scholarly journals Genetic differences in red cell osmotic fragility: analysis in allophenic mice

Blood ◽  
1982 ◽  
Vol 59 (5) ◽  
pp. 986-989 ◽  
Author(s):  
MJ Dewey ◽  
JL Brown ◽  
FS Nallaseth
Keyword(s):  
Phenotypic Variation ◽  
Blood Cells ◽  
Osmotic Fragility ◽  
Red Cells ◽  
Fragility Analysis ◽  
Red Cell ◽  
F1 Hybrid ◽  
Osmotic Lysis ◽  
Per Se ◽  
Genetically Determined

Abstract Mice of strain DBA/2J were found to produce red cells considerably more resistant to osmotic lysis than cells from C57BL/6J or the F1 hybrid between the two strains. Such strain-specific differences in osmotic fragility could be the result of genetically determined humoral or other systemic differences that indirectly influence red cell properties. Alternatively, this phenotypic variation might be an inherent property of the erythrocyte themselves and be directly controlled by their genotype. Analysis of red cells from allophenic (mosaic) mice of the strain composition C57BL/6J in equilibrium DBA/2J demonstrated that the latter possibility is the case. In such mice, erythrocytes of the DBA/2J genotype are relatively more resistant to osmotic lysis than are those of the C57BL/6J genotype; partial lysis of allophenic blood at intermediate salt concentrations results in marked enrichment for DBA/2J cells among the survivors. Future experiments designed to determine the mechanism underlying this difference can now focus on the properties of the red blood cells per se with the certainty that this property is inherent to the genotype of each cell.

scholarly journals Genetic differences in red cell osmotic fragility: analysis in allophenic mice

Blood ◽  
1982 ◽  
Vol 59 (5) ◽  
pp. 986-989
Author(s):  
MJ Dewey ◽  
JL Brown ◽  
FS Nallaseth
Keyword(s):  
Phenotypic Variation ◽  
Blood Cells ◽  
Osmotic Fragility ◽  
Red Cells ◽  
Fragility Analysis ◽  
Red Cell ◽  
F1 Hybrid ◽  
Osmotic Lysis ◽  
Per Se ◽  
Genetically Determined

Mice of strain DBA/2J were found to produce red cells considerably more resistant to osmotic lysis than cells from C57BL/6J or the F1 hybrid between the two strains. Such strain-specific differences in osmotic fragility could be the result of genetically determined humoral or other systemic differences that indirectly influence red cell properties. Alternatively, this phenotypic variation might be an inherent property of the erythrocyte themselves and be directly controlled by their genotype. Analysis of red cells from allophenic (mosaic) mice of the strain composition C57BL/6J in equilibrium DBA/2J demonstrated that the latter possibility is the case. In such mice, erythrocytes of the DBA/2J genotype are relatively more resistant to osmotic lysis than are those of the C57BL/6J genotype; partial lysis of allophenic blood at intermediate salt concentrations results in marked enrichment for DBA/2J cells among the survivors. Future experiments designed to determine the mechanism underlying this difference can now focus on the properties of the red blood cells per se with the certainty that this property is inherent to the genotype of each cell.

Red-cell Adhesion in Trypanosomiasis of Man and other Animals

Parasitology ◽  
1931 ◽  
Vol 23 (3) ◽  
pp. 346-359 ◽  
Author(s):  
James Montague Wallace ◽  
Arthur Wormall
Keyword(s):  
Cell Adhesion ◽  
Guinea Pig ◽  
Blood Cells ◽  
Infected Animal ◽  
Glucose Solution ◽  
Red Cells ◽  
Red Cell ◽  
Good Adhesion ◽  
Destructive Action ◽  
Per Se

