Infection and Immunity最新文献

{"title":"Filamentous bacteriophage M13 induces proinflammatory responses in intestinal epithelial cells.","authors":"Ambarish C Varadan, Juris A Grasis","doi":"10.1128/iai.00618-24","DOIUrl":"10.1128/iai.00618-24","url":null,"abstract":"<p><p>Bacteriophages are the dominant members of the human enteric virome and can shape bacterial communities in the gut; however, our understanding of how they directly impact health and disease is limited. Previous studies have shown that specific bacteriophage populations are expanded in patients with Crohn's disease (CD) and ulcerative colitis (UC), suggesting that fluctuations in the enteric virome may contribute to intestinal inflammation. Based on these studies, we hypothesized that a high bacteriophage burden directly induces intestinal epithelial responses. We found that filamentous bacteriophages M13 and Fd induced dose-dependent IL-8 expression in the human intestinal epithelial cell line HT-29 to a greater degree than their lytic counterparts, T4 and ϕX174. We also found that M13, but not Fd, reduced bacterial internalization in HT-29 cells. This led us to investigate the mechanism underlying M13-mediated inhibition of bacterial internalization by examining the antiviral and antimicrobial responses in these cells. M13 upregulated type I and III IFN expressions and augmented short-chain fatty acid (SCFA)-mediated LL-37 expression in HT-29 cells. Taken together, our data establish that filamentous bacteriophages directly affect human intestinal epithelial cells. These results provide new insights into the complex interactions between bacteriophages and the intestinal mucosa, which may underlie disease pathogenesis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"93 5","pages":"e0061824"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968660","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>Candida albicans</i> biofilm extracellular vesicles deliver candidalysin to epithelial cell membranes and induce host cell responses.","authors":"Sejeong Lee, Antzela Tsavou, Robert Zarnowski, Rita Pforte, Stefanie Allert, Thomas Krüger, Olaf Kniemeyer, Axel A Brakhage, Tam T T Bui, David R Andes, Jonathan P Richardson, Bernhard Hube, Julian R Naglik","doi":"10.1128/iai.00404-24","DOIUrl":"10.1128/iai.00404-24","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are heterogeneous particles encapsulated with a phospholipid bilayer membrane. EVs have evolved diverse biological functions, serving mainly as prominent mediators and regulators of cell-cell communication. This study investigated whether candidalysin, a key virulence factor in <i>Candida albicans</i> infections, is present within EVs derived from <i>C. albicans</i> biofilms and retains activity by inducing host immune responses. We found that biofilm EVs contain candidalysin and can permeabilize planar lipid bilayer membranes in a dose-dependent manner. However, biofilm EVs were unable to damage oral epithelial cells (OECs) but were able to induce cytokine responses. Notably, EVs obtained from biofilms cultured for 24 h and 48 h exhibited differences in cargo composition and their ability to activate OECs. This study highlights the potential of biofilm EVs as a toxin delivery system during <i>C. albicans</i> infection and identifies temporal differences in the ability of EVs to activate epithelial cells.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0040424"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763680","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":"A <i>Salmonella enterica</i> serovar Typhimurium genome-wide CRISPRi screen reveals a role for type 1 fimbriae in evasion of antibody-mediated agglutination.","authors":"Samantha K Lindberg, Graham G Willsey, Nicholas J Mantis","doi":"10.1128/iai.00574-24","DOIUrl":"10.1128/iai.00574-24","url":null,"abstract":"<p><p>The O5-specific monoclonal IgA antibody, Sal4, mediates the conversion of <i>Salmonella enterica</i> serovar Typhimurium (STm) from virulent, free-swimming cells to non-motile, multicellular biofilm-like aggregates within a matter of hours. We hypothesize that the rapid transition from an invasive to a non-invasive state is an adaptation of STm to Sal4 IgA exposure. In this report, we performed a genome-wide CRISPR interference (CRISPRi) screen to identify STm genes that influence multicellular aggregate formation in response to Sal4 IgA treatment. From a customized library of >36,000 spacers, ~1% (373) were enriched at the top of the culture supernatant after two consecutive rounds of Sal4 IgA treatment. The enriched spacers mapped to a diversity of targets, including genes involved in O-antigen modification, cyclic-di-GMP metabolism, outer membrane biosynthesis/signaling, and invasion/virulence, with the most frequently targeted gene being <i>fimW</i>, which encodes a negative regulator of type 1 fimbriae (T1F) expression. Generation of a STm Δ<i>fimW</i> strain confirmed that the loss of FimW activity results in a hyperfimbriated phenotype and evasion of Sal4 IgA-mediated agglutination in solution. Closer examination of the <i>fimW</i> mutant revealed its propensity to form biofilms at the air-liquid interface in response to Sal4 exposure, suggesting that T1F \"primes\" STm to transition from a planktonic to a sessile state, possibly by facilitating bacterial attachment to abiotic surfaces. These findings shed light on the mechanism by which IgA antibodies influence STm virulence in the intestinal environment.