Understanding the pathomechanisms of infection through biochemical and molecular studies of the Acanthamoeba spp.-host system is essential for the development of new diagnostic procedures and the identification of new therapeutic targets that will limit the degree of cell and organ damage. Animal studies, on the other hand, have clearly revealed that amoebae are transported in the blood system and penetrate the kidneys where they can cause dysfunction. Many clinical cases described in the scientific literature do not report whether the kidneys were studied for the presence of amoebae during post-mortem examinations. However, there is no data on the true number of patients with kidneys affected by amoebae. infection in the kidneys has been described only in one patient in whom urinalysis showed no abnormalities. The average time of infection for a patient with systemic acanthamoebiasis, based on current literature, is 18 months (range: 3 months to 6 years). Disseminated acanthamoebiasis is characterized by multi-organ and multi-symptom lesions with a rapid course leading to the death of the host. These amoebae are the etiological factor of granulomatous amebic encephalitis, amoebic keratitis (AK) and systemic acanthamoebiasis, following invasion of various tissues and organs. The only exception is Acanthamoeba pyriformis which additionally includes facultative sporocarp fruiting in its life-cycle. They occur in water, soil and air in the form of metabolically active trophozoites and resistant cysts, which enable the amoebae not only to survive without nutrients but also to resist disinfection and treatment measures. are protozoa with pathogenic properties that are ubiquitously distributed in the environment. In immunocompetent hosts, amoebae inhibit the apoptosis of kidney cells, and in immunosuppressed hosts, they lead to increased apoptosis by the intrinsic pathway and thus to a more severe course of the disease. have various strategies concerning apoptosis. with the host cell surface and/or the oxidative burst caused by elevated levels of NOXs lead to an antioxidant response enhanced by the Nrf2 pathway. This study is the first to address the mechanisms occurring in the kidneys of hosts infected with Acanthamoeba sp. In contrast, the AS group showed lower gene and protein expression of Bcl-2, and higher gene as well as protein expression of Bax, caspases 3 and 9. Additionally in A group, higher gene and protein expression of Bcl-2, and lower gene as well as protein expression of Bax, caspases 3 and 9 were noted. Compared to control mice, in the AS group the expression of the Nrf2 gene was upregulated while the concentration of Nrf2 protein was decreased. Gene expression and/or protein concentration of Nrf2 were higher in group A than in control animals. Increased gene expression and/or protein concentration of NOX2 and NOX4 were found in both immunocompetent and immunosuppressed mice infected with Acanthamoeba sp. NOX2, NOX4 and Nrf2 were analyzed by quantitative reverse transcription PCR (qRT-PCR) and ELISA methods, while pro-apoptotic and anti-apoptotic proteins (Bax and Bcl-2, respectively), Cas9, Cas3 were analyzed by qRT-PCR and western blot methods. Mice were divided into four groups based on their immunological status and Acanthamoeba sp. infection: A, immunocompetent Acanthamoeba sp.-infected mice AS, immunosuppressed Acanthamoeba sp.- infected mice C, immunocompetent uninfected mice CS, immunosuppressed uninfected mice. ![]() We also aimed to determine the protein and gene expressions of Bcl2, Bax, caspases 3 and 9. The aim of the study was to analyze the gene expression and protein concentration of NADPH oxidase 2 and 4 (NOX2 and NOX4, respectively) and nuclear erythroid 2-related factor (Nrf2) in the kidneys of hosts with systemic acanthamoebiasis. Recent reports indicate kidney dysfunction in hosts with systemic acanthamoebiasis. ![]() are opportunistic pathogens that cause inflammation, mostly in the brain, lungs and cornea.
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