1. The red-cell adhesion phenomenon in trypanosomiasis of man and other animals, first described by Duke and Wallace (1930) and shown by these authors to be due to the presence in the blood of the infected animal of a sub-stance (adhesin) which appears during the course of an infection, has been investigated further. Several strains of T. rhodesiense and T. gambiense have been used for this study.2. Red-cell adhesion of this nature has been obtained with the red blood cells of primates only, thus confirming the earlier finding.3. No relationship appears to exist between red-cell adhesion and isohaemagglutination, or other types of haemagglutination. The removal, by absorption, of the α and β isohaemagglutinins from a human adhesin serum of blood group O, or the removal from a monkey adhesin serum of agglutinins for baboon, rabbit and guinea-pig red cells does not lead to the removal of the adhesin.4. Centrifuging, per se, does not destroy to any appreciable extent the power of trypanosomes to adhere to red cells.5. Trypanosomes which have been freed from plasma by centrifuging and subsequent washing with citrate-Ringer-glucose solution give good adhesion with human or monkey red cells when a fresh adhesin serum or plasma is used. Little or no adhesion is obtained with these washed trypanosomes however, if the adhesin serum is very old or if it has been previously filtered through a Berkefeld filter candle or if the adhesin serum or plasma has been heated at 56° C. for 30 minutes.6. From this and other evidence the conclusion is reached that in addition to the red cells, trypanosomes and the adhesin some other factor (designated the “X” factor) is necessary for red-cell adhesion.7. This “X” factor is present in the serum or plasma of humans, monkeys, baboons, rabbits and guinea-pigs and has properties similar to those of complement. It is removed, as is most of the haemolytic complement, when the serum is filtered through a Berkefeld filter, it is destroyed by heating at 56° C. for 30 minutes, and, like haemolytic complement, it is inactivated when the serum is subjected to the action of dilute ammonia for about 1½ hours. Filtration, heating at 56° C. for 30 minutes and dilute ammonia appear to have no significant destructive action on the adhesin.8. The requirements for this red-cell adhesion phenomenon are (a) the red cells of a primate, (b) an adhesin, which is probably an antibody-like sub-stance produced during infection with trypanosomes, (c) trypanosomes of a strain related to that which gave rise to the formation of the adhesin, and (d) a complement-like component (“X” factor) present in the plasma and serum of most, if not all, normal animals.

HEMOLYTIC DISEASE OF THE NEWBORN DUE TO ANTI-A AND ANTI-B

PEDIATRICS ◽  
1955 ◽  
Vol 15 (1) ◽  
pp. 54-62
Author(s):  
Clare N. Shumway ◽  
Gerald Miller ◽  
Lawrence E. Young
Keyword(s):  
B Cells ◽  
Red Blood Cells ◽  
Blood Group ◽  
Newborn Infant ◽  
Blood Cells ◽  
Osmotic Fragility ◽  
Red Cells ◽  
Hemolytic Disease ◽  
Abo Incompatibility

Ten infants with hemolytic disease of the newborn due to ABO incompatibility were studied. In every case the investigations were undertaken because of jaundice occurring in the first 24 hours of life. The clinical, hematologic and serologic observations in the infants and the serologic findings in the maternal sera are described. Evidence is presented to show that the diagnosis of the disorder rests largely upon the demonstration of spherocytosis, increased osmotic fragility of the red cells, reticulocytosis, and hyperbilirubinemia in a newborn infant whose red blood cells are incompatible with the maternal major blood group isoantibody and against whose cells no other maternal isoantibody is demonstrable. The anti-A or anti-B in each of the maternal sera tested in this series hemolyzed A or B cells in the presence of complement. Other serologic findings in the maternal sera were less consistently demonstrated.

scholarly journals Normal Functions of the Spleen Relative to Red Blood Cells: A Review

Blood ◽  
1959 ◽  
Vol 14 (4) ◽  
pp. 399-408 ◽  
Author(s):  
WILLIAM H. CROSBY
Keyword(s):  
Cell Surface ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Normal Function ◽  
Red Cells ◽  
Red Cell ◽  
Cell Production ◽  
Normal Functions ◽  
Normal Spleen ◽  
And Storage

Abstract During all the stages of a red cell’s life the normal spleen exerts a normal function. Eight of these functions have been considered: (1) erythropoiesis; (2) an effect upon red cell production; (3) an effect upon maturation of the red cell surface; (4) the reservoir function; (5) the "culling function"; (6) iron turnover and storage; (7) the "pitting function"; (8) destruction of old red cells.

The squeezing of red blood cells through capillaries with near-minimal diameters

1989 ◽  
Vol 203 ◽  
pp. 381-400 ◽  
Author(s):  
D. Halpern ◽  
T. W. Secomb
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Cell Shape ◽  
Numerical Solutions ◽  
Tube Diameter ◽  
Red Cells ◽  
Rheological Parameters ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Intact Cells

