BackgroundAcanthamoebiasis is most often found in patients with immune deficiency, with infections facilitated by the intake of immunosuppressive drugs. The host immune response to Acanthamoeba spp. infection is poorly understood. Thus, in this study, we aimed to examine the course of Acanthamoeba spp. infection taking into account the host’s immunological status, including assessment of the hematological parameters, cytokine analysis, immunophenotypic changes in spleen populations, and histological spleen changes, which could help clarify some aspects of the immune response to acanthamoebiasis. In our experimental study, we used Acanthamoeba strain AM 22 isolated from the bronchoaspirate of a patient with acute myeloid leukaemia (AML) and atypical pneumonia symptoms.ResultsAcanthamoeba spp. affected the hematological parameters in immunocompetent and immunosuppressed mice and induced a change in spleen weight during infection. Moreover, analysis of anti-inflammatory (IL-4 and IL-10) and pro-inflammatory (IL-17A and IFN-γ) cytokines produced by splenocytes stimulated with concanavalin A demonstrated that Acanthamoeba spp. induced a selective Th1, Th2 and Th17 response at later stages of the infection in immunocompetent hosts. In the case of hosts with low immunity, Acanthamoeba elicited robust Th1 cell-mediated immunity without the participation of Th17. We observed suppression of CD8+ and CD4+ T lymphocytes and CD3+CD4-CD8- double-negative (DN) T lymphocyte populations in the beginning, and in the case of CD3+/CD4+/CD8+ double-positive (DP) T cells in the final phase of Acanthamoeba spp. infection in hosts with low immunity. Also, CD4+T lymphocytes and CD3+/CD4+ and CD3+/CD8+ lymphocyte counts during each stage of acanthamoebiasis were shown to be upregulated.ConclusionsWe demonstrated that analysis of the immune response and pathogenesis mechanisms of clinical isolates of Acanthamoeba spp. in an animal model not only has purely cognitive significance but above all, may help in the development of effective methods of pharmacological therapy especially in patients with low immunity.
The diverse clinical picture and the non-specificity of symptoms in Lyme disease (LD) require the implementation of effective diagnostics, which should take into account the heterogeneity of Borrelia antigens. According to available guidelines, laboratories should use a two-tier serological diagnosis based on the enzyme-linked immunosorbent (ELISA) screening test and confirmation of the immunoblot (IB). The aim of the study was to investigate the immunoreactivity of LD patient sera to Borrelia antigens and to attempt to identify the genospecies responsible for LD using an ELISA–IB assay combination. Eighty patients with suspected LD and 22 healthy people participated in the study. All samples were tested with ELISA and IB assays in both IgM and IgG antibodies. In the case of the ELISA assay, more positive results were obtained in the IgM class than in the IgG class. In the case of the IB assay, positive results dominated in the IgG class. Positive results obtained in the IB assay most often showed IgM antibodies against the OspC and flagellin antigens, whereas the IgG antibodies were against VlsE, BmpA, OspC, p41, and p83 antigens. The IB assay is an important part of LD serodiagnosis and should be mandatory in diagnostic laboratories.
This experimental study assessed the impact of medications frequently used after kidney transplantation on the immune system of pregnant female Wistar rats. The study evaluates medications, both approved and contraindicated during pregnancy in common therapeutic combinations. The study was conducted on 32 female Wistar rats, subjected to immunosuppressive regimens most commonly used in therapy of human kidney transplant recipients (cyclosporine A, mycophenolate mofetil and prednisone; tacrolimus, mycophenolate mofetil and prednisone; and cyclosporine A, everolimus and prednisone). The animals received drugs by oral gavage 2 weeks before pregnancy and at 3 weeks of pregnancy. We found drug regimen-dependent differences in cytometry from spleen. Many subpopulations of lymphocytes were suppressed in rats treated with cyclosporine A, mycophenolate mofetil and prednisone and tacrolimus, mycophenolate mofetil and prednisone; the number of NK cells was increased in group of rats treated with cyclosporine A, everolimus and prednisone. We also found changes in histological examination of thymus and spleen of all treated dams. In cytokine assay, we noticed increasing levels of IL-17 with increasing doses of concanavalin A in control group and in group of dams treated with cyclosporine A, mycophenolate mofetil and prednisone. This increase was blocked in rats treated with tacrolimus, mycophenolate mofetil and prednisone and cyclosporine A, everolimus and prednisone. Qualitative, quantitative and morphological changes of immune system in pharmacologically immunosuppressed females have been observed. Thymus structure, spleen composition and splenocytes IL-17 production were mostly affected in drug regimen-dependent manner.
Clinical transplantology is a constantly evolving field of medicine. Kidney transplantation has become standard clinical practice, and it has a significant impact on reducing mortality and improving the quality of life of patients. Allogenic transplantation induces an immune response, which may lead to the rejection of the transplanted organ. The gold standard for evaluating rejection of the transplanted kidney by the recipient’s organism is a biopsy of this organ. However, due to the high invasiveness of this procedure, alternative diagnostic methods are being sought. Therefore, the biomarkers may play an essential predictive role in transplant rejection. A review of the most promising biomarkers for early diagnosis and prognosis prediction of allogenic kidney transplant rejection summarizes novel data on neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), C-X-C motif chemokine 10 (CXCL-10), cystatin C (CysC), osteopontin (OPN), and clusterin (CLU) and analyses the dynamics of changes of the biomarkers mentioned above in kidney diseases and the mechanism of rejection of the transplanted kidney.
The course of Acanthamoeba spp. infection depends on the age and immune status of the host, and the virulence of the Acanthamoeba spp. strain. Some strains of free-living amoebae exhibit organ specificity, during the course of infection, while others may cause changes in many organs or completely lose pathogenicity. The aim of the current study was to investigate the pathological properties of Acanthamoeba spp. isolated from a patient with acute myeloid leukemia and atypical pneumonia (AM22). Moreover, the objective was to investigate the histopathological changes in the kidneys and heart of immunocompetent and immunosuppressed mice infected with Acanthamoeba spp. Amoebae were re-isolated from both the kidneys and hearts of the inoculated mice, although no cysts or trophozoites of the amoebae were detected in microscopic slides of the fragments of these organs. Acanthamoeba spp. induced changes in the kidney and heart weight of infected mice. In immunocompetent and immunosuppressed Acanthamoeba spp. infected mice, we found some histopathological changes, including areas with less acidic cytoplasm and a relaxation of muscle fibers. In further studies, it is important to analyze changes in gene and protein expressions in the heart and kidneys of hosts with disseminated acanthamoebiasis to better understand the course of infection in these organs, because the results of histological analysis varied depending on the immune status and duration of infection.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.