Infection and Immunity最新文献

{"title":"Heterogeneity of <i>Salmonella enterica</i> lipopolysaccharide counteracts macrophage and antimicrobial peptide defenses.","authors":"Linda M Heffernan, Anna-Lisa E Lawrence, Haley A Marcotte, Amit Sharma, Aria X Jenkins, Damilola Iguwe, Jennifer Rood, Scott W Herke, Mary X O'Riordan, Basel H Abuaita","doi":"10.1128/iai.00251-24","DOIUrl":"10.1128/iai.00251-24","url":null,"abstract":"<p><p>S<i>almonella enterica</i> is comprised of over 2,500 serovars, in which non-typhoidal serovars (NTS), Enteritidis (SE), and Typhimurium (STM) are the most clinically associated with human infections. Although NTS have similar genetic elements to cause disease, phenotypic variation including differences in lipopolysaccharide (LPS) composition may control immune evasion. Here, we demonstrate that macrophage host defenses and LL-37 antimicrobial efficacy against SE and STM are substantially altered by LPS heterogeneity. We found that SE evades macrophage killing by inhibiting phagocytosis while STM survives better intracellularly post-phagocytosis. SE-infected macrophages failed to activate the inflammasomes and subsequently produced less interleukin-1β (IL-1β), IL-18, and interferon λ. Inactivation of LPS biosynthesis genes altered LPS composition, and the SE LPS-altered mutants could no longer inhibit phagocytosis, inflammasome activation, and type II interferon signaling. In addition, SE and STM showed differential susceptibility to the antimicrobials LL-37 and colistin, and alteration of LPS structure substantially increased susceptibility to these molecules. Collectively, our findings highlight that modification of LPS composition by <i>Salmonella</i> increases resistance to host defenses and antibiotics.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119729","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":"Molecular, structural, and functional characterization of delta subunit of T-complex protein-1 from <i>Leishmania donovani</i>.","authors":"Apeksha Anand, Gunjan Gautam, Gaurava Srivastava, Shailendra Yadav, Karthik Ramalingam, Mohammad Imran Siddiqi, Neena Goyal","doi":"10.1128/iai.00234-24","DOIUrl":"10.1128/iai.00234-24","url":null,"abstract":"<p><p>Chaperonins/Heat shock protein 60 are ubiquitous multimeric protein complexes that assist in the folding of partially and/or misfolded proteins using metabolic energy into their native stage. The eukaryotic group II chaperonin, also referred as T-complex protein-1 ring complex (TRiC)/T-complex protein-1 (TCP1)/chaperonin containing T-complex protein (CCT), contains 8-9 paralogous subunits, arranged in each of the two rings of hetero-oligomeric complex. In <i>Leishmania</i>, till date, only one subunit, LdTCP1γ, has been well studied. Here, we report the molecular, structural, and functional characterization of TCP1δ subunit of <i>Leishmania donovani</i> (LdTCP1δ), the causative agent of Indian kala-azar. LdTCP1δ gene exhibited only 27.9% identity with LdTCP1γ and clustered in a separate branch in the phylogenic tree of LdTCP1 subunits. The purified recombinant protein formed a high molecular weight complex (0.75 MDa), arranged into 16-mer assembly, and performed <i>in vitro</i> chaperonin activity as assayed by ATP-dependent luciferase folding. LdTCP1δ exhibits 1.8-fold upregulated expression in metabolically active, rapidly dividing log phase promastigotes. Over-expression of LdTCP1δ in promastigotes results in increased infectivity and rate of multiplication of intracellular amastigotes. The study thus establishes the existence of an individual functionally active homo-oligomeric complex of LdTCP1δ chaperonin with its role in parasite infectivity and multiplication.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153922","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":"Inhibition of transient receptor potential vanilloid 1 reduces shedding and transmission during <i>Streptococcus pneumoniae</i> co-infection with influenza.","authors":"Daichi Murakami, Masamitsu Kono, Hideki Sakatani, Takuro Iyo, Masayoshi Hijiya, Tatsuya Shiga, Tetsuya Kinoshita, Takayoshi Sumioka, Yuka Okada, Shizuya Saika, Yusuke Koizumi, Muneki Hotomi","doi":"10.1128/iai.00146-24","DOIUrl":"10.1128/iai.00146-24","url":null,"abstract":"<p><p>Transmission is the first step for a microorganism to establish colonization in the respiratory tract and subsequent development of infectious disease. <i>Streptococcus pneumoniae</i> is a leading pathogen that colonizes the mucosal surfaces of the human upper respiratory tract and causes subsequent transmission and invasive infections especially in co-infection with influenza A virus. Host factors contributing to respiratory contagion are poorly understood. Transient receptor potential vanilloid (TRPV) channels have various roles in response to microoorganism. Inhibition of TRPV exacerbates invasive infection by <i>Streptococcus pneumoniae</i>, but