Infection and Immunity最新文献

{"title":"Bacterial surface lipoproteins mediate epithelial microinvasion by Streptococcus pneumoniae","authors":"Jia Mun ChanElisa Ramos-SevillanoModupeh BettsHolly U. WilsonCaroline M. WeightAmbrine Houhou-OusalahGabriele PollaraJeremy S. BrownRobert S. Heyderman1Research Department of Infection, Division of Infection and Immunity, University College London, London, United Kingdom2UCL Respiratory, Division of Medicine, University College London, London, United Kingdom, Nancy E. Freitag","doi":"10.1128/iai.00447-23","DOIUrl":"https://doi.org/10.1128/iai.00447-23","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":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140617114","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":"Plasmodium yoelii surface-related antigen (PySRA) modulates the host pro-inflammatory responses via binding to CD68 on macrophage membrane","authors":"Xin Feng, Jia-Li Yu, Yi-Fan Sun, Chen-Yan Du, Yao Shen, Lu Zhang, Wei-Zhong Kong, Su Han, Yang Cheng","doi":"10.1128/iai.00113-24","DOIUrl":"https://doi.org/10.1128/iai.00113-24","url":null,"abstract":"Malaria is an important mosquito-borne disease that seriously endangers human life\u0000and health. In 2021, global reports indicate that nearly 247 million malaria cases\u0000caused 619,000 deaths (1). Malaria is a highly complex disease with a variety of pathologic manifestations.\u0000In the early stages of infection, most patients showed general symptoms such as fever,\u0000sweat, and headache. Meanwhile, the symptoms of cerebral malaria, severe anemia, and\u0000respiratory distress occurred with the increase in parasites during the erythrocytic\u0000stage, leading to severe malaria (2–4).","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140617196","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":"Flagellin-modulated inflammasome pathways characterize the human alveolar macrophage response to Burkholderia pseudomallei, a lung-tropic pathogen","authors":"Lara Lovelace-MaconSarah M. BakerDeirdre DuckenSudeshna SealGuilhem RerolleDiane TomitaKelly D. SmithSandra SchwarzT. Eoin West1Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington, USA2Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington, USA3Department of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington, USA4Interfaculty Institute of Microbiology and Infection Medicine, University of Tuebingen, Tuebingen, Germany5Department of Global Health, University of Washington, Seattle, Washington, USA, Victor J. Torres","doi":"10.1128/iai.00060-24","DOIUrl":"https://doi.org/10.1128/iai.00060-24","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":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140578477","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":"Retraction for Billington et al., “Clostridium perfringens Type E Animal Enteritis Isolates with Highly Conserved, Silent Enterotoxin Gene Sequences”","authors":"Stephen J. BillingtonEva U. WieckowskiMahfuzur R. SarkerDawn BueschelJ. Glenn SongerBruce A. McClane","doi":"10.1128/iai.00066-24","DOIUrl":"https://doi.org/10.1128/iai.00066-24","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":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140578226","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":"An infant mouse model of influenza-driven nontypeable Haemophilus influenzae colonization and acute otitis media suitable for preclinical testing of novel therapies","authors":"Katherine R. Landwehr, Caitlyn M. Granland, Kelly M. Martinovich, Naomi M. Scott, Elke J. Seppanen, Luke Berry, Deborah Strickland, Alma Fulurija, Peter C. Richmond, Lea-Ann S. Kirkham","doi":"10.1128/iai.00453-23","DOIUrl":"https://doi.org/10.1128/iai.00453-23","url":null,"abstract":"Nontypeable Haemophilus influenzae (NTHi) is a Gram-negative bacterium that exhibits opportunistic pathogenic behavior\u0000in humans (1). Asymptomatic nasopharyngeal colonization with NTHi is common and transient in children,\u0000with carriage frequencies ranging from ~15% to 100% depending upon age and geographic\u0000region (2–5). NTHi can also cause a range of diseases including sinusitis, conjunctivitis, pharyngitis,\u0000meningitis, bacteraemia, pneumonia, and otitis media (OM) (6, 7). Globally, NTHi is the predominant pathogen associated with chronic OM with effusion,\u0000recurrent acute OM, or acute OM with failure to treat (8). Early and dense NTHi colonization is associated with the development of acute and\u0000recurrent OM (6, 9–13). Triggers for the development of asymptomatic NTHi colonization into OM are thought\u0000to involve virus-induced inflammation, which permits proliferation and dissemination\u0000of NTHi from the nasopharynx along the Eustachian tube and into the middle ear (14, 15).","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140578328","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":"Deciphering the gastrointestinal carriage of Klebsiella pneumoniae","authors":"Andrew S. Bray, M. Ammar Zafar","doi":"10.1128/iai.00482-23","DOIUrl":"https://doi.org/10.1128/iai.00482-23","url":null,"abstract":"Carl Friedländer’s identification of bacteria in the lungs of pneumonia patients in\u00001882 marked a pivotal moment, attributing the disease to bacterial causation, naming\u0000the bacterium Friedländer bacillus, which was subsequently named Klebsiella pneumoniae (K. pneumoniae) after microbiologist Edwin Klebs (1–3). In the ensuing 141 years, K. pneumoniae, a gram negative, encapsulated, non-motile, and