Providencia alcalifaciens</i> is a gut commensal bacterium and also an emerging enteric pathogen associated with sporadic infections and outbreak cases in humans. The most notable outbreak caused by this bacterium occurred in 1996 in Fukui Prefecture, Japan, affecting 270 individuals. However, the pathogenic mechanisms responsible for this outbreak remain unknown. In this study, we identified the key virulence determinants of the Fukui outbreak strains through genomic and functional analyses. These strains uniquely carry a ~162 kb large plasmid encoding a type III secretion system (T3SS) closely homologous to the <i>Salmonella</i> SPI-1 T3SS. We also show that the plasmid-encoded T3SS (T3SSp) constitutes a functional secretion system and is essential for the pathogenicity of the Fukui outbreak strain, including the invasion of cultured epithelial cells and the induction of diarrhea in a rabbit model. Secretome analysis identified effectors secreted in a T3SSp-dependent manner, among which PipA-sharing limited sequence similarity with SipA, a SPI-1 T3SS effector-plays a crucial role in inducing diarrhea. Ectopic expression of PipA in HeLa cells caused focal accumulation of F-actin, indicating its cytoskeleton-modulating activity. Comparative genomics with other <i>Providencia</i> species revealed the dissemination of the large plasmid, with structural variations among enteropathogenic strains of <i>P. alcalifaciens</i> and <i>Providencia rustigianii</i> associated with clinical cases in humans and animals. Thus, our findings underscore the molecular basis of <i>P. alcalifaciens</i> pathogenicity in the Fukui outbreak and highlight the significance of the large plasmids encoding T3SS in driving pathogenic evolution among <i>Providencia</i> species.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0015126"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influenza A virus co-infection alters <i>Streptococcus pneumoniae</i> gene expression during upper respiratory tract colonization.","authors":"Noah A Nutter, Alicia Costa-Terryll, Lance M Miller, Ming Leung, Pengbo Zhang, Md Maidul Islam, Daniel Fecko, M Ammar Zafar","doi":"10.1128/iai.00323-26","DOIUrl":"https://doi.org/10.1128/iai.00323-26","url":null,"abstract":"<p><p><i>Streptococcus pneumoniae</i> (<i>Spn</i>) asymptomatically colonizes the upper respiratory tract (URT), a niche from which it can transmit to another host or cause invasive disease in the same host. The <i>in vivo</i> transcriptional adaptations that <i>Spn</i> undergoes during nasopharyngeal colonization, particularly during influenza A virus (IAV) co-infection, are poorly understood. Here, we leveraged an established infant mouse model of colonization, shedding, and transmission to perform genome-wide transcriptomic profiling of <i>Spn</i> during mono- and during IAV co-infection. Compared with broth-grown controls, pneumococci isolated from the URT exhibited distinct transcriptional programs, with over 200 genes differentially expressed across time points. Genes involved in carbohydrate uptake and metabolism, glycan degradation, amino sugar and nucleotide sugar metabolism, and amino acid biosynthesis were consistently enriched during colonization, highlighting metabolic adaptation to the nasopharyngeal niche. In contrast, IAV co-infection induced a markedly distinct transcriptional signature, including upregulation of branched-chain amino acid biosynthesis, bacteriocin production, and phosphate acquisition systems. Notably, the pilus islet-1 locus was upregulated during <i>Spn</i>-IAV co-infection. Functional studies demonstrated that while the pilus was dispensable for colonization under mono- and co-infection conditions, it promoted high-shedding events and enhanced inflammatory responses during IAV co-infection. However, reduced inflammation and reduced high-shedding events from pups inoculated with a pilus-deficient mutant did not alter transmission frequency in the infant mouse model. Collectively, our findings define the <i>in vivo</i> transcriptional landscape of <i>Spn</i> during URT colonization and reveal distinct bacterial adaptations during viral co-infection, providing insight into mechanisms that influence pneumococcal persistence, inflammation, and transmission.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0032326"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon crosstalk at the lung barrier in viral and fungal infection.","authors":"Maria Velez-Brochero, Amariliz Rivera","doi":"10.1128/iai.00295-26","DOIUrl":"https://doi.org/10.1128/iai.00295-26","url":null,"abstract":"<p><p>Interferons (IFNs) coordinate host defense at the lung barrier by linking pathogen recognition to epithelial and immune-cell responses. Their effects are highly context-dependent and can be protective or pathological according to IFN class and ligand, cellular source and target, and the timing and duration of signaling. In this minireview, we compare the induction of type I, II, and III IFNs during respiratory viral infection and pulmonary <i>Aspergillus fumigatus</i> infection, highlighting epithelial-led antiviral sensing and predominantly myeloid-centered antifungal sensing. We then examine how receptor distribution, ligand identity, JAK-STAT complex assembly, and integration with inflammatory pathways generate cell type-specific transcriptional and functional programs. Finally, we discuss three