Infection and Immunity最新文献

{"title":"Pathogenic diversification of the gut commensal Providencia alcalifaciens via acquisition of a second type III secretion system","authors":"Jessica A. KleinAlexander V. PredeusAimee R. GreisslMattie M. Clark-HerreraEddy CruzJennifer A. CundiffAmanda L. HaeberleMaya HowellAaditi LeleDonna J. RobinsonTrina L. WestermanMarie WrandeSarah J. WrightNicole M. GreenBruce A. VallanceMichael McClellandAndres MejiaAlan G. GoodmanJohanna R. ElfenbeinLeigh A. Knodler1Paul G. Allen School for Global Health, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA2Wellcome Sanger Institute, Hinxton, Cambridgeshire, United Kingdom3Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, USA4Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA5Public Health Laboratory, Los Angeles County Department of Public Health, Downey, California, USA6Division of Gastroenterology, Hepatology and Nutrition, BC Children’s Hospital and the University of British Columbia, Vancou..","doi":"10.1128/iai.00314-24","DOIUrl":"https://doi.org/10.1128/iai.00314-24","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":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142224024","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 Noh et al., “Identification of Anaplasma marginale adhesins for entry into Dermacentor andersoni tick cells using phage display”","authors":"Susan M. NohJessica UjczoDebra C. AlperinShelby M. JarvisMuna S. M. SolymanRoberta KokuOlalekan C. AkinsulieElizabeth J. Hoffmann","doi":"10.1128/iai.00377-24","DOIUrl":"https://doi.org/10.1128/iai.00377-24","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":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142224026","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":"T6SS in plant pathogens: unique mechanisms in complex hosts.","authors":"Lexie M Matte, Abigail V Genal, Emily F Landolt, Elizabeth S Danka","doi":"10.1128/iai.00500-23","DOIUrl":"10.1128/iai.00500-23","url":null,"abstract":"<p><p>Type VI secretion systems (T6SSs) are complex molecular machines that allow bacteria to deliver toxic effector proteins to neighboring bacterial and eukaryotic cells. Although initial work focused on the T6SS as a virulence mechanism of human pathogens, the field shifted to examine the use of T6SSs for interbacterial competition in various environments, including in the plant rhizosphere. Genes encoding the T6SS are estimated to be found in a quarter of all Gram-negative bacteria and are especially highly represented in <i>Proteobacteria</i>, a group which includes the most important bacterial phytopathogens. Many of these pathogens encode multiple distinct T6SS gene clusters which can include the core components of the apparatus as well as effector proteins. The T6SS is deployed by pathogens at multiple points as they colonize their hosts and establish an infection. In this review, we describe what is known about the use of T6SS by phytopathogens against plant hosts and non-plant organisms, keeping in mind that the structure of plants requires unique mechanisms of attack that are distinct from the mechanisms used for interbacterial interactions and against animal hosts. While the interactions of specific effectors (such as phospholipases, endonucleases, peptidases, and amidases) with targets have been well described in the context of interbacterial competition and in some eukaryotic interactions, this review highlights the need for future studies to assess the activity of phytobacterial T6SS effectors against plant cells.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017316","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":"Eosinophils respond to, but are not essential for control of an acute <i>Salmonella enterica</i> serovar Typhimurium infection in mice.","authors":"Rachael D FitzPatrick, Jonathan R Noone, Richard A Cartwright, Dominique M Gatti, Tara P Brosschot, Jenna M Lane, Erik L Jensen, Isabella Kroker Kimber, Lisa A Reynolds","doi":"10.1128/iai.00325-24","DOIUrl":"https://doi.org/10.1128/iai.00325-24","url":null,"abstract":"<p><p>Eosinophils are a highly abundant cell type in the gastrointestinal tract during homeostatic conditions, where they have recently been reported to take on an activated phenotype following colonization by the bacterial microbiota. To date, there have been few studies investigating whether eosinophils respond to infection with enteric bacterial pathogens and/or investigating the requirements for eosinophils for effective bacterial pathogen control. In this study, we investigated the response of eosinophils to an acute enteric infection of mice with the bacterial pathogen <i>Salmonella enterica</i> serovar Typhimurium. We also assessed whether eosinophil deficiency impacted <i>Salmonella</i> burdens in the intestinal tract or impacted the systemic dissemination of <i>Salmonella</i> following an oral infection of littermate wild-type BALB/cJ and eosinophil-deficient ΔdblGATA BALB/cJ mice. We found comparable <i>Salmonella</i> burdens in the intestinal tract of wild-type and eosinophil-deficient mice and no significant differences in the levels of <i>Salmonella</i> disseminating to systemic organs within 3 days of infection. Despite our evidence suggesting that eosinophils are not an essential cell type for controlling bacterial burdens in this acute infection setting, we found higher levels of eosinophils in gut-draining lymph nodes following infection, indicating that eosinophils do respond to <i>Salmonella</i> infection. Our data contribute to the growing evidence that eosinophils are responsive to bacterial stimuli, yet the influence of and requirements for eosinophils during bacterial infection appear to be highly context-dependent.