An analysis is presented of the mechanics of red blood cells flowing in very narrow tubes. Mammalian red cells are highly flexible, but their deformations satisfy two significant constraints. They must deform at constant volume, because the contents of the cell are incompressible, and also at nearly constant surface area, because the red cell membrane strongly resists dilation. Consequently, there exists a minimal tube diameter below which passage of intact cells is not possible. A cell in a tube with this diameter has its critical shape: a cylinder with hemispherical ends. Here, flow of red cells in tubes with near-minimal diameters is analysed using lubrication theory. When the tube diameter is slightly larger than the minimal value, the cell shape is close to its shape in the critical case. However, the rear end of the cell becomes flattened and then concave with a relatively small further increase in the diameter. The changes in cell shape and the resulting rheological parameters are analysed using matched asymptotic expansions for the high-velocity limit and using numerical solutions. Predictions of rheological parameters are also obtained using the assumption that the cell is effectively rigid with its critical shape, yielding very similar results. A rapid decrease in the apparent viscosity of red cell suspensions with increasing tube diameter is predicted over the range of diameters considered. The red cell velocity is found to exceed the mean bulk velocity by an amount that increases with increasing tube diameter.

scholarly journals Macrophages and iron trafficking at the birth and death of red cells

Blood ◽  
2015 ◽  
Vol 125 (19) ◽  
pp. 2893-2897 ◽  
Author(s):  
Tamara Korolnek ◽  
Iqbal Hamza
Keyword(s):  
Growth Factors ◽  
Blood Cells ◽  
Iron Homeostasis ◽  
Critical Role ◽  
The Body ◽  
Red Cells ◽  
Physical Contact ◽  
Red Cell ◽  
Iron Trafficking ◽  
Intimate Association

Abstract Macrophages play a critical role in iron homeostasis via their intimate association with developing and dying red cells. Central nurse macrophages promote erythropoiesis in the erythroblastic island niche. These macrophages make physical contact with erythroblasts, enabling signaling and the transfer of growth factors and possibly nutrients to the cells in their care. Human mature red cells have a lifespan of 120 days before they become senescent and again come into contact with macrophages. Phagocytosis of red blood cells is the main source of iron flux in the body, because heme must be recycled from approximately 270 billion hemoglobin molecules in each red cell, and roughly 2 million senescent red cells are recycled each second. Here we will review pathways for iron trafficking found at the macrophage-erythroid axis, with a focus on possible roles for the transport of heme in toto.

scholarly journals How Do Red Blood Cells Die?

2021 ◽  
Vol 12 ◽  
Author(s):  
Perumal Thiagarajan ◽  
Charles J. Parker ◽  
Josef T. Prchal
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Red Cells ◽  
Cell Labeling ◽  
Red Cell ◽  
Average Life Span ◽  
Human Red Blood Cells ◽  
Physicochemical Changes ◽  
Cell Clearance

Normal human red blood cells have an average life span of about 120 days in the circulation after which they are engulfed by macrophages. This is an extremely efficient process as macrophages phagocytose about 5 million erythrocytes every second without any significant release of hemoglobin in the circulation. Despite large number of investigations, the precise molecular mechanism by which macrophages recognize senescent red blood cells for clearance remains elusive. Red cells undergo several physicochemical changes as they age in the circulation. Several of these changes have been proposed as a recognition tag for macrophages. Most prevalent hypotheses for red cell clearance mechanism(s) are expression of neoantigens on red cell surface, exposure phosphatidylserine and decreased deformability. While there is some correlation between these changes with aging their causal role for red cell clearance has not been established. Despite plethora of investigations, we still have incomplete understanding of the molecular details of red cell clearance. In this review, we have reviewed the recent data on clearance of senescent red cells. We anticipate recent progresses in in vivo red cell labeling and the explosion of modern proteomic techniques will, in near future, facilitate our understanding of red cell senescence and their destruction.

scholarly journals Single locus (rol) control of extreme resistance to red cell osmotic lysis: intrinsic mode of gene action.

Genetics ◽  
1989 ◽  
Vol 121 (2) ◽  
pp. 353-358
Author(s):  
C A Schaefer ◽  
M J Dewey
Keyword(s):  
Gene Action ◽  
Allelic Variation ◽  
Recombinant Inbred Strain ◽  
Inbred Mouse ◽  
Red Cells ◽  
Mouse Strains ◽  
Red Cell ◽  
Extreme Resistance ◽  
Extracellular Milieu ◽  
Osmotic Lysis

