Acceso abierto

Acute Pulmonary Embolism and Immunity in Animal Models

Anna M. Imiela
Anna M. Imiela
, 
Tomasz P. Mikołajczyk
Tomasz P. Mikołajczyk
, 
Tomasz J. Guzik
Tomasz J. Guzik
 y 
Piotr Pruszczyk
Piotr Pruszczyk
   | 24 ene 2024
Archivum Immunologiae et Therapiae Experimentalis's Cover Image
Acerca de este artículo
Artículo anterior
Artículo siguiente
Cite
Article Category: Review
Publicado en línea: 24 ene 2024
Páginas: -
Recibido: 24 ago 2023
Aceptado: 05 dic 2023
DOI: https://doi.org/10.2478/aite-2024-0003
Palabras clave
© 2023 Anna M. Imiela et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Fig 1.

A mosaic theory of acute pulmonary embolism – an interplay between inflammation and other essential factors in the pathophysiology of pulmonary embolism.
A mosaic theory of acute pulmonary embolism – an interplay between inflammation and other essential factors in the pathophysiology of pulmonary embolism.

Fig 2.

Chemokine accumulation and pro-inflammatory cell influx in the lung parenchyma as well as in the pulmonary artery wall during acute pulmonary embolism episode. Recruitment of inflammatory cells into lung parenchyma, bronchoalveolar lavage (BAL) and pulmonary artery (PA) wall. Shortly after acute pulmonary episode starts, a rapid and robust influx of macrophages occurs. In lung parenchyma the inflammatory cell response is caused mainly by macrophages, while in PA wall the inflammatory response is related to neutrophil with simultaneous rise in macrophages. Higher accumulation of proteins, eosinophils and macrophages is present in BAL, Increased chemokines and cytokines expression is observed under hypoxic conditions in lung parenchyma and PA wall. This figure has been created with BioRender.com. Abbreviations: CINC-1, Cytokine-induced neutrophil chemoattractant; CXCL, Chemokine (C-X-C motif) ligand; FI, Fibrynolysis inhibitor; IL, Interleukin; MCP, Monocyte-chemoattractant protein; MIP, Macrophage inflammatory protein; ROS, Reactive oxygen species; TNF, Tumor necrosis factor; TPA, Tissue plasminogen activator.
Chemokine accumulation and pro-inflammatory cell influx in the lung parenchyma as well as in the pulmonary artery wall during acute pulmonary embolism episode. Recruitment of inflammatory cells into lung parenchyma, bronchoalveolar lavage (BAL) and pulmonary artery (PA) wall. Shortly after acute pulmonary episode starts, a rapid and robust influx of macrophages occurs. In lung parenchyma the inflammatory cell response is caused mainly by macrophages, while in PA wall the inflammatory response is related to neutrophil with simultaneous rise in macrophages. Higher accumulation of proteins, eosinophils and macrophages is present in BAL, Increased chemokines and cytokines expression is observed under hypoxic conditions in lung parenchyma and PA wall. This figure has been created with BioRender.com. Abbreviations: CINC-1, Cytokine-induced neutrophil chemoattractant; CXCL, Chemokine (C-X-C motif) ligand; FI, Fibrynolysis inhibitor; IL, Interleukin; MCP, Monocyte-chemoattractant protein; MIP, Macrophage inflammatory protein; ROS, Reactive oxygen species; TNF, Tumor necrosis factor; TPA, Tissue plasminogen activator.

Fig 3.

Cardiac inflammatory processes in right ventricle during acute pulmonary embolism episode. Schematic overview of the contribution of pro-inflammatory cells in the pathogenesis of right ventricular (RV) failure during acute pulmonary embolism (APE) episode. During APE, neutrophils, and macrophage infiltrate myocardium. Mononuclear cells with M1 phenotype occur during early phase of APE episode and convert into M2 phenotype in the later phase. RV inflammation is characterized by exaggerated chemokines accumulation, cytokine storm and oxidative stress. Chronic inflammation and hypoxia results in myocardial damage, necrosis and fibrosis. Treatment with selective antibodies such as anti-CINC and anti-PMN resulted in RV failure amelioration. This figure has been created with BioRender.com. Abbreviations: CCL, C-C motif chemokine ligand; CCR, CC Chemokine receptor; CINC, cytokine-induced neutrophil chemoattractant; CXCL, C-X-C motif chemokine ligand; M, macrophage; MCP, monocyte chemoattractant protein; MIP, macrophage inflammatory protein; MPO, Myeloperoxidase; PMN, polymorphonuclear cell antibody; RV, right ventricle.
Cardiac inflammatory processes in right ventricle during acute pulmonary embolism episode. Schematic overview of the contribution of pro-inflammatory cells in the pathogenesis of right ventricular (RV) failure during acute pulmonary embolism (APE) episode. During APE, neutrophils, and macrophage infiltrate myocardium. Mononuclear cells with M1 phenotype occur during early phase of APE episode and convert into M2 phenotype in the later phase. RV inflammation is characterized by exaggerated chemokines accumulation, cytokine storm and oxidative stress. Chronic inflammation and hypoxia results in myocardial damage, necrosis and fibrosis. Treatment with selective antibodies such as anti-CINC and anti-PMN resulted in RV failure amelioration. This figure has been created with BioRender.com. Abbreviations: CCL, C-C motif chemokine ligand; CCR, CC Chemokine receptor; CINC, cytokine-induced neutrophil chemoattractant; CXCL, C-X-C motif chemokine ligand; M, macrophage; MCP, monocyte chemoattractant protein; MIP, macrophage inflammatory protein; MPO, Myeloperoxidase; PMN, polymorphonuclear cell antibody; RV, right ventricle.
eISSN:
1661-4917
Idioma:
Inglés
Calendario de la edición:
Volume Open
Temas de la revista:
Medicine, Basic Medical Science, Biochemistry, Immunology, Clinical Medicine, other, Clinical Chemistry
RSS Feed de revista