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  • American Society for Microbiology  (4)
  • 1
    Online Resource
    Online Resource
    Protein Kinase C-α Is a Gatekeeper of Cryptosporidium Sporozoite Adherence and Invasion
    American Society for Microbiology ; 2022
    In:  Infection and Immunity Vol. 90, No. 3 ( 2022-03-17)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 90, No. 3 ( 2022-03-17)
    Abstract: Cryptosporidium infection is a leading cause of diarrhea-associated morbidity and mortality in young children globally. Single nucleotide polymorphisms (SNPs) in the human protein kinase C-α ( PRKCA ) gene region have been associated with susceptibility to cryptosporidiosis. Here, we examined the role of protein kinase C-α (PKCα) activity in human HCT-8 intestinal epithelial cells during infection with Cryptosporidium parvum sporozoites. To delineate the role of PKCα in infection, we developed a fluorescence-based imaging assay to differentiate adherent from intracellular parasites. We tested pharmacological agonists and antagonists of PKCα and measured the effect on C. parvum sporozoite adherence to and invasion of HCT-8 cells. We demonstrate that both PKCα agonists and antagonists significantly alter parasite adherence and invasion in vitro . We found that HCT-8 cell PKCα is activated by C. parvum infection. Our findings suggest intestinal epithelial cell PKCα as a potential host-directed therapeutic target for cryptosporidiosis and implicate PKCα activity as a mediator of parasite adherence and invasion.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/iai.00679-21
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2022
    detail.hit.zdb_id: 1483247-1
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  • 2
    Online Resource
    Online Resource
    Novel Biomarkers, Including tcdB PCR Cycle Threshold, for Predicting Recurrent Clostridioides difficile Infection
    American Society for Microbiology ; 2023
    In:  Infection and Immunity Vol. 91, No. 4 ( 2023-04-18)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 91, No. 4 ( 2023-04-18)
    Abstract: Traditional clinical models for predicting recurrent Clostridioides difficile infection do not perform well, likely owing to the complex host-pathogen interactions involved. Accurate risk stratification using novel biomarkers could help prevent recurrence by improving underutilization of effective therapies (i.e., fecal transplant, fidaxomicin, bezlotoxumab). We used a biorepository of 257 hospitalized patients with 24 features collected at diagnosis, including 17 plasma cytokines, total/neutralizing anti-toxin B IgG, stool toxins, and PCR cycle threshold ( C T ) (a proxy for stool organism burden). The best set of predictors for recurrent infection was selected by Bayesian model averaging for inclusion in a final Bayesian logistic regression model. We then used a large PCR-only data set to confirm the finding that PCR C T predicts recurrence-free survival using Cox proportional hazards regression. The top model-averaged features were (probabilities of 〉 0.05, greatest to least): interleukin 6 (IL-6), PCR C T , endothelial growth factor, IL-8, eotaxin, IL-10, hepatocyte growth factor, and IL-4. The accuracy of the final model was 0.88. Among 1,660 cases with PCR-only data, cycle threshold was significantly associated with recurrence-free survival (hazard ratio, 0.95; P  〈   0.005). Certain biomarkers associated with C. difficile infection severity were especially important for predicting recurrence; PCR C T and markers of type 2 immunity (endothelial growth factor [EGF], eotaxin) emerged as positive predictors of recurrence, while type 17 immune markers (IL-6, IL-8) were negative predictors. In addition to novel serum biomarkers (particularly, IL-6, EGF, and IL-8), the readily available PCR C T may be critical to augment underperforming clinical models for C. difficile recurrence.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/iai.00092-23
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2023
    detail.hit.zdb_id: 1483247-1
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  • 3
    Online Resource
    Online Resource
    Fresh Isolates from Children with Severe Plasmodium falciparum Malaria Bind to Multiple Receptors
    American Society for Microbiology ; 2001
    In:  Infection and Immunity Vol. 69, No. 9 ( 2001-09), p. 5849-5856
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 69, No. 9 ( 2001-09), p. 5849-5856
    Abstract: The sequestration of Plasmodium falciparum -infected erythrocytes (pRBC) away from the peripheral circulation is a property of all field isolates. Here we have examined the pRBC of 111 fresh clinical isolates from children with malaria for a number of adhesive features in order to study their possible coexpression and association with severity of disease. A large number of adhesion assays were performed studying rosetting, giant rosetting, and binding to CD36, intercellular adhesion molecule 1, platelet endothelial cell adhesion molecule 1, thrombospondin, heparin, blood group A, and immunoglobulins. Suspension assays were performed at the actual parasitemia of the isolate, while all the static adhesion assays were carried out at an equal adjusted parasitemia. The ability to bind to multiple receptors, as well as the ability to form rosettes and giant rosettes, was found to be more frequent among isolates from children with severe versus mild malaria ( P = 0.0015). Rosettes and giant rosettes were more frequent for children with severe malaria, and the cell aggregates were larger and tighter, than for those with mild disease ( P = 0.0023). Binding of immunoglobulins (97% of isolates) and of heparin (81% of isolates) to infected erythrocytes was common, and binding to heparin and blood group A was associated with severity of disease ( P = 0.011 and P = 0.031, respectively). These results support the idea that isolates that bind to multiple receptors are involved in the causation of severe malaria and that several receptor-ligand interactions work synergistically in bringing about severe disease.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.69.9.5849-5856.2001
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
    detail.hit.zdb_id: 1483247-1
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  • 4
    Online Resource
    Online Resource
    Type 3 Immunity during Clostridioides difficile Infection: Too Much of a Good Thing?
    American Society for Microbiology ; 2019
    In:  Infection and Immunity Vol. 88, No. 1 ( 2019-12-17)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 88, No. 1 ( 2019-12-17)
    Abstract: Clostridioides (formerly known as Clostridium ) difficile is the leading cause of hospital-acquired gastrointestinal infections in the United States and one of three urgent health care threats identified by the Centers for Disease Control and Prevention. C. difficile disease is mediated by the production of toxins that disrupt the epithelial barrier and cause a robust host inflammatory response. Studies in humans as well as animal models of disease have shown that the type of immune response generated against the infection dictates the outcome of disease, often irrespective of bacterial burden. Much of the focus on immunity during C. difficile infection (CDI) has been on type 3 immunity because of the established role for this arm of the immune system in other gastrointestinal inflammatory conditions such as inflammatory bowel disease (IBD). For example, interleukin-22 (IL-22) production by group 3 innate lymphoid cells (ILC3s) protects against pathobionts translocating across the epithelium during CDI. On the other hand, interleukin-17 (IL-17) production by Th17 cells increases CDI-associated mortality. Additionally, neutropenia has been associated with increased susceptibility to CDI in humans, but increased neutrophilia in mouse models correlates with host pathology. Taking the data together, these findings suggest dual roles for type 3 immune responses during infection. Here, we review the complex role of type 3 immunity during CDI and delineate what is known about innate and adaptive cellular immunity as well as the downstream effector cytokines known to be important during this infection.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00306-19
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2019
    detail.hit.zdb_id: 1483247-1
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