Infection and Immunity最新文献

{"title":"Articles of Significant Interest in This Issue.","authors":"","doi":"10.1128/iai.00231-24","DOIUrl":"https://doi.org/10.1128/iai.00231-24","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"92 6","pages":"e0023124"},"PeriodicalIF":3.1,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300551","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":"Lipid A modification of colistin-resistant <i>Klebsiella pneumoniae</i> does not alter innate immune response in a mouse model of pneumonia.","authors":"Gitanjali Bhushan, Victor Castano, Tania Wong Fok Lung, Courtney Chandler, Thomas H McConville, Robert K Ernst, Alice S Prince, Danielle Ahn","doi":"10.1128/iai.00016-24","DOIUrl":"10.1128/iai.00016-24","url":null,"abstract":"<p><p>Polymyxin resistance in carbapenem-resistant <i>Klebsiella pneumoniae</i> bacteria is associated with high morbidity and mortality in vulnerable populations throughout the world. Ineffective antimicrobial activity by these last resort therapeutics can occur by transfer of <i>mcr-1</i>, a plasmid-mediated resistance gene, causing modification of the lipid A portion of lipopolysaccharide (LPS) and disruption of the interactions between polymyxins and lipid A. Whether this modification alters the innate host immune response or carries a high fitness cost in the bacteria is not well established. To investigate this, we studied infection with <i>K. pneumoniae</i> (KP) ATCC 13883 harboring either the <i>mcr-1</i> plasmid (p<i>mcr-1</i>) or the vector control (pBCSK) ATCC 13883. Bacterial fitness characteristics of <i>mcr-1</i> acquisition were evaluated. Differentiated human monocytes (THP-1s) were stimulated with KP bacterial strains or purified LPS from both parent isolates and isolates harboring <i>mcr-1</i>. Cell culture supernatants were analyzed for cytokine production. A bacterial pneumonia model in WT C57/BL6J mice was used to monitor immune cell recruitment, cytokine induction, and bacterial clearance in the bronchoalveolar lavage fluid (BALF). Isolates harboring <i>mcr-1</i> had increased colistin MIC compared to the parent isolates but did not alter bacterial fitness. Few differences in cytokines were observed with purified LPS from <i>mcr-1</i> expressing bacteria <i>in vitro</i>. However, in a mouse pneumonia model, no bacterial clearance defect was observed between p<i>mcr-1</i>-harboring KP and parent isolates. Consistently, no differences in cytokine production or immune cell recruitment in the BALF were observed, suggesting that other mechanisms outweigh the effect of these lipid A mutations in LPS.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0001624"},"PeriodicalIF":2.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070936","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":"Effect of hepatocyte damage in hepatic fibrogenesis of patients infected with <i>Schistosoma japonicum</i>.","authors":"Yaqi Lu, Wangxian Tang, Heng Zhang, Jing Liu, Shan Zhong","doi":"10.1128/iai.00026-24","DOIUrl":"10.1128/iai.00026-24","url":null,"abstract":"<p><p>Schistosomiasis is a serious public health problem, and previous studies found that liver function and hepatic cells are damaged. To evaluate the serum parameters of liver function and fibrosis in schistosomiasis patients infected with <i>Schistosoma japonicum</i> (<i>Schistosoma J</i>.) and analyze the correlations between liver function and serum fibrosis markers in patients infected with <i>Schistosoma J</i>., this retrospective study enrolled 133 patients. The study population was divided into four groups: healthy people control group (<i>n</i> = 20), chronic schistosomiasis without liver cirrhosis (CS) group (<i>n</i> = 21), schistosomiasis cirrhosis without hypoalbuminemia (SC-HA) group (<i>n</i> = 68), and schistosomiasis cirrhosis with hypoalbuminemia (SC +HA) group (<i>n</i> = 24). Clinical and laboratory data were collected for analysis. In the multiple comparison of abnormal rates of aspartate aminotransferase (AST) and total bilirubin (TBIL), the abnormal rate of the SC +HA group was significantly higher than that of the other three groups (<i>P</i> < 0.05), and the abnormal rate of γ-GT in the SC +HA group was significantly higher than that in the control group (<i>P</i> < 0.05). Multiple comparison results of serum levels of fibrosis markers showed that the SC group had a significantly higher level of indexes than other groups (<i>P</i> < 0.05). The levels of TGF-β1 in the CS group, SC-HA group and SC +HA group were significantly higher than those in the control group (<i>P</i> < 0.001). Our study demonstrated that the liver function and hepatic cells were damaged with the progression of liver disease in patients infected with <i>Schistosoma J.</i>, and they played an important role in the occurrence and development of liver fibrosis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0002624"},"PeriodicalIF":2.