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153921","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":"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":"https://doi.org/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":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic glycan-specific antibody binding mediates protection during primary amoebic meningoencephalitis.","authors":"Annie Park Moseman, Ching-Wen Chen, Xiaoe Liang, Dongmei Liao, Masayuki Kuraoka, E Ashley Moseman","doi":"10.1128/iai.00183-24","DOIUrl":"https://doi.org/10.1128/iai.00183-24","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;i&gt;Naegleria fowleri&lt;/i&gt; (&lt;i&gt;N. fowleri&lt;/i&gt;) infection &lt;i&gt;via&lt;/i&gt; the upper respiratory tract causes a fatal CNS disease known as primary amoebic meningoencephalitis (PAM). The robust &lt;i&gt;in vivo&lt;/i&gt; immune response to &lt;i&gt;N. fowleri infection&lt;/i&gt; underlies the immunopathology that characterizes the disease. However, little is known about why this pathogen evades immune control. Infections occur in seemingly healthy individuals and effective clinical options are lacking, thus a nearly 98% fatality rate. It is unclear how or if host factors may contribute to susceptibility or disease exacerbation, yet mechanistic studies of the &lt;i&gt;in vivo&lt;/i&gt; immune response and disease progression are hampered by a lack of tools. In this study, we have generated monoclonal antibodies to &lt;i&gt;N. fowleri&lt;/i&gt; surface antigens and shown them to be excellent tools for studying the &lt;i&gt;in vivo&lt;/i&gt; immune response. We also identified one monoclonal, 2B6, with potent inherent anti-amoebastatic activity &lt;i&gt;in vitro&lt;/i&gt;. This antibody is also able to therapeutically prolong host survival &lt;i&gt;in vivo&lt;/i&gt; and furthermore, recombinant antibodies with an isotype more capable of directing immune effector activity further improved survival when given therapeutically. Thus, we report the generation of a novel monoclonal antibody to &lt;i&gt;N. fowleri&lt;/i&gt; that can enhance beneficial immune functions, even when given therapeutically during disease. We believe this provides evidence for the potential of therapeutic antibody treatments in PAM.IMPORTANCE&lt;i&gt;Naegleria fowleri&lt;/i&gt; (&lt;i&gt;N. fowleri&lt;/i&gt;) is a free-living amoeba that is found ubiquitously in warm freshwater. While human exposure is common, it rarely results in pathogenesis. However, when &lt;i&gt;N. fowleri&lt;/i&gt; gains access to the upper airway, specifically the olfactory mucosa, infection leads to a lethal disease known as primary amoebic meningoencephalitis (PAM). As a free-living amoeba, &lt;i&gt;N. fowleri&lt;/i&gt; does not need a mammalian host; indeed, it can be accurately described as an accidental opportunistic pathogen. While most opportunistic infections occur in humans who are immunocompromised, there are no reported immune dysfunctions associated with &lt;i&gt;N. fowleri&lt;/i&gt; infection. Therefore, the basis for &lt;i&gt;N. fowleri&lt;/i&gt; opportunism is not known, and the reasons why some humans develop PAM while others do not are simply not well understood. It is reasonable to speculate that local or acute immune failures, potentially even a lack of prior adaptive immunity, are related to disease susceptibility. Careful immune profiling and characterization of the &lt;i&gt;in vivo&lt;/i&gt; immune response to &lt;i&gt;N. fowleri&lt;/i&gt; in a mammalian host are desperately needed to understand which host factors are critical to defense, and how these responses might be compromised in a way that results in lethal infection. To identify genes and pathways that provide resistance against &lt;i&gt;in vivo N. fowleri&lt;/i&gt; infection, we generated surface reactive monoclonal antibodies (A","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132619","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":"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":"https://doi.org/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":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","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":"https://doi.org/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":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Akkermansia muciniphila</i> alleviates abdominal aortic aneurysms via restoring CITED2 activated by EPAS1.","authors":"Siqing Wang, Hang Shi, Yue Cheng, Lei Jiang, Yang Lou, Manish Kumar, Mingfei Sun, Xianze Shao, Xuan Zhao, Baichun Wang","doi":"10.1128/iai.00172-24","DOIUrl":"https://doi.org/10.1128/iai.00172-24","url":null,"abstract":"<p><p>Abdominal aortic aneurysm (AAA) is a life-threatening cardiovascular disease that has been linked to gut microbiome dysbiosis. Therefore, this study aims to investigate the effects of <i>Akkermansia muciniphila</i> (<i>Am</i>) on AAA mice and the biomolecules involved. AAA mice were generated using angiotensin II (Ang II), and 16sRNA sequencing was used to identify an altered abundance of microbiota in the feces of AAA mice. Vascular smooth muscle cell (VSMC) markers and apoptosis, and macrophage infiltration in mouse aortic tissues were examined. The abundance of <i>Am</i> was reduced in AAA mouse feces, and endothelial PAS domain-containing protein 1 (EPAS1) was downregulated in AAA mice and VSMC induced with Ang II. <i>Am</i> delayed AAA progression in mice, which was blunted by knockdown of EPAS1. EPAS1 was bound to the Cbp/p300-interacting transactivator 2 (CITED2) promoter and promoted CITED2 transcription. CITED2 reduced VSMC apoptosis and delayed AAA progression. Moreover, EPAS1 inhibited macrophage inflammatory response by promoting CITED2 transcription. In conclusion, gut microbiome dysbiosis in AAA induces EPAS1-mediated dysregulation of CITED2 to promote macrophage inflammatory response and VSMC apoptosis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107026","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":"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":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}