Possible role for a plasma factor in the induction and/or maintenance of the state of leukocyte adhesiveness/aggregation in the peripheral blood. A study of mothers and their newborns

Lidor, Arie; Arber, Nadir; Berliner, Shlomo; Lifshitz, A; G, Segal; Aronson, Moshe; Neri, Alexander; Pinkhas, J; Mp, David

doi:10.3109/00365519109091643

Cited by 11 publications

(6 citation statements)

References 34 publications

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“…in the newborns, the differences not being significant). However, the differences in the state of LAA were significant (15 ±6.4% in the mothers and 5 ±3.3% in the newborns; p< 0.0001) suggesting that the state of LAA in the peripheral blood does not result from a simple chance collision [24], Finally, an increased lymphocyte aggregation re sponse was noted in some of the patients under stress. It is known that during stress the absolute number of lymphocytes in the peripheral blood is in creased [25,26] and it is possible that they aggregate during stress [20].…”

Section: Discussionmentioning

confidence: 85%

Detection of Aggregated Leukocytes in the Circulating Pool during Stress – Demargination Is Not Necessarily a Result of Decreased Leukocyte Adhesiveness

Arber¹,

Berliner²,

Rotenberg

et al. 1991

Acta Haematol

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Leukocyte endothelial interactions are essential for a normal immune response. It is known that this response is influenced by stress and that the latter induces demargination. We examined the question of whether stress demargination results from a decreased state of leukocyte adhesiveness. Included were various volunteers and patients under different degrees of stress. 66 young athletes before beginning their daily exercises, 67 middle-aged healthy volunteers, 25 patients before ergometry for evaluation of chest pain, 75 patients who were referred to the emergency room with chest pain without ischemia/infarction, 78 patients with ischemia/infarction, 65 patients with minor trauma, 25 with a fracture and 12 with polytrauma. The leukocyte adhesiveness/aggregation (LAA) values were measured with a direct slide test. The respective LAA values were 7.4 ± 4.7, 6.3 ± 4.4, 5.8 ± 3.6, 5.2 ± 3.5, 10.8 ± 8.5, 9.1 ± 5.8, 12.2 ± 6.6 and 19 ± 12.6% of aggregated leukocytes. We conclude that an increase in aggregated white blood cells can be detected in the circulating pool during major stress. It is therefore suggested that stress demargination is not necessarily a result of diminished leukocyte adhesiveness.

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Section: Discussionmentioning

confidence: 85%

Detection of Aggregated Leukocytes in the Circulating Pool during Stress – Demargination Is Not Necessarily a Result of Decreased Leukocyte Adhesiveness

Arber¹,

Berliner²,

Rotenberg

et al. 1991

Acta Haematol

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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%

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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“…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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Possible role for a plasma factor in the induction and/or maintenance of the state of leukocyte adhesiveness/aggregation in the peripheral blood. A study of mothers and their newborns

Cited by 11 publications

References 34 publications

Detection of Aggregated Leukocytes in the Circulating Pool during Stress – Demargination Is Not Necessarily a Result of Decreased Leukocyte Adhesiveness

Detection of Aggregated Leukocytes in the Circulating Pool during Stress – Demargination Is Not Necessarily a Result of Decreased Leukocyte Adhesiveness

Rheological determinants in patients with Gaucher disease and internal inflammation

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

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