Possible Role of Fibrinogen in the Aggregation of White Blood Cells

Berliner, S; Fuchs, Jacob; Seligsohn, Uri; Kariv, Naam; Hazaz, Bilha; Rotenberg, Z; Weinberger, I; Agmon, Jacob; Pinkhas, J; Aronson, Moshe

doi:10.1055/s-0038-1645963

Cited by 34 publications

(13 citation statements)

References 10 publications

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“…In fact, it can be induced by an in vivo infusion of immunoglobulins [22] and abolished by plasmapheresis [23]. This dependence on plasma factors have been shown also for the enhanced leukocyte adhesiveness/aggregation [21,24]. In addition, rheological studies have suggested that increased erythrocyte [25] or leukocyte [26] aggregability might have deleterious rheological consequences in term of tissue hypoperfusion and less efficient oxygenation [10].…”

Section: Discussionmentioning

confidence: 96%

“…We have raised the possibility that this stimulation might have rheological consequences in terms of the appearance of adhesive erythrocytes and leukocytes in the peripheral blood. This assumption is based on the knowledge that the acute-phase response is accompanied by the synthesis of multiple adhesive proteins and that part of them might be involved in the induction and/or maintenance of enhanced red [8,9,20] or white [21] blood cells adhesiveness/aggregation in the peripheral blood.…”

Section: Discussionmentioning

confidence: 99%

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Rheological determinants in patients with Gaucher disease and internal inflammation

et al. 2004

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The purpose of this study was to determine whether the inflammatory response in patients with Gaucher disease (GD) is accompanied by enhanced adhesiveness/aggregation of both red and white blood cells. Sixty patients with GD and matched controls were included. The degree of erythrocyte and leukocyte adhesiveness/aggregation was determined by using a simple slide test and image analysis. Patients with GD had significantly elevated concentrations of fibrinogen (328 vs. 262 mg/dl, P < 0.0001) and accelerated erythrocyte sedimentation rates (27 vs. 13 mm/H, P < 0.005). This was accompanied by a significantly enhanced degree of erythrocyte (75 vs. 85, P < 0.0001) and leukocyte (3.5 vs. 1.3, P < 0.002) adhesiveness/aggregation. The low-grade, smoldering, and subclinical internal inflammation in individuals with GD is accompanied by an increased degree of erythrocyte and leukocyte adhesiveness/aggregation. These findings might have rheological consequences in terms of microcirculatory slow flow and tissue hypoxemia. Am.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Rheological determinants in patients with Gaucher disease and internal inflammation

et al. 2004

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“…Both membrane adhesive proteins on the surface of white blood cells [27,28] and plasmatic proteins [29,30] might participate in the induction and/or maintenance of increased LAA in the peripheral blood during in£ammation. The present study addresses both topics of the expression of adhesive proteins of white blood cells as well as the possibility that plasma proteins are involved as well.…”

Section: Discussionmentioning

confidence: 99%

The leukocyte adhesiveness/aggregation test as an inflammation-related, plasma-dependent agglutination phenomenon

Zeltser¹,

Kassirer²,

Shapira³

et al. 1998

Scandinavian Journal of Clinical and Laboratory Investigation

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The leukocyte adhesiveness/aggregation test (LAAT) is a non-specific marker of inflammation. In the present study, we examined the expression of the CD11b/CD18 as well as the CD62L antigens on the surface of peripheral blood leukocytes in 84 patients with various inflammatory conditions and 60 controls by using whole blood flow cytometry. We also conducted several in vitro experiments in order to explain the mechanism of the leukocyte adhesiveness/aggregation. A significant (r= -0.36, p<0.001) negative correlation was found between the expression of CD62L on the surface of peripheral blood polymorphonuclears and the state of LAA. There was no correlation between the availability of the CD11b/CD18 antigen and the adhesive state of these cells. In a series of in vitro experiments, we could show that it is possible to significantly reduce the number of aggregated leukocytes in the peripheral blood by using dilutions with buffer but not with plasma. There is no change in the degree of aggregation following incubation at low temperature in the presence of an aerobic metabolism blocker or following incubation with a divalent ion chelator. Additionally, white blood cells could be seen to adhere to protein-rich areas in the peripheral slides. We assume that the state of LAA in the peripheral blood as revealed by the LAA test is more a plasma factor-dependent agglutination than a firm aggregation phenomenon. Factors other than the leukocyte integrins or selectins should be sought as being responsible for this LAA phenomenon.

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“…Increased adhesiveness/aggregation of WBC can be attributed to both cellular [19] and plasmatic factors [20]. We addressed this issue by studying the presence of leukocyte adhesion molecules that participate in WBC adhesiveness, namely CD11b/CD18 and CD62L antigens.…”

Section: Discussionmentioning

confidence: 99%

Reduced Leukocyte Adhesiveness in Response to Viral versus Nonviral Infection/Inflammation

et al. 2001

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Possible Role of Fibrinogen in the Aggregation of White Blood Cells

Cited by 34 publications

References 10 publications

Rheological determinants in patients with Gaucher disease and internal inflammation

Rheological determinants in patients with Gaucher disease and internal inflammation

The leukocyte adhesiveness/aggregation test as an inflammation-related, plasma-dependent agglutination phenomenon

Reduced Leukocyte Adhesiveness in Response to Viral versus Nonviral Infection/Inflammation

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