interconnected consequences of IFN crosstalk at the respiratory barrier: regulation of epithelial permeability and repair, licensing or pathological reprogramming of immune effector cells during primary infection, and loss of coordination during viral-fungal coinfection, including influenza-associated and COVID-19-associated pulmonary aspergillosis. Collectively, the available evidence supports a model in which spatially restricted and appropriately timed IFN responses promote pathogen control and preserve barrier function, whereas excessive, prolonged, or mistimed signaling impairs epithelial recovery, disrupts phagocyte activity, and increases susceptibility to secondary fungal invasion. Defining these context-dependent circuits may guide therapeutic strategies that modulate IFN signaling with greater temporal and cell type specificity.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0029526"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chondroitin sulfate degradation bolsters <i>Proteus mirabilis</i> growth and colonization of the catheterized urinary tract.","authors":"Benjamin C Hunt, Vitus Brix, Namrata Deka, Brian S Learman, Aimee L Brauer, Brianna M Shipman, Nicole J De Nisco, Chelsie E Armbruster","doi":"10.1128/iai.00223-26","DOIUrl":"https://doi.org/10.1128/iai.00223-26","url":null,"abstract":"<p><p>Glycosaminoglycans (GAGs) are negatively charged polysaccharides composed of repeating disaccharide units and are essential components of the extracellular matrix throughout numerous tissues. The bladder urothelium has a protective GAG layer that primarily consists of chondroitin sulfate (CS), heparan sulfate (HS), and hyaluronic acid (HA), and urinary tract pathogens must either degrade or otherwise circumvent this layer to infect the urothelium. In this study, we investigated GAG degradation by <i>Proteus mirabilis,</i> a common and persistent colonizer of the catheterized urinary tract. Almost all <i>P. mirabilis</i> urinary tract isolates harbor a putative chondroitin endolyase (PMI2127), exolyase (PMI2128), and sulfatase (PMI2124). By generating mutant and complemented strains of these genes, we determined that <i>P. mirabilis</i> strain HI4320 degrades multiple forms of CS under numerous culture conditions, including during growth in human urine, and can use CS degradation products as a carbon source. Sulfatase and endolyase activities were required for efficient degradation of all CS types, while the exolyase only contributed to using CS-B or CS-C as a carbon source. Interestingly, only endolyase activity contributed to colonization in a murine model of catheter-associated urinary tract infection (CAUTI), although the colonization defect was even more pronounced when both the endolyase and exolyase were disrupted. The colonization defect was specific to the CAUTI model, likely due to the impact of catheterization on the GAG landscape of the bladder. Limiting CS degradation by <i>P. mirabilis</i> may therefore reduce the risk of ascending infection in catheterized patients.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0022326"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of <i>Galleria mellonella</i>, epithelial cell cytotoxicity, and mouse model of bacteremia to measure <i>Pseudomonas aeruginosa</i> virulence.","authors":"Aliki Valdes, Christopher Axline, Travis J Kochan, Sophia Nozick, Timothy Ward, Issay Niki, Ethan VanGosen, David Hynes, Julia Nelson, Preeti Garai, Tania Afzal, Daniel Amusin, Sumitra D Mitra, Timothy L Turner, William Cheng, Joanne J Lee, Prarthana Prashanth, Nathan B Pincus, Jonathan P Allen, Jake Hauser, Egon A Ozer, Kelly E R Bachta, Cheng-Hsun Chiu, Antonio Oliver, Alan R Hauser","doi":"10.1128/iai.00335-26","DOIUrl":"10.1128/iai.00335-26","url":null,"abstract":"<p><p>Considerable effort has focused on identifying alternatives to mouse models in research studies. In the field of bacterial pathogenesis, <i>Galleria mellonella</i> and epithelial cell lines have been widely used for this purpose, but the concordance of these models with mice remains unclear. To begin to address this knowledge gap, we used 105 clinical isolates of <i>Pseudomonas aeruginosa</i> for which virulence had previously been determined in a mouse bacteremia model. A semistrong correlation was observed between <i>G. mellonella</i> median time to 50% mortality and mouse 50% pre-lethal dose (LD₅₀) values (Spearman's rank correlation coefficient [ρ] = 0.75), whereas percent A549 epithelial-like cell lysis during co-culture showed a weak correlation to mouse LD₅₀ values (ρ=-0.47). Given the stronger correlation between <i>G. mellonella</i> and mouse virulence, we next examined whether <i>G. mellonella</i> could substitute for mice when asking questions about the virulence of large numbers of <i>P. aeruginosa</i> isolates. Results from mice indicated that isolates with resistance to more antibiotics were significantly less virulent, and the use of <i>G. mellonella</i> identified the same inverse correlation. Furthermore, both models found no evidence for the existence of hypervirulent clonal lineages. In particular, isolates belonging to sequence types defined as high-risk clones were not consistently more virulent than other isolates, despite the known association of high-risk clones with poor clinical outcomes. These findings suggest that <i>G. mellonella</i> can serve as an adequate substitute for mice when addressing specific population-based virulence questions, although conclusions should be confirmed in mice.