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"93 5","pages":"e0057424"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020563","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":"Involvement of CD146 in the <i>Cryptococcus neoformans</i> adhesion and infection of brain endothelial cells.","authors":"Wei Liu, Junhong Chen, Ting Wang, Ying Gong, Chen Yang, Yuwei Li, Xiyun Yan, Hongxia Duan, Xiaoming Wang, Mingshun Zhang","doi":"10.1128/iai.00145-25","DOIUrl":"10.1128/iai.00145-25","url":null,"abstract":"<p><p>Cryptococcal meningitis is a common and refractory central nervous system (CNS) infection with high mortality and disability. For <i>Cryptococcus neoformans</i> (<i>C. neoformans</i>) to penetrate the CNS, it first adheres to and breaches the blood‒brain barrier (BBB). Here, we explored the roles of CD146, an adhesion molecule expressed on the surface of brain microvascular endothelial cells (BMECs), in cryptococcal vascular adhesion and BBB invasion. Following cryptococcal infection, we observed a reduction in CD146 expression in BMECs, which was at least partially mediated by metalloproteinase-9. Once overexpressed on BMECs, CD146 increased <i>C. neoformans</i> adhesion; in contrast, CD146 knockout decreased the attachment of fungi to endothelial cells <i>in vitro</i>. Unexpectedly, CD146 knockout failed to reduce fungal infection in the brain following intravascular instillation of <i>C. neoformans</i>. However, <i>the</i> anti-CD146 antibody AA98 significantly increased the fungemia (spleen CFU), suggesting that CD146 may be involved in the early adhesion and invasion of Cryptococcus into cerebral vessels. AA98, however, failed to extend the survival of <i>C. neoformans</i> infected mice. These results suggest that CD146 may play dispensable roles in the <i>C. neoformans</i> brain infection.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"93 5","pages":"e0014525"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006592","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>MBOVJF4278_00820</i> encodes a novel cytoadhesin of <i>Mycoplasma bovis</i> binding to heparin.","authors":"Qi Wu, Zhixin Ma, Qiao Pan, Tong Liu, Jiuqing Xin, Qingyuan Xu","doi":"10.1128/iai.00606-24","DOIUrl":"10.1128/iai.00606-24","url":null,"abstract":"<p><p><i>Mycoplasma bovis</i>, a minimal bacterium but a notorious cattle pathogen, leads to serious economic losses. This pathogen binding to host cells is emerging as a complex process involving a broad range of surface-exposed structures. For mycoplasma, adhering to host tissue is the first and crucial step of infection. It is well known that the molecules contributing to microbial cytoadhesion are important virulence factors. Here, we cloned, expressed, and purified the recombinant protein, which is encoded by <i>MBOVJF4278_00820</i>, and induced polyclonal antibodies for it in mice. The cytoadhesive properties of this surface-exposed protein were demonstrated on embryonic bovine lung (EBL) and Madin-Darby bovine kidney (MDBK) cells. Furthermore, heparin as the binding target was confirmed, and the characteristics of the interaction between this protein and heparin have also been analyzed. Our data indicate that the surface-associated <i>MBOVJF4278_00820</i>-encoded protein is a novel adhesion-related factor of <i>Mycoplasma bovis</i>.IMPORTANCEAdhesins are crucial in facilitating <i>Mycoplasma bovis</i> infection. In this study, we identified a specific <i>Mycoplasma bovis</i> adhesin that interacts with heparin on the surface of host cells. Given that heparin is ubiquitously distributed across a wide range of tissue cells, the identification of the heparin-binding adhesin is significant for elucidating how <i>Mycoplasma bovis</i> targets diverse host cells and triggers a spectrum of clinical manifestations.