it is unclear how TRPV channels influence pneumococcal transmission. Here, we describe the effect of inhibition of TRPV1 on pneumococcal transmission. We adopted a TRPV1-deficient infant mouse model of pneumococcal transmission during co-infection with influenza A virus. We also analyzed the expression of nasal mucin or pro-inflammatory cytokines. TRPV1 deficiency attenuated pneumococcal transmission and shedding during co-infection with influenza A virus. TRPV1 deficiency suppressed the expression of nasal mucin. In addition, there were increases in the expression of tumor necrosis factor-α and type I interferon, followed by the suppressed replication of influenza A virus in TRPV1-deficient mice. Inhibition of TRPV1 was shown to attenuate pneumococcal transmission by reducing shedding through the suppression of nasal mucin during co-infection with influenza A virus. Inhibition of TRPV1 suppressed nasal mucin by modulation of pro-inflammatory responses and regulation of replication of influenza A virus. TRPV1 could be a new target in preventive strategy against pneumococcal transmission.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897275","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":"RSV enhances <i>Staphylococcus aureus</i> bacterial growth in the lung.","authors":"Helen E Rich, Simran Bhutia, Francina Gonzales de Los Santos, Gabrielle P Entrup, Helen I Warheit-Niemi, Stephen J Gurczynski, Monica Bame, Michael T Douglas, Susan B Morris, Rachel L Zemans, Nicholas W Lukacs, Bethany B Moore","doi":"10.1128/iai.00304-24","DOIUrl":"10.1128/iai.00304-24","url":null,"abstract":"<p><p>Patients coinfected with respiratory syncytial virus (RSV) and bacteria have longer hospital stays, higher risk of intensive care unit admission, and worse outcomes. We describe a model of RSV line 19F/methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) USA300 coinfection that does not impair viral clearance, but prior RSV infection enhances USA300 MRSA bacterial growth in the lung. The increased bacterial burden post-RSV correlates with reduced accumulation of neutrophils and impaired bacterial killing by alveolar macrophages. Surprisingly, reduced neutrophil accumulation is likely not explained by reductions in phagocyte-recruiting chemokines or alterations in proinflammatory cytokine production compared with mice infected with <i>S. aureus</i> alone. Neutrophils from RSV-infected mice retain their ability to migrate toward chemokine signals, and neutrophils from the RSV-infected lung are better able to phagocytize and kill <i>S. aureus ex vivo</i> on a per cell basis. In contrast, while alveolar macrophages could ingest USA300 post-RSV, intracellular bacterial killing was impaired. The RSV/<i>S. aureus</i> coinfected lung promotes a state of overactivation in neutrophils, demonstrated by increased production of reactive oxygen species (ROS) that can drive formation of neutrophil extracellular traps (NETs), resulting in cell death. Mice with RSV/<i>S. aureus</i> coinfection had increased extracellular DNA and protein in bronchoalveolar lavage fluid and histological evidence confirmed NETosis <i>in vivo</i>. Taken together, these data highlight that prior RSV infection can prime the overactivation of neutrophils leading to cell death that impairs neutrophil accumulation in the lung. Additionally, alveolar macrophage killing of bacteria is impaired post-RSV. Together, these defects enhance USA300 MRSA bacterial growth in the lung post-RSV.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987857","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":"Host cell-specific metabolism of linoleic acid controls <i>Toxoplasma gondii</i> growth in cell culture.","authors":"Nicole D Hryckowian, Carlos J Ramírez-Flores, Caitlin Zinda, Sung Chul Park, Martin T Kelty, Laura J Knoll","doi":"10.1128/iai.00299-24","DOIUrl":"10.1128/iai.00299-24","url":null,"abstract":"<p><p>The obligate intracellular parasite <i>Toxoplasma gondii</i> can infect and replicate in any warm-blooded cell tested to date, but much of our knowledge about <i>T. gondii</i> cell biology comes from just one host cell type: human foreskin fibroblasts (HFFs). To expand our knowledge of host-parasite lipid interactions, we studied <i>T. gondii</i> in intestinal epithelial cells, the first site of host-parasite contact following oral infection and the exclusive site of parasite sexual development in feline hosts. We found that highly metabolic Caco-2 cells are permissive to <i>T. gondii</i> growth even when treated with high levels of linoleic acid (LA), a polyunsaturated fatty acid (PUFA) that kills parasites in HFFs. Caco-2 cells appear to sequester LA away from the parasite, preventing membrane disruptions and lipotoxicity that characterize LA-induced parasite death in HFFs. Our work is an important step toward understanding host-parasite interactions in feline intestinal epithelial cells, an understudied but important cell type in the <i>T. gondii</i> life cycle.