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0033526"},"PeriodicalIF":3.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What goes around comes around: updates in the study of <i>Coxiella burnetii</i> lipopolysaccharide phase variation.","authors":"Kathleen N Pierce, Rebecca Anderson, Megan Brose, Jessica McCormick-Ell, Carrie Mae Long","doi":"10.1128/iai.00030-26","DOIUrl":"https://doi.org/10.1128/iai.00030-26","url":null,"abstract":"<p><p>Lipopolysaccharide (LPS) is a major outer membrane component of Gram-negative bacteria that can modulate host immune responses during infection. Extensive studies on the LPS of well-studied organisms, such as <i>Escherichia coli</i> and <i>Salmonella</i> spp., have elucidated many LPS pathways; however, knowledge of unique LPS structures of lesser-studied bacteria, such as <i>Coxiella burnetii</i>, remains limited. <i>C. burnetii</i> is an intracellular pathogen that is the cause of the zoonotic disease Q fever. The highly infectious nature of <i>C. burnetii</i> warrants designation as a select agent by the United States Federal Select Agent Program and must be contained in a Biosafety Level three facility. Contributing to the organism's biothreat potential, <i>C. burnetii</i> LPS is a critical virulence determinant that dictates bacterial survival and pathogenesis. Several reviews have extensively covered <i>C. burnetii</i> LPS structure and function prior to 2017, though recent findings regarding mechanisms of LPS biosynthesis, LPS-induced host immunity, and LPS elongation pose biosafety and regulatory questions that necessitate careful consideration. Here, we discuss recent (post-2017) findings related to <i>C. burnetii</i> LPS from scientific and biosafety perspectives that may be applicable across many fields of research. From the discovery of <i>C. burnetii</i> LPS phase variation by Fiset and Stoker in 1956 to the recent elucidation of specific genetic mechanisms underlying this process, the study of <i>C. burnetii</i> LPS is a reminder that what goes around comes around, even in research.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0003026"},"PeriodicalIF":3.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum for Honorato et al., \"Extracellular vesicles of <i>Emergomyces africanus</i> modulate host immune responses and reflect metabolic adaptations to nutrient availability\".","authors":"Leandro Honorato, Albaniza Liuane Ribeiro do Nascimento Sabino, Jhon Jhamilton Artunduaga Bonilla, Susana Ruiz Mendoza, Julio Kornetz, Flavia C G Dos Reis, Elaine C Albergoni, Vinicius Alves, Susana Frases, Allan Jefferson Guimarães, Daniel Zamith-Miranda, Simone Sidoli, Joshua D Nosanchuk, Marcio L Rodrigues, Leonardo Nimrichter","doi":"10.1128/iai.00434-26","DOIUrl":"https://doi.org/10.1128/iai.00434-26","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0043426"},"PeriodicalIF":3.4,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptional analyses of peripheral blood lymphocytes obtained shortly after primary immunization discriminate vaccines against <i>Francisella tularensis</i>.","authors":"Roberto De Pascalis, Scott Espich, Hamda Khan, Mykia Toney, Chou Chao-Kai, Wu Wells, Karen L Elkins","doi":"10.1128/iai.00208-26","DOIUrl":"https://doi.org/10.1128/iai.00208-26","url":null,"abstract":"<p><p>The high virulence and pathogenesis of <i>Francisella tularensis</i> (<i>Ft</i>), responsible for tularemia, made it a target for bioweapon development during the \"Cold War.\" This prompted investigation of vaccines, starting with an older vaccine candidate denoted <i>Ft</i> live vaccine strain (LVS). LVS has limited efficacy against aerosol challenge with <i>Ft</i> subsp. Tularensis (Type A), the most virulent subtype. However, no vaccines, including LVS, have been licensed in the U.S. Animal studies indicate that <i>Ft</i> vaccines induce protective T-cell-mediated immune responses. In previous studies, analyses of leukocytes from vaccinated animals that were restimulated <i>in vitro</i> facilitated screening and selection of vaccines for more extensive <i>in vivo</i> evaluation. These studies demonstrated that a novel live attenuated vaccine strain derived from Type A <i>Ft</i>, denoted <i>ΔclpB</i>, was protective against aerosol challenge in animal models. In this study, we focused on evaluating immune responses immediately after vaccination of Fischer 344 rats with LVS and <i>ΔclpB</i> using multiple analytical approaches. While humoral immune responses were comparable between the two vaccines, we identified multiple differences in immune responses by analyses of peripheral blood leukocytes by flow cytometry and by relative gene expression. In particular, vaccination with LVS or <i>ΔclpB</i> resulted in differential expression of multiple genes at selected time points. Gene expression, in turn, predicted activation or inhibition of multiple biological pathways. These results suggest that immune responses shortly after primary vaccination may discriminate vaccines with different degrees of <i>in vivo</i> protection that could potentially be used as correlates of protection and extrapolate efficacy from animals to people.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0020826"},"PeriodicalIF":3.4,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}