Platelet biology of the rapidly failing lung

Washington, A. Valance; Esponda, Omar L.; Gibson, Angelia D.

doi:10.1111/bjh.16315

Cited by 28 publications

(36 citation statements)

References 125 publications

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“…Megakaryocytes (MKs) are normally present in the human lung and play a role in platelet homeostasis [1,2]. Originally described by Aschoff in 1893, the interest in pulmonary MKs and their platelet production has raised considerably during the last decade [1][2][3]. Several studies have shown that platelets participate in lung damage, particularly in acute lung injury [2,3].…”

Section: Introductionmentioning

confidence: 99%

Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage: an autopsy study with clinical correlation and review of the literature

et al. 2020

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Pulmonary megakaryocytes participate in the pathogenesis of lung damage, particularly in acute lung injury. Although megakaryocytes are not mentioned as a characteristic histologic finding associated to pulmonary injury, a few studies reveal that their number is increased in diffuse alveolar damage (DAD). In this autopsy study, we have observed a relevant number of pulmonary megakaryocytes in COVID-19 patients dying with acute lung injury (7.61 ± 5.59 megakaryocytes per 25 high-power fields vs. 1.14 ± 0.86 for the control group, p < 0.05). We analyzed samples of 18 patients, most of whom died after prolonged disease and use of mechanical ventilation. Most patients showed advanced DAD and abnormal coagulation parameters with high levels of fibrinogen, D-dimers, and variable thrombocytopenia. For comparison, pulmonary samples from a group of 14 non-COVID-19 patients dying with DAD were reviewed. They showed similar pulmonary histopathologic findings and an increase in the number of megakaryocytes (4 ± 4.17 vs. 1.14 ± 0.86 for the control group, p < 0.05). Megakaryocyte count in the COVID-19 group was greater but did not reach statistical significance (7.61 ± 5.59 vs. 4 ± 4.17, p = 0.063). Regardless of the cause, pulmonary megakaryocytes are increased in patients with DAD. Their high number seen in COVID-19 patients suggests a relation with the thrombotic events so often seen these patients. Since the lung is considered an active site of megakaryopoiesis, a prothrombotic status leading to platelet activation, aggregation and consumption may trigger a compensatory pulmonary response.

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Section: Introductionmentioning

confidence: 99%

Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage: an autopsy study with clinical correlation and review of the literature

et al. 2020

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“…It is known that platelets act as important mediators of innate defenses: platelet adhesion, activation, and degranulation are the essential steps in this process, in which platelet-associated surface receptor molecules play a pivotal role in the development of inflammation ( 148 ).…”

Section: Aβ Is a Vital Defense Protein With Multiple Rolesmentioning

confidence: 99%

On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications

et al. 2020

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As do many other immunity-related blood cells, platelets release antimicrobial peptides that kill bacteria, fungi, and even certain viruses. Here we review the literature suggesting that there is a similarity between the antimicrobials released by other blood cells and the amyloid-related Aβ peptide released by platelets. Analyzing the literature, we also propose that platelet-generated Aβ amyloidosis may be more common than currently recognized. This systemic Aβ from a platelet source may participate in various forms of amyloidosis in pathologies ranging from brain cancer, glaucoma, skin Aβ accumulation, and preeclampsia to Alzheimer’s disease and late-stage Parkinson’s disease. We also discuss the advantages and disadvantages of specific animal models for studying platelet-related Aβ. This field is undergoing rapid change, as it evaluates competing ideas in the light of new experimental observations. We summarized both in order to clarify the role of platelet-generated Aβ peptides in amyloidosis-related health disorders, which may be helpful to researchers interested in this growing area of investigation.

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“…Originally described by Aschoff in 1893, the interest in pulmonary MKs and their platelet production has raised considerably during the last decade [1][2][3]. Several studies have shown that platelets participate in lung damage, particularly in acute lung injury [2,3]. MKs are usually not mentioned as a characteristic histopathologic nding associated to acute pulmonary injury [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

“…In ammatory injury to alveolar epithelium and endothelial cells, resulting in intra-alveolar edema, deposition of brin and formation of microthrombi are important pathogenic mechanisms of DAD. There is experimental and clinical evidence that platelets contribute to alveolar damage and repair in acute respiratory distress syndrome (ARDS) and other forms of acute lung injury [2,3].…”

Section: Introductionmentioning

confidence: 99%

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Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage. An autopsy study with clinical correlation and review of the literature.

Valdivia-Mazeyra

Salas

Nieves-Alonso

et al. 2020

Preprint

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Megakaryocytes are normally present in the lung where they play a role in platelet homeostasis. The latter are well known to participate in the pathogenesis of lung damage, particularly in acute lung injury. Although megakaryocytes are usually not mentioned as a characteristic histopathologic finding associated to acute pulmonary injury, a few studies point out that their number is increased in the lungs of patients with diffuse alveolar damage. In this autopsy study we have observed a relevant number of pulmonary megakaryocytes in COVID-19 patients dying with acute respiratory distress syndrome. We have studied pulmonary tissue samples of 18 patients most of which died after prolonged disease and use of mechanical ventilation. Most samples showed fibroproliferative or fibrotic diffuse alveolar damage and an increased number of megakaryocytes. In six, thrombi of the pulmonary microcirculation were seen. We compare our findings with previous published autopsy reports, mainly focusing on the description of megakaryocytes. Our patients showed abnormal coagulation parameters with high levels of fibrinogen, D-dimers and variable thrombocytopenia. Since the lung is considered an active site of megakariopoiesis, a prothrombotic status leading to platelet activation, aggregation and consumption may trigger a compensatory pulmonary response. An increased number of pulmonary megakaryocytes suggests and supports a relation with the thrombotic events so often seen in COVID-19. Regardless of its etiology, future studies of patients dying with acute pulmonary injury should include pulmonary megakaryocytes as a histologic variable of interest.

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Platelet biology of the rapidly failing lung

Cited by 28 publications

References 125 publications

Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage: an autopsy study with clinical correlation and review of the literature

Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage: an autopsy study with clinical correlation and review of the literature

On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications

Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage. An autopsy study with clinical correlation and review of the literature.

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