Claudia Mickael, Mariah Jordan, Janelle N. Posey, Rubin N. Tuder, Eva Nozik, Joshua M. Thurman, Kurt R. Stenmark, Brian B. Graham, Cassidy Delaney
University of Colorado Anschutz Medical Campus. University of California, San Francisco.
United States
American Journal of Physiology Lung Cellular and Molecular Physiology
Am J Physiol Lung Cell Mol Physiol 2024;
DOI: 10.1152/ajplung.00165.2024
Abstract
Schistosomiasis-induced pulmonary hypertension (PH) presents a significant global health burden, yet the underlying mechanisms remain poorly understood. Here, we investigate the involvement of platelets and the complement system in the initiation events leading to Schistosoma-induced PH. We demonstrate that Schistosoma exposure leads to thrombocytopenia, platelet accumulation in the lung, and platelet activation. Additionally, we observed increased plasma complement anaphylatoxins C3a and C5a, indicative of complement system activation, and elevated platelet expression of C1q, C3, decay activating factor (DAF), and complement C3a and C5a receptors. Our findings suggest the active involvement of platelets in responding to complement system signals induced by Schistosoma exposure and form the basis for future mechanistic studies on how complement may regulate platelet activation and promote the development of Schistosoma-induced PH.
Category
Class I. Pulmonary Hypertension Associated with Infection
Acquired Patient Factors Associated with Pulmonary Vascular Disease
Age Focus: Pediatric Pulmonary Vascular Disease or Adult Pulmonary Vascular Disease
Fresh or Filed Publication: Fresh (PHresh). Less than 1-2 years since publication
Article Access
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