Cholesterol-mediated inflammation activation in alveolar macrophages
Registered Report in principle acceptance
Surfactant protein C and cholesterol
In this project, we investigate the role of cholesterol and lipid metabolism in the development of lung fibrosis. We are want to know if accumulation of cholesterol in the lung initiate an inflammatory response, such as activation of the NLRP3 inflammasome. Interestingly, this happens in the absence of SP-C and we are looking for its relation to familial forms of lung fibrosis, where patients present mutations on the SP-C gene. With this knowledge we aim to develop a therapy for this disease.
Resting time after phorbol 12-myristate 13-acetate in THP-1 derived macrophages provides a non-biased model for the study of NLRP3 inflammasome
Differentiation of THP-1 with 5ng/ml PMA followed by 24h resting period provides a model that morphologically and molecularly resembles macrophages.
Alveolar Dynamics and Beyond - The Importance of Surfactant Protein C and Cholesterol in Lung Homeostasis and Fibrosis
Sehlmeyer, K., Ruwisch, J., Roldan, N., Lopez-Rodriguez, E.: Front Physiol. 2020;11:386.
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Surfactant protein C (SP-C) is an important player in enhancing the interfacial adsorption of lung surfactant lipid films to the alveolar air-liquid interface. Doing so, surface tension drops down enough
Air Space Distension Precedes Spontaneous Fibrotic Remodeling and Impaired Cholesterol Metabolism in the Absence of Surfactant Protein C
Ruwisch, J., Sehlmeyer, K., Roldan, N., Garcia-Alvarez, B., Perez-Gil, J., Weaver, T.E., Ochs, M., Knudsen, L., Lopez-Rodriguez, E.: Am J Resp Cell Mol. 2020;62(4):466-78.
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Surfactant protein (SP)-C deficiency is found in samples from patients with idiopathic pulmonary fibrosis,
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