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"93 5","pages":"e0060624"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012953","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":"Probiotic colonization of <i>Xenopus laevis</i> skin causes short-term changes in skin microbiomes and gene expression.","authors":"Joseph D Madison, Owen G Osborne, Amy Ellison, Christina N Garvey Griffith, Lindsey Gentry, Harald Gross, Brian Gratwicke, Leon Grayfer, Carly R Muletz-Wolz","doi":"10.1128/iai.00569-24","DOIUrl":"10.1128/iai.00569-24","url":null,"abstract":"<p><p>Probiotic therapies have been suggested for amelioration efforts of wildlife disease such as chytridiomycosis caused by <i>Batrachochytrium</i> spp. in amphibians. However, there is a lack of information on how probiotic application affects resident microbial communities and immune responses. To better understand these interactions, we hypothesized that probiotic application would alter microbial community composition and host immune expression in <i>Xenopus laevis</i>. Accordingly, we applied three amphibian-derived and anti-<i>Batrachochytrium</i> bacteria strains (two <i>Pseudomonas</i> spp. and one <i>Stenotrophomonas</i> sp.) to <i>X. laevis</i> in monoculture and also as a cocktail. We quantified microbial community structure using 16S rRNA gene sequencing. We also quantified genes involved in <i>X. laevis</i> immune responses using quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) and skin transcriptomics over 1 and 3-week periods. All probiotic treatments successfully colonized <i>X. laevis</i> skin for 3 weeks, but with differential amplicon sequence variant (ASV) sequence counts over time. Bacterial community and immune gene effects were most pronounced at week 1 post-probiotic exposure and decreased thereafter. All probiotic treatments caused initial changes to bacterial community alpha and beta diversity, including reduction in diversity from pre-exposure anti-<i>Batrachochytrium</i> bacterial ASV relative abundance. Probiotic colonization by <i>Pseudomonas</i> probiotic strain RSB5.4 reduced expression of regulatory T cell marker (<i>FOXP3,</i> measured with RT-qPCR) and caused the greatest gene expression changes detected by transcriptomics. Single bacterial strains and mixed cultures, therefore, altered amphibian microbiome-immune interactions. This work will help to improve our understanding of the role of the microbiome-immune interface underlying both disease dynamics and emergent eco-evolutionary processes.IMPORTANCEAmphibian skin microbial communities have an important role in determining disease outcomes, in part through complex yet poorly understood interactions with host immune systems. Here we report that probiotic-induced changes to the <i>Xenopus laevis</i> frog skin microbial communities also result in significant alterations to these animals' immune gene expression. These findings underscore the interdependence of amphibian skin immune-microbiome interactions.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0056924"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763649","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":"Type I IFNs contribute to upregulation of PD-L1 during <i>Chlamydia trachomatis</i> infection.","authors":"Nicole V Reinhold-Larsson, Michael N Starnbach","doi":"10.1128/iai.00040-25","DOIUrl":"10.1128/iai.00040-25","url":null,"abstract":"<p><p><i>Chlamydia trachomatis</i> is an obligate intracellular bacterial pathogen that if left untreated can cause reproductive harm. Failure of natural adaptive immunity results in chronic and repeat infections. In efforts to understand the failure of adaptive immunity, we have previously discovered that CD8⁺ T cells, normally integral for controlling intracellular pathogen infections, are misprogrammed by PD-1/PD-L1 signaling during <i>in vivo C. trachomatis</i> infection and fail to mount a protective response. Seeking to uncover the pathways and host factors involved in PD-L1 upregulation that may lead to CD8⁺ T-cell inhibition, we discovered that <i>C. trachomatis</i> triggers the secretion of host type I interferons (IFNs) that are necessary and sufficient to upregulate PD-L1 <i>in vitro</i>. Additionally, secretion of type I IFNs is dependent on <i>C. trachomatis</i> development and its type III secretion system. We have also validated that type I IFNs contribute to upregulation of PD-L1 during <i>C. trachomatis</i> infection <i>in vivo</i> using a mouse model of infection. Overall, these findings reveal that <i>C. trachomatis</i> induction of this host pathway may contribute to adaptive immune evasion.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0004025"},"PeriodicalIF":2.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604762","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":"Heterologous prime-boost immunization of two-component vaccine candidate PWDVax protected pigs against F18 enterotoxigenic <i>Escherichia coli</i> post-weaning diarrhea.","authors":"Chongyang Zhang, Siqi Li, Ipshita Upadhyay, Sai Simah Reddy Vakamalla, Kathyrn L Lauder, Chance Hansen, Kristen Ann Massey, Courtney Hayes, Nicole L Herndon, Weiping Zhang","doi":"10.1128/iai.00406-24","DOIUrl":"10.1128/iai.00406-24","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Post-weaning diarrhea (PWD) is associated predominantly with enterotoxigenic &lt;i&gt;Escherichia coli&lt;/i&gt; (ETEC) and continuously causes significant economic losses to swine producers