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A Brief Note on Erythrocytes
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Journal of Blood & Lymph

ISSN: 2165-7831

Open Access

Commentary - (2021) Volume 11, Issue 11

A Brief Note on Erythrocytes

Agung Lestari*
*Correspondence: Dr. Agung Lestari, Department of Medicine, University of Gadjah Mada, Caturtunggal, Kec, Depok, Sleman Regency, Yogyakarta Special Region, Indonesia, Email:
Department of Medicine, University of Gadjah Mada, Caturtunggal, Kec, Depok, Sleman Regency, Yogyakarta Special Region, Indonesia

Received: 01-Nov-2021 Published: 22-Nov-2021
Citation: Lestari, Agung. "A Brief Note on Erythrocytes ." J Blood Lymph 11 (2021) : 270.
Copyright: © 2021 Lestari A. This is an open-access article distributed under the terms of the creative commons attribution license which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Description

Erythrocytes are biconcave enucleate red blood cells that transport O2/CO2 between the body's tissues and lungs; their high haemoglobin content contributes to their oxygen-carrying capacity. The hormone erythropoietin regulates the process by which red blood cells are produced from hemopoietic stem cells. The oxygenation of the erythrocyte in the lung capillaries promotes CO2 unloading, resulting in shrinkage and ATP release. ATP stimulates endothelial cells to produce Nitric Oxide (NO), some of which binds to haemoglobin. Deoxygenation in peripheral tissues causes NO release and CO2 loading, resulting in purple cellular swelling. Red cell deficiencies can have an impact on the lungs. Anemias can cause respiratory problems, but polycythemias rarely cause respiratory problems. Hemoglobinopathies, such as sickle cell disease, frequently result in pulmonary complications that cause significant morbidity and mortality. When erythrocytes come into contact with lung fibroblasts because of lung harm, they stimulate the discharge of interleukin-8 (IL-8), which enhances inflammatory responses. Mutations in the ATP-transporting Cystic Fibrosis Tran's membrane conductance regulator (CFTR) gene cause a variety of lung pathologies in CF patients. Because CF erythrocytes are unable to release ATP in response to mechanical deformation in the lung, ATP-stimulated synthesis of NO from endothelial cells is inhibited, resulting in pulmonary hypertension. Malaria-infected erythrocytes show off a spread of abnormalities, ensuing in alveolar and endothelial damage.

With a few exceptions, erythrocytes are present in teleosts and most teleosts are nucleated. They have an oval to rounded nucleus and are generally oval in shape. Rainbow trout erythrocytes appear to have immune responses. In vitro, erythrocytes exposed to Candida albicans have a tendency to cluster around macrophage-like cells, stimulating their phagocytic activity toward the fungus. Erythrocytes exposed to diverse antigens do specific Pathogen Recognition Receptor (PRR) mRNA transcripts, and stimulation with the aid of poly (I:C) might also result in the secretion of molecules that may modify macrophage antiviral responses. Another erythrocyte defense mechanism is shown by respiratory proteins, which can mediate the production of reactive oxygen species even in invertebrates after activation by microbial proteases and pathogen-associated.

Erythrocytes are typically biconcave discs. They are circular on stained smears with distinct, smooth margins. Rodent erythrocytes are 4-7 m in diameter and have a similar morphology to human erythrocytes. Human erythrocytes are 6-8 m in diameter (similar to the size of a resting lymphocyte nucleus) and 1.5-2.5 m thick, with a central pallor that accounts for approximately one-third of the cell's diameter. Erythrocytse morphology is best appreciated inside the feathered edge, where cells are well distributed. Reticulocytes can account for up to 10% of erythrocytes in young rodents.

Circulating erythrocytes have a lifespan of about 120 days. Aging of red cells is related to a decrease in enzymatic activities, a modern increase in hemoglobin awareness and pink cellular viscosity due to loss of general cation and water content material ('dense red cells,' and structural changes of the membrane with a decrease in the floor: extent ratio, ensuing within the formation of a rigid spherocyte with improved osmotic fragility. These functions arise in physiologic situations, but they'll also be visible in a diffusion of pathologic disorders related to hemolytic procedures.

The final event in the life of these cells is the trapping of senescent erythrocytes by reticuloendothelial cells. This phenomenon may be viewed as an immunologic method characterised by means of the publicity of hidden antigenic sites, that is followed by way of the binding of obviously going on autologous antibodies (immunoglobulin G), which causes phagocytosis. Exposure of band 3 epitopes may be one of the events closely associated with erythrocyte senescence.

Several other damaging processes (oxidative, proteolytic) may intervene during the life of circulating erythrocytes; some of these act concurrently with the presence of molecular defects in the cytoskeleton or hemoglobin structure, accelerating red cell clearance.

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