Abstract
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.
Highlights
Acanthamoebiasis is most often found in patients with immune deficiency, with infections facilitated by the intake of immunosuppressive drugs
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
Animal model Our experimental model of acanthamoebiasis involved BALB/c mice (n = 96) aged about 6–10 weeks, divided into four groups: (i) Group C: immunocompetent animals not infected with Acanthamoeba spp., (n = 18); (ii) Group A: immunocompetent animals infected with Acanthamoeba spp., (n = 30); (iii) Group Immunosuppressed uninfected control group mice (CS): immunosuppressed animals not infected by Acanthamoeba spp.; immunosuppression induced by methylprednisolone (MPS) (n = 18); and (iv) Group Immunosuppressed Acanthamoeba spp. infected mice (AS): immunosuppressed animals infected by Acanthamoeba spp.; immunosuppression induced by MPS (n = 30)
Summary
Acanthamoebiasis 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. Acanthamoebiasis is an opportunistic invasion caused by protozoans of the genus Acanthamoeba and is much more frequently noted in patients with immune deficiency, such as immunosuppressed patients following solid organ and bone marrow transplants and patients with HIV/AIDS [1]. Several hundred cases of amoebic brain infections have been reported worldwide, with the first identified human case of GAE occurring in an immunosuppressed patient with Hodgkin’s disease [7]. The host immune response to Acanthamoeba spp. infection is poorly understood, even though 50–90% of people are known to be seropositive [8]. Immunocompetent patients are more likely to have brain invasions and secondary cutaneous lesions, while patients with low immunity more frequently have isolated primary cutaneous skin infections [9]. Immunocompetent patients develop a granulomatous reaction, while in immunosuppressed individuals, granuloma formation is weak, especially in HIV patients [10, 11]
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