Abstract Previous work has indicated that inbred mouse strains C57BL/6 and DBA/2 produce red cells differing in their sensitivity to osmotic lysis and that the trait is under multigene control. A recombinant inbred strain (BXD-31), produced from C57BL/6 and DBA/2, has red cells manifesting resistance to osmotic lysis far greater than that of either progenitor. We demonstrate here that the fragility difference between BXD-31 and DBA/2 is the consequence of allelic variation at a single autosomal locus, termed rol. The resistance allele (rol') is almost completely recessive to the sensitive one (rols). Results of bone marrow chimera analyses indicate that (1) the mode of rol gene action is by a direct influence on the properties of the red cells rather than an indirect influence on their extracellular milieu, and (2) rol does not affect erythrocyte production and turnover. The fragility difference caused by rol variation is likely to involve the erythrocyte membrane or underlying cytoskeleton, since various red cell properties sensitive to ion metabolism differences are unaffected by the gene.

scholarly journals Diminished osmotic fragility of human erythrocytes following the membrane insertion of oxygenated sterol compounds

Blood ◽  
1981 ◽  
Vol 58 (2) ◽  
pp. 317-325
Author(s):  
RA Streuli ◽  
JR Kanofsky ◽  
RB Gunn ◽  
S Yachnin
Keyword(s):  
Cell Membrane ◽  
Hereditary Spherocytosis ◽  
Osmotic Fragility ◽  
Human Erythrocytes ◽  
Fragility Curve ◽  
Membrane Insertion ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Mean Cell Volume ◽  
Osmotic Lysis

Oxygenated sterol compounds (OSC), when incubated for 1 hr with human erythrocytes in lipoprotein-depleted medium at concentrations of 0.625- 5 X 10(-5) M, are inserted into the cell membrane and remain there despite subsequent washing of the cells. The insertion results in expansion of the surface area of the red cell ghost membrane, an increase in critical hemolytic volume, and as a consequence, in diminished osmotic fragility of the erythrocytes. This effect is seen with echinocyte-forming as well as with non-echinocyte-forming OSC. Erythrocytes treated with OSC do not differ from control cells with respect to their mean cell volume (MCV) in isotonic solution, water content, ion fluxes, and filterability through polycarbonate filters. The shift of the osmotic fragility curve toward lower NaCl concentrations is proportional to the amount of OSC inserted into the red cell membrane. 7 beta-Hydroxycholesterol, 22-ketocholesterol, and 20 alpha-hydroxycholesterol are the most potent inhibitors of osmotic lysis. The effect of OSC on osmotic fragility is diminished if the erythrocytes are incubated in a lipoprotein-containing medium; free cholesterol, however, does not change this effect. Various progesterones also protect red cell from osmotic lysis, but only if the erythrocytes are directly exposed to the compounds present in the hypotonic NaCl solutions used for measurement of their osmotic fragility. Progesterones do not remain in the membrane after the cells have been washed. The OSC are also capable of correcting the osmotic fragility curve of red cells from patients with hereditary spherocytosis. These experiments may suggest an approach to the pharmacologic treatment of hereditary spherocytosis.

scholarly journals Two distinct categories of warm autoantibody reactivity with age- fractionated red cells

Blood ◽  
1984 ◽  
Vol 63 (1) ◽  
pp. 177-180 ◽  
Author(s):  
DR Branch ◽  
IA Shulman ◽  
AL Sy Siok Hian ◽  
LD Petz
Keyword(s):  
Blood Cells ◽  
Clinical Evidence ◽  
Red Cells ◽  
Type I ◽  
Severe Anemia ◽  
Red Cell ◽  
Type Ii ◽  
Antiglobulin Test ◽  
Moderate Anemia ◽  
Cell Fractions

Abstract Using age-fractionated erythrocytes, warm autoantibodies can be classified into two distinct categories, depending on their reactivity with reticulocyte-enriched (younger) or reticulocyte-poor (older) red cell fractions. The strength of the direct antiglobulin test (DAT) on the age-fractionated red cells of 24 patients indicated that 19 (79%) had an IgG warm autoantibody that reacted preferentially with older red blood cells. In 7 of these 19 patients (37%), the DAT was negative using reticulocyte-enriched red cell fractions. We have termed this preferential reactivity of warm autoantibodies with older red cells as type I. Five of the 24 patients studied (21%) had an IgG warm autoantibody that demonstrated no preference for young or older red cells. We have termed this pattern of warm autoantibody reactivity as type II. All 5 patients having type II warm autoantibodies had severe anemia. In contrast, 6 of 19 patients having type I warm autoantibody did not have clinical evidence of anemia when tested, and 11 of the 19 had only slight to moderate anemia. Additionally, our results using type I warm autoantibody raise questions regarding the blood group specificity of warm autoantibodies. The antigen recognized by type I warm autoantibody may be a cryptantigen. Rh specificity or relative Rh specificity, often associated with warm autoantibodies, may simply be a coincidental finding.

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