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080198","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":"crANKing up the infection: ankyrin domains in <i>Rickettsiales</i> and their role in host manipulation.","authors":"William C Hamilton, Irene L G Newton","doi":"10.1128/iai.00059-24","DOIUrl":"10.1128/iai.00059-24","url":null,"abstract":"<p><p>Intracellular bacteria use secreted effector proteins to modify host biology and facilitate infection. For many of these microbes, a particular eukaryotic domain-the ankyrin repeat (ANK)-plays a central role in specifying the host proteins and pathways targeted by the microbe. While we understand much of how some ANKs function in model organisms like <i>Legionella</i> and <i>Coxiella</i>, the understudied <i>Rickettsiales</i> species harbor many proteins with ANKs, some of which play critical roles during infection. This minireview is meant to organize and summarize the research progress made in understanding some of these <i>Rickettsiales</i> ANKs as well as document some of the techniques that have driven much of this progress.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107027","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 cynomolgus monkey <i>E. coli</i> urinary tract infection model confirms efficacy of new FimH vaccine candidates.","authors":"Laurent Chorro, Tara Ciolino, Caresse Lynn Torres, Arthur Illenberger, JohnPaul Aglione, Paula Corts, Jacqueline Lypowy, Christopher Ponce, Annalena La Porte, Deborah Burt, Gretchen L Volberg, Lila Ramaiah, Kathryn McGovern, Jianfang Hu, Annaliesa S Anderson, Natalie C Silmon de Monerri, Isis Kanevsky, Robert G K Donald","doi":"10.1128/iai.00169-24","DOIUrl":"10.1128/iai.00169-24","url":null,"abstract":"<p><p>The increase in urinary tract infections (UTI) caused by antibiotic-resistant <i>Escherichia coli</i> requires the development of new therapeutic agents and prophylactic vaccines. To evaluate the efficacy of new lead candidates, we implemented a cynomolgus macaque UTI challenge model that mimics human uncomplicated cystitis in response to transurethral challenge with a multidrug-resistant (MDR) <i>E. coli</i> serotype O25b ST131 isolate. <i>E. coli</i> fimbrial adhesin FimH and O-antigens are separately under clinical evaluation by others as vaccine candidates to prevent UTI and invasive urosepsis disease, respectively. Accordingly, we assessed the protective efficacy of three 50-µg intramuscular doses of a novel recombinant FimH antigen adjuvanted with liposomal QS21/MPLA compared with saline placebo in groups of nine animals. A third group was vaccinated with this FimH formulation in combination with 1 µg each of a four-valent mixture of serotype O1a, O2, O6, and O25b O-antigen CRM₁₉₇ lattice glycoconjugates. Both vaccines elicited high levels of serum FimH IgG and adhesin blocking antibodies at the time of bacterial challenge and, for the combination group, O-antigen-specific antibodies. Following bacterial challenge, both vaccinated groups showed >200- and >700-fold reduction in bacteriuria at day 2 and day 7 post-infection compared with placebo, respectively. In parallel, both vaccines significantly reduced levels of inflammatory biomarkers IL-8 and myeloperoxidase in the urine at day 2 post-infection relative to placebo. Results provide preclinical proof-of-concept for the prevention of an MDR UTI infection by these new vaccine formulations.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286099","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":"The plasmid-encoded members of paralogous gene family 52 are dispensable to the enzootic cycle of <i>Borrelia burgdorferi</i>.","authors":"Ashley M Groshong, Nora E Gibbons, Brendan P Moore, William T Bellamy, Jon S Blevins","doi":"10.1128/iai.00214-24","DOIUrl":"10.1128/iai.00214-24","url":null,"abstract":"<p><p>Lyme disease, the leading vector-borne disease in the United States and Europe, develops after infection with <i>Borrelia burgdorferi sensu lato</i> bacteria. Transmission of the spirochete from the tick vector to a vertebrate host requires global changes in gene expression that are controlled, in part, by the Rrp2/RpoN/RpoS alternative sigma factor cascade. Transcriptional studies defining the <i>B. burgdorferi</i> RpoS regulon have suggested that RpoS activates the transcription of paralogous family 52 (PFam52) genes. In strain B31, PFam52 genes (<i>bbi42</i>, <i>bbk53</i>, and <i>bbq03</i>) encode a set of conserved hypothetical proteins with >89% amino acid identity that are predicted to be surface-localized. Extensive homology among members of paralogous families complicates studies of protein contributions to pathogenicity as the potential for functional redundancy will obfuscate findings. Using a sequential mutagenesis approach, we generated clones expressing a single PFam52 paralog, as well as a strain deficient in all three. The single paralog expressing strains were used to confirm BBI42, BBK53, and BBQ03 surface localization and RpoS regulation. Surprisingly, the PFam52-deficient strain was able to infect mice and complete the enzootic cycle similar to the wild-type parental strain. Indeed, the presence of numerous pseudogenes that contain frameshifts or internal stop codons among the PFam52 genes suggests that they may be subjected to gene loss in <i>B. burgdorferi</i>'s reduced genome. Alternatively, the lack of phenotype might reflect the limitations of the experimental mouse infection model.