rod-shaped bacterium, has been extensively\u0000studied as it can readily colonize human mucosal surfaces and is considered an opportunistic\u0000pathogen that can cause the development of pneumonia, bacteremia, pyogenic liver abscesses,\u0000and urinary tract infections (UTIs) (Fig. 1A) (4). What has been historically referred to as “Klebsiella pneumoniae” has since been demonstrated to be a complex of very closely related Klebsiella species (5–8), known as the K. pneumoniae species complex (KpSC), which comprises clinically relevant species that include K. pneumoniae, K. quasipneumoniae subsp. quasipneumoniae and similipneumoniae, K. variicola subsp. variicola and tropica, K. quasivariicola, and K. africana. This review will focus on K. pneumoniae sensu stricto, comprising ~85% of KpSC isolates (5, 9–12).","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140578475","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":"Suppression of host humoral immunity by <i>Borrelia burgdorferi</i> varies over the course of infection.","authors":"Megan T Williams, Yan Zhang, Mark E Pulse, Rance E Berg, Michael S Allen","doi":"10.1128/iai.00018-24","DOIUrl":"10.1128/iai.00018-24","url":null,"abstract":"<p><p><i>Borrelia burgdorferi</i>, the spirochetal agent of Lyme disease, utilizes a variety of strategies to evade and suppress the host immune response, which enables it to chronically persist in the host. The resulting immune response is characterized by unusually strong IgM production and a lack of long-term protective immunity. Previous studies in mice have shown that infection with <i>B. burgdorferi</i> also broadly suppresses host antibody responses against unrelated antigens. Here, we show that mice infected with <i>B. burgdorferi</i> and concomitantly immunized with recombinant severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein had an abrogated antibody response to the immunization. To further define how long this humoral immune suppression lasts, mice were immunized at 2, 4, and 6 weeks post-infection. Suppression of host antibody production against the SARS-CoV-2 spike protein peaked at 2 weeks post-infection but continued for all timepoints measured. Antibody responses against the SARS-CoV-2 spike protein were also assessed following antibiotic treatment to determine whether this immune suppression persists or resolves following clearance of <i>B. burgdorferi</i>. Host antibody production against the SARS-CoV-2 spike protein returned to baseline following antibiotic treatment; however, anti-SARS-CoV-2 IgM remained high, comparable to levels found in <i>B. burgdorferi</i>-infected but untreated mice. Thus, our data demonstrate restored IgG responses following antibiotic treatment but persistently elevated IgM levels, indicating lingering effects of <i>B. burgdorferi</i> infection on the immune system following treatment.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11003232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140184390","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":"Phospholipase C epsilon-1 (PLCƐ1) mediates macrophage activation and protection against tuberculosis.","authors":"Ananya Gupta, Shyamala Thirunavukkarasu, Javier Rangel-Moreno, Mushtaq Ahmed, Rosemary V Swanson, Stanley Kimbung Mbandi, Alan V Smrcka, Deepak Kaushal, Thomas J Scriba, Shabaana A Khader","doi":"10.1128/iai.00495-23","DOIUrl":"10.1128/iai.00495-23","url":null,"abstract":"<p><p>Tuberculosis (TB) caused by <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) infects up to a quarter of the world's population. Although immune responses can control <i>Mtb</i> infection, 5%-10% of infected individuals can progress to active TB disease (progressors). A myriad of host factors regulate disease progression in TB and a better understanding of immune correlates of protection and disease is pivotal for the development of new therapeutics. Comparison of human whole blood transcriptomic metadata with that of macaque TB progressors and <i>Mtb</i>-infected diversity outbred mice (DO) led to the identification of differentially regulated gene (DEG) signatures, associated with TB progression or control. The current study assessed the function of Phospholipase C epsilon (<i>PLCƐ1</i>), the top downregulated gene across species in TB progressors, using a gene-specific knockout mouse model of <i>Mtb</i> infection and in vitro <i>Mtb</i>-infected bone marrow-derived macrophages. <i>PLCƐ1</i> gene expression was downregulated in TB progressors across species. <i>PLCε1</i> deficiency in the mouse model resulted in increased susceptibility to <i>Mtb</i> infection<i>,</i> coincident accumulation of lung myeloid cells, and reduced ability to mount antibacterial responses. However, <i>PLCε1</i> was not required for the activation and accumulation of T cells in mice. Our results suggest an important early role for <i>PLCƐ1</i> in shaping innate immune response to TB and may represent a putative target for host-directed therapy.