worldwide. Currently, there are no effective countermeasures against this significant swine disease. Challenges persist in developing vaccines against PWD since ETEC strains produce heterogeneous virulence factors, including F4 (K88) and F18 fimbria and heat-labile toxin (LT), heat-stable toxin type I (STa), heat-stable toxin II (STb), and Shiga toxin type 2e (Stx2e, also causes edema disease). An effective PWD vaccine would induce broadly protective immunity, ideally against two fimbriae and four toxins. In this study, by applying a novel epitope- and structure-based multiepitope-fusion-antigen (MEFA) vaccinology platform, we created a monomeric polyvalent fimbria-toxin protein (fimbria-toxin MEFA) and a holotoxin-structured protein to target PWD virulence determinants (F4 and F18 fimbriae and LT, STa, STb, and Stx2e toxins) and developed a two-component multivalent PWD vaccine candidate, PWDVax. We further applied a heterologous prime-boost immunization strategy and assessed vaccine protection against F18 ETEC-associated PWD. Piglets, after being primed intramuscularly with a fimbria-toxin MEFA monomer protein and boosted orally with live &lt;i&gt;Escherichia coli&lt;/i&gt; bacteria producing GM&lt;sub&gt;1&lt;/sub&gt;-binding holotoxin-structured fimbria-toxin MEFA, developed IgG and secretory IgA responses to the target fimbriae and toxins. Challenged with an F18ac ETEC strain, the immunized piglets were protected against watery diarrhea (87.5%) or any diarrhea (66.7%). These data indicated that PWDVax protects against F18 ETEC-associated PWD and can become an effective PWD vaccine. The two-component vaccine and heterologous prime-boost immunization strategy may be instructive for developing neonatal vaccines in general.IMPORTANCEEnterotoxigenic &lt;i&gt;Escherichia coli&lt;/i&gt; (ETEC)-associated post-weaning diarrhea (PWD) is a global swine disease, remains a major threat to pig health and well-being, and causes significant economic losses. Currently, there are no effective vaccines available against this disease because of challenges including heterogeneity among ETEC strains (or virulence factors) and difficulties in inducing protective immunity against some key virulence determinants. PWDVax, a two-component PWD vaccine candidate, unprecedentedly targeted two ETEC fimbriae (F4 and F18) and four toxins (LT, STa, STb, and Stx2e), the virulence factors associated with nearly all PWD clinical cases. Under a heterologous prime-boost immunization schedule, it induced broad systemic and mucosal antigen-specific antibodies but also protected weaned piglets against F18 ETEC diarrhea. This makes PWDVax potentially an effective vaccine to protect against PWD, particularly the current F18 ETEC-associated severe PWD outbreaks in the United States. Additionally, the two-component vaccine and heterologous","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0040624"},"PeriodicalIF":2.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604757","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":"A call for healing and unity.","authors":"Patrick D Schloss","doi":"10.1128/iai.00098-25","DOIUrl":"10.1128/iai.00098-25","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0009825"},"PeriodicalIF":2.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515499","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":"Extracellular adherence proteins reduce matrix porosity and enhance <i>Staphylococcus aureus</i> biofilm survival during prosthetic joint infection.","authors":"Mohini Bhattacharya, Tyler D Scherr, Jessica Lister, Tammy Kielian, Alexander R Horswill","doi":"10.1128/iai.00086-25","DOIUrl":"10.1128/iai.00086-25","url":null,"abstract":"<p><p>Biofilms are a cause of chronic, non-healing infections. <i>Staphylococcus aureus</i> is a proficient biofilm-forming pathogen commonly isolated from prosthetic joint infections that develop following primary arthroplasty. Extracellular adherence protein (Eap), previously characterized in planktonic or non-biofilm populations as being an adhesin and immune evasion factor, was recently identified in the exoproteome of <i>S. aureus</i> biofilms. This work demonstrates that Eap and its two functionally orphaned homologs EapH1 and EapH2 contribute to biofilm structure and prevent macrophage invasion and phagocytosis in these communities. Biofilms unable to express Eap proteins demonstrated increased porosity and reduced biomass. We describe the role of Eap proteins <i>in vivo</i> using a mouse model of <i>S. aureus</i> prosthetic joint infection. The Results suggest that the protection conferred to biofilms by Eap proteins is a function of biofilm structural stability that interferes with the leukocyte response to biofilm-associated bacteria.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0008625"},"PeriodicalIF":2.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673773","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}