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

Citation
D. Zeltser et al., The leukocyte adhesiveness/aggregation test as an inflammation-related plasma-dependent agglutination phenomenon, SC J CL INV, 58(7), 1998, pp. 593-601
Citations number
34
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION
ISSN journal
00365513 → ACNP
Volume
58
Issue
7
Year of publication
1998
Pages
593 - 601
Database
ISI
SICI code
0036-5513(199811)58:7<593:TLATAA>2.0.ZU;2-T
Abstract
The leukocyte adhesiveness/aggregation test (LAAT) is a non-specific marker of inflammation. In the present study, we examined the expression of the C D11b/CD18 as well as the CD62L antigens on the surface of peripheral blood leukocytes in 84 patients with various inflammatory conditions and 60 contr ols by using whole Mood 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 p olymorphonuclears and the state of LAA. There was no correlation between th e availability of the CD11b/CD18 antigen and the adhesive state of these ce lls. In a series of in vitro experiments, we could show that it is possible to significantly reduce the number of aggregated leukocytes in the periphe ral blood by using dilutions with buffer but not with plasma. There is no c hange in the degree of aggregation following incubation at low temperature in the presence of an aerobic metabolism blocker or following incubation wi th a divalent ion chelator. Additionally, white blood cells could be seen t o 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.