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906517","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":"Lactate promotes the biofilm-to-invasive-planktonic transition in <i>Salmonella enterica</i> serovar Typhimurium via the <i>de novo</i> purine pathway.","authors":"Francisco J Albicoro, Shingo Bessho, Kaitlyn Grando, Sophia Olubajo, Vincent Tam, Çagla Tükel","doi":"10.1128/iai.00266-24","DOIUrl":"10.1128/iai.00266-24","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;i&gt;Salmonella enterica&lt;/i&gt; serovar Typhimurium (&lt;i&gt;S&lt;/i&gt;. Typhimurium) infection triggers an inflammatory response that changes the concentration of metabolites in the gut impacting the luminal environment. Some of these environmental adjustments are conducive to &lt;i&gt;S&lt;/i&gt;. Typhimurium growth, such as the increased concentrations of nitrate and tetrathionate or the reduced levels of Clostridia-produced butyrate. We recently demonstrated that &lt;i&gt;S&lt;/i&gt;. Typhimurium can form biofilms within the host environment and respond to nitrate as a signaling molecule, enabling it to transition between sessile and planktonic states. To investigate whether &lt;i&gt;S&lt;/i&gt;. Typhimurium utilizes additional metabolites to regulate its behavior, our study delved into the impact of inflammatory metabolites on biofilm formation. The results revealed that lactate, the most prevalent metabolite in the inflammatory environment, impedes biofilm development by reducing intracellular c-di-GMP levels, suppressing the expression of curli and cellulose, and increasing the expression of flagellar genes. A transcriptomic analysis determined that the expression of the &lt;i&gt;de novo&lt;/i&gt; purine pathway increases during high lactate conditions, and a transposon mutagenesis genetic screen identified that PurA and PurG, in particular, play a significant role in the inhibition of curli expression and biofilm formation. Lactate also increases the transcription of the type III secretion system genes involved in tissue invasion. Finally, we show that the pyruvate-modulated two-component system BtsSR is activated in the presence of high lactate, which suggests that lactate-derived pyruvate activates BtsSR system after being exported from the cytosol. All these findings propose that lactate is an important inflammatory metabolite used by &lt;i&gt;S&lt;/i&gt;. Typhimurium to transition from a biofilm to a motile state and fine-tune its virulence.IMPORTANCEWhen colonizing the gut, &lt;i&gt;Salmonella enterica&lt;/i&gt; serovar Typhimurium (&lt;i&gt;S&lt;/i&gt;. Typhimurium) adopts a dynamic lifestyle that alternates between a virulent planktonic state and a multicellular biofilm state. The coexistence of biofilm formers and planktonic &lt;i&gt;S&lt;/i&gt;. Typhimurium in the gut suggests the presence of regulatory mechanisms that control planktonic-to-sessile transition. The signals triggering the transition of &lt;i&gt;S&lt;/i&gt;. Typhimurium between these two lifestyles are not fully explored. In this work, we demonstrated that in the presence of lactate, the most dominant host-derived metabolite in the inflamed gut, there is a reduction of c-di-GMP in &lt;i&gt;S&lt;/i&gt;. Typhimurium, which subsequently inhibits biofilm formation and induces the expression of its invasion machinery, motility genes, and &lt;i&gt;de novo&lt;/i&gt; purine metabolic pathway genes. Furthermore, high levels of lactate activate the BtsSR two-component system. Collectively, this work presents new insights toward the comprehension of host metabolism and gut microenvironment roles in the regulation o","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916558","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":"Salmonella Typhimurium infection inhibits macrophage IFNβ signaling in a TLR4-dependent manner","authors":"Michael ShusterZhihui LyuJacques AugenstreichShrestha MathurAkshaya GaneshJiqiang LingVolker Briken1Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland, USASunny Shin","doi":"10.1128/iai.00098-24","DOIUrl":"https://doi.org/10.1128/iai.00098-24","url":null,"abstract":"Infection and Immunity, Ahead of Print. <br/>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142224023","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}