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065335","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":"Exploring the versatile roles of the endocannabinoid system and phytocannabinoids in modulating bacterial infections.","authors":"Hailey Barker, Mariola J Ferraro","doi":"10.1128/iai.00020-24","DOIUrl":"10.1128/iai.00020-24","url":null,"abstract":"<p><p>The endocannabinoid system (ECS), initially identified for its role in maintaining homeostasis, particularly in regulating brain function, has evolved into a complex orchestrator influencing various physiological processes beyond its original association with the nervous system. Notably, an expanding body of evidence emphasizes the ECS's crucial involvement in regulating immune responses. While the specific role of the ECS in bacterial infections remains under ongoing investigation, compelling indications suggest its active participation in host-pathogen interactions. Incorporating the ECS into the framework of bacterial pathogen infections introduces a layer of complexity to our understanding of its functions. While some studies propose the potential of cannabinoids to modulate bacterial function and immune responses, the outcomes inherently hinge on the specific infection and cannabinoid under consideration. Moreover, the bidirectional relationship between the ECS and the gut microbiota underscores the intricate interplay among diverse physiological processes. The ECS extends its influence far beyond its initial discovery, emerging as a promising therapeutic target across a spectrum of medical conditions, encompassing bacterial infections, dysbiosis, and sepsis. This review comprehensively explores the complex roles of the ECS in the modulation of bacteria, the host's response to bacterial infections, and the dynamics of the microbiome. Special emphasis is placed on the roles of cannabinoid receptor types 1 and 2, whose signaling intricately influences immune cell function in microbe-host interactions.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0002024"},"PeriodicalIF":2.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075952","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":"Identification of <i>Anaplasma marginale</i> adhesins for entry into <i>Dermacentor andersoni</i> tick cells using phage display.","authors":"Susan M Noh, Jessica Ujczo, Debra C Alperin, Shelby M Jarvis, Muna S M Solyman, Roberta Koku, Olalekan C Akinsulie, Elizabeth E Hoffmann","doi":"10.1128/iai.00540-23","DOIUrl":"10.1128/iai.00540-23","url":null,"abstract":"<p><p><i>Anaplasma marginale</i> is an obligate, intracellular, tick-borne bacterial pathogen that causes bovine anaplasmosis, an often severe, production-limiting disease of cattle found worldwide. Methods to control this disease are lacking, in large part due to major knowledge gaps in our understanding of the molecular underpinnings of basic host-pathogen interactions. For example, the surface proteins that serve as adhesins and, thus, likely play a role in pathogen entry into tick cells are largely unknown. To address this knowledge gap, we developed a phage display library and screened 66 <i>A</i>. <i>marginale</i> proteins for their ability to adhere to <i>Dermacentor andersoni</i> tick cells. From this screen, 17 candidate adhesins were identified, including OmpA and multiple members of the Msp1 family, including Msp1b, Mlp3, and Mlp4. We then measured the transcript of <i>ompA</i> and all members of the <i>msp1</i> gene family through time, and determined that <i>msp1b</i>, <i>mlp2</i>, and <i>mlp4</i> have increased transcript during tick cell infection, suggesting a possible role in host cell binding or entry. Finally, Msp1a, Msp1b, Mlp3, and OmpA were expressed as recombinant protein. When added to cultured tick cells prior to <i>A. marginale</i> infection, all proteins except the C-terminus of Msp1a reduced <i>A. marginale</i> entry by 2.2- to 4.7-fold. Except OmpA, these adhesins lack orthologs in related pathogens of humans and animals, including <i>Anaplasma phagocytophilum</i> and the <i>Ehrlichia</i> spp., thus limiting their utility in a universal tick transmission-blocking vaccine. However, this work greatly advances efforts toward developing methods to control bovine anaplasmosis and, thus, may help improve global food security.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0054023"},"PeriodicalIF":2.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140897406","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":"Mucosal vaccination in a murine gnotobiotic model of <i>Giardia lamblia</i> infection.","authors":"Sozaburo Ihara, Brian V Nguyen, Yukiko Miyamoto, Lars Eckmann","doi":"10.1128/iai.00065-24","DOIUrl":"10.1128/iai.00065-24","url":null,"abstract":"<p><p><i>Giardia lamblia</i> is an important protozoan cause of diarrheal disease worldwide, delayed development and cognitive impairment in children in low- and middle-income countries, and protracted post-infectious syndromes in developed regions. <i>G. lamblia</i> resides in the lumen and at the epithelial surface of the proximal small intestine but is not mucosa invasive. The protozoan parasite is genetically diverse with significant genome differences across strains and assemblages. Animal models, particularly murine models, have been instrumental in defining mechanisms of host defense against <i>G. lamblia</i>, but mice cannot be readily infected with most human pathogenic strains. Antibiotic pretreatment can increase susceptibility, suggesting that the normal microbiota plays a role in controlling <i>G. lamblia</i> infection in mice, but the broader implications on susceptibility to diverse strains are not known. Here, we have used gnotobiotic mice to demonstrate that robust intestinal infection can be achieved for a broad set of human-pathogenic strains of the genetic assemblages A and B. Furthermore, gnotobiotic mice were able to eradicate infection with a similar kinetics to conventional mice after trophozoite challenge. Germ-free mice could also be effectively immunized by the mucosal route with a protective antigen, α1-giardin, in a manner dependent on CD4 T cells. These results indicate that the gnotobiotic mouse model is powerful for investigating acquired host defenses in giardiasis, as the mice are broadly susceptible to diverse <i>G. lamblia</i> strains yet display no apparent defects in mucosal immunity needed for controlling and eradicating this lumen-dwelling pathogen.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0006524"},"PeriodicalIF":2.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140897407","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":"Caspase-8 activity mediates TNFα production and restricts Coxiella burnetii replication during murine macrophage infection","authors":"Chelsea A. OsbronCrystal LawsonNolan HannaHeather S. KoehlerAlan G. Goodman1School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA2Paul G. Allen School for Global Health, College of Veterinary Medicine, Washington State University, Pullman, Washington, USASunny Shin","doi":"10.1128/iai.00053-24","DOIUrl":"https://doi.org/10.1128/iai.00053-24","url":null,"abstract":"Infection and Immunity, Ahead of Print. <br/>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"30 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141259310","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":"Continuous in vitro propagation of Babesia microti","authors":"Lee Fuller1Fuller Laboratories, Fullerton, California, USADe’Broski R. Herbert","doi":"10.1128/iai.00481-23","DOIUrl":"https://doi.org/10.1128/iai.00481-23","url":null,"abstract":"Infection and Immunity, Ahead of Print. <br/>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"74 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141259859","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":"Article of Significant Interest in This Issue.","authors":"","doi":"10.1128/iai.00182-24","DOIUrl":"10.1128/iai.00182-24","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"92 5","pages":"e0018224"},"PeriodicalIF":3.1,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11075452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140859504","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":"IL-22-dependent responses and their role during <i>Citrobacter rodentium</i> infection.","authors":"Karine Melchior, Romana R Gerner, Suzana Hossain, Sean-Paul Nuccio, Cristiano Gallina Moreira, Manuela Raffatellu","doi":"10.1128/iai.00099-24","DOIUrl":"10.1128/iai.00099-24","url":null,"abstract":"<p><p>The mouse pathogen <i>Citrobacter rodentium</i> is utilized as a model organism for studying infections caused by the human pathogens enteropathogenic <i>Escherichia coli</i> (EPEC) and enterohemorrhagic <i>E. coli</i> (EHEC) and to elucidate mechanisms of mucosal immunity. In response to <i>C. rodentium</i> infection, innate lymphoid cells and T cells secrete interleukin (IL)-22, a cytokine that promotes mucosal barrier function. IL-22 plays a pivotal role in enabling mice to survive and recover from <i>C. rodentium</i> infection, although the exact mechanisms involved remain incompletely understood. Here, we investigated whether particular components of the host response downstream of IL-22 contribute to the cytokine's protective effects during <i>C. rodentium</i> infection. In line with previous research, mice lacking the IL-22 gene (<i>Il22</i>^-/- mice) were highly susceptible to <i>C. rodentium</i> infection. To elucidate the role of specific antimicrobial proteins modulated by IL-22, we infected the following knockout mice: <i>S100A9</i>^-/- (calprotectin), <i>Lcn2</i>^-/- (lipocalin-2), <i>Reg3b</i>^-/- (Reg3β), <i>Reg3g</i>^-/- (Reg3γ), and <i>C3</i>^-/- (C3). All knockout mice tested displayed a considerable level of resistance to <i>C. rodentium</i> infection, and none phenocopied the lethality observed in <i>Il22</i>^-/- mice. By investigating another arm of the IL-22 response, we observed that <i>C. rodentium</i>-infected <i>Il22^-/</i>^- mice exhibited an overall decrease in gene expression related to intestinal barrier integrity as well as significantly elevated colonic inflammation, gut permeability, and pathogen levels in the spleen. Taken together, these results indicate that host resistance to lethal <i>C. rodentium</i> infection may depend on multiple antimicrobial responses acting in concert, or that other IL-22-regulated processes, such as tissue repair and maintenance of epithelial integrity, play crucial roles in host defense to attaching and effacing pathogens.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0009924"},"PeriodicalIF":2.9,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11075456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140335528","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}