Key result
ROS-induced oxidative modifications of cardiac proteins, such as titin, significantly enhanced their immunogenicity and recognition by serum antibodies in human patients and rodents with Chagas disease.
Why the study?
Do ROS-induced cardiac-oxidized antigens serve as targets of immune recognition and contribute to pathogenesis in Chagas disease?
Observational
Do ROS-induced cardiac-oxidized antigens serve as targets of immune recognition and contribute to pathogenesis in Chagas disease?
ROS-induced oxidative modifications of cardiac proteins create antigens that are targeted by immune recognition, contributing to the pathogenesis of Chagas disease cardiomyopathy.
ROS-modified cardiac proteins may drive autoimmunity in Chagas cardiomyopathy; hypothesis-generating and leaves open therapeutic targeting pending clinical trials.
Trypanosoma cruzi elicits reactive oxygen species (ROS) of inflammatory and mitochondrial origin in infected hosts. In this study, we examined ROS-induced oxidative modifications in the heart and determined whether the resultant oxidized cardiac proteins are targets of immune response and of pathological significance in Chagas disease. Heart biopsies from chagasic mice, rats and human patients exhibited, when compared to those from normal controls, a substantial increase in protein 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), carbonyl, and 3-nitrotyrosine (3-NT) adducts. To evaluate whether oxidized proteins gain antigenic properties, heart homogenates or isolated cardiomyocytes were oxidized in vitro and one- or two-dimensional gel electrophoresis (2D-GE)/Western blotting (WB) was performed to investigate the proteomic oxidative changes and recognition of oxidized proteins by sera antibodies in chagasic rodents (mice, rats) and human patients. Human cardiomyocytes exhibited LD(50) sensitivity to 30 µM 4-HNE and 100 µM H(2)O(2) at 6 h and 12 h, respectively. In vitro oxidation with 4-HNE or H(2)O(2) resulted in a substantial increase in 4-HNE- and carbonyl-modified proteins that correlated with increased recognition of cardiac (cardiomyocytes) proteins by sera antibodies of chagasic rodents and human patients. 2D-GE/Western blotting followed by MALDI-TOF-MS/MS analysis to identify cardiac proteins that were oxidized and recognized by human chagasic sera yielded 82 unique proteins. We validated the 2D-GE results by enzyme-linked immunosorbent assay (ELISA) and WB and demonstrated that oxidation of recombinant titin enhanced its immunogenicity and recognition by sera antibodies from chagasic hosts (rats and humans). Treatment of infected rats with phenyl-α-tert-butyl nitrone (PBN, antioxidant) resulted in normalized immune detection of cardiac proteins associated with control of cardiac pathology and preservation of heart contractile function in chagasic rats. We conclude that ROS-induced, cardiac-oxidized antigens are targets of immune recognition by antibodies and molecular determinants for pathogenesis during Chagas disease.
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Dhiman et al. (2012) conducted an observational in Chagas disease. Trypanosoma cruzi infection and ROS-induced oxidative stress vs. Healthy/uninfected controls was evaluated on Immune recognition of cardiac-oxidized antigens by sera antibodies. ROS-induced oxidative modifications of cardiac proteins, such as titin, significantly enhanced their immunogenicity and recognition by serum antibodies in human patients and rodents with Chagas disease.
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