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11003233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140049371","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":"Enterohemorrhagic <i>Escherichia coli</i> effector EspF triggers oxidative DNA lesions in intestinal epithelial cells.","authors":"Yuting Fang, Muqing Fu, Xinyue Li, Bao Zhang, Chengsong Wan","doi":"10.1128/iai.00001-24","DOIUrl":"10.1128/iai.00001-24","url":null,"abstract":"<p><p>Attaching/effacing (A/E) pathogens induce DNA damage and colorectal cancer by injecting effector proteins into host cells via the type III secretion system (T3SS). EspF is one of the T3SS-dependent effector proteins exclusive to A/E pathogens, which include enterohemorrhagic <i>Escherichia coli</i>. The role of EspF in the induction of double-strand breaks (DSBs) and the phosphorylation of the repair protein SMC1 has been demonstrated previously. However, the process of damage accumulation and DSB formation has remained enigmatic, and the damage response is not well understood. Here, we first showed a compensatory increase in the mismatch repair proteins MutS homolog 2 (MSH2) and MSH6, as well as poly(ADP-ribose) polymerase 1, followed by a dramatic decrease, threatening cell survival in the presence of EspF. Flow cytometry revealed that EspF arrested the cell cycle at the G2/M phase to facilitate DNA repair. Subsequently, 8-oxoguanine (8-oxoG) lesions, a marker of oxidative damage, were assayed by ELISA and immunofluorescence, which revealed the accumulation of 8-oxoG from the cytosol to the nucleus. Furthermore, the status of single-stranded DNA (ssDNA) and DSBs was confirmed. We observed that EspF accelerated the course of DNA lesions, including 8-oxoG and unrepaired ssDNA, which were converted into DSBs; this was accompanied by the phosphorylation of replication protein A 32 in repair-defective cells. Collectively, these findings reveal that EspF triggers various types of oxidative DNA lesions with impairment of the DNA damage response and may result in genomic instability and cell death, offering novel insight into the tumorigenic potential of EspF.IMPORTANCEOxidative DNA lesions play causative roles in colitis-associated colon cancer. Accumulating evidence shows strong links between attaching/effacing (A/E) pathogens and colorectal cancer (CRC). EspF is one of many effector proteins exclusive to A/E pathogens with defined roles in the induction of oxidative stress, double-strand breaks (DSBs), and repair dysregulation. Here, we found that EspF promotes reactive oxygen species generation and 8-oxoguanine (8-oxoG) lesions when the repair system is activated, contributing to sustained cell survival. However, infected cells exposed to EspF presented 8-oxoG, which results in DSBs and ssDNA accumulation when the cell cycle is arrested at the G2/M phase and the repair system is defective or saturated by DNA lesions. In addition, we found that EspF could intensify the accumulation of nuclear DNA lesions through oxidative and replication stress. Overall, our work highlights the involvement of EspF in DNA lesions and DNA damage response, providing a novel avenue by which A/E pathogens may contribute to CRC.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11003234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982884","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":"Why put yourself on a pedestal? The pathogenic role of the A/E pedestal","authors":"M. V. Miner, I. Rauch","doi":"10.1128/iai.00489-23","DOIUrl":"https://doi.org/10.1128/iai.00489-23","url":null,"abstract":"The study of enterobacterial pathogens is of critical importance, given the nearly\u000063,000 annual diarrheagenic Escherichia coli (E. coli)-related deaths worldwide (1, 2). In particular, enteropathogenic E. coli (EPEC) is a leading cause of infantile diarrhea, often contracted through the fecal-oral\u0000route via food or water (3). Attaching and effacing (A/E) pathogens, like EPEC, are named for their signature\u0000lesion on the intestinal epithelium during infection. The characteristics of these\u0000attaching and effacing lesions are effacement of the intestinal brush border, intimate\u0000attachment to the host epithelium, and the formation of actin-rich pedestals below\u0000the site of bacterial adherence. These pedestals are derived from bacterial-driven\u0000actin nucleation inside the host cell, creating a protrusion in the plasma membrane.\u0000Enterohemorrhagic E. coli (EHEC) is another human A/E pathogen that is similar to EPEC but can be distinguished\u0000from EPEC by its pathogenic and geographic features. Although EPEC is prevalent in\u0000low- and middle-income countries, EHEC is pervasive in developed countries. EPEC preferentially\u0000infects the small intestine, and EHEC preferentially infects the colon. Additionally,\u0000only EHEC produces Shiga toxin (Stx) that can inhibit protein synthesis in eukaryotic\u0000cells and is a cause of many of the systemic symptoms experienced, including long-term\u0000renal damage and hemolytic uremic syndrome (4, 5). Regardless of their clinical differences, both EPEC and EHEC are often studied\u0000using the murine pathogen Citrobacter rodentium (C. rodentium) as a proxy (6–8). All three pathogens encode the Locus of enterocyte effacement (LEE) pathogenicity\u0000island, which encodes a type III secretion system and is required for virulence. C. rodentium possesses the same LEE pathogenicity island-encoded effectors that are required for\u0000EPEC and EHEC virulence (9–11). However, the three AE pathogens have other effectors that are not a part of the\u0000LEE pathogenicity island, contributing to distinct characteristics in each pathogen.\u0000These A/E lesion pathogens are a continuous object of study due, in part, to their\u0000unique ability to form pedestals and the unknown role the pedestals play in infection.","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140603144","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}