Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent

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Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent. / Vainer, B.; Berliner, S.; Nielsen, O. H.

In: Inflammation Research, Vol. 53, No. 9, 01.09.2004, p. 458-461.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Vainer, B, Berliner, S & Nielsen, OH 2004, 'Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent', Inflammation Research, vol. 53, no. 9, pp. 458-461. https://doi.org/10.1007/s00011-004-1280-2

APA

Vainer, B., Berliner, S., & Nielsen, O. H. (2004). Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent. Inflammation Research, 53(9), 458-461. https://doi.org/10.1007/s00011-004-1280-2

Vancouver

Vainer B, Berliner S, Nielsen OH. Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent. Inflammation Research. 2004 Sep 1;53(9):458-461. https://doi.org/10.1007/s00011-004-1280-2

Author

Vainer, B. ; Berliner, S. ; Nielsen, O. H. / Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent. In: Inflammation Research. 2004 ; Vol. 53, No. 9. pp. 458-461.

Bibtex

@article{ffdb5dd5b605467aab843acabf3e6ed0,
title = "Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent",
abstract = "Objective: In active stages of ulcerative colitis (UC), a tendency for neutrophils to aggregate in the colonic lamina propria is mediated by yet unidentified surface receptors. The aim was to assess the spontaneous leukocyte aggregation and the aggregation induced by bacteria-derived products in UC and to evaluate the involvement of ICAM-1 and β2-integrins in this aggregation. Materials and methods: Blood was drawn from 10 patients with quiescent UC, 10 patients with active UC, and 10 healthy volunteers. The blood was stimulated with LPS or fMLP with subsequent blocking of CD11b or ICAM-1 with specific antibodies. The aggregation was assessed on glass slides with an automated image analyzer (Inflamet{\texttrademark}). Results: The spontaneous leukocyte aggregation was increased in quiescent and active UC as compared to healthy controls (p < 0.05). Although not statistically significant, LPS and fMLP seemed to increase the leukocyte adhesiveness, and also a tendency towards inhibition of the leukocyte aggregation was observed by blocking ICAM-1. Conclusions: Increased adhesiveness of circulating leukocytes seems to be involved in the pathogenesis of UC, and ICAM-1 is suggested to be a part of this phenomenon. The results indicate an altered basic neutrophil response in UC.",
keywords = "Colitis, ICAM-1, Integrins, Leukocyte aggregation, Ulcerative",
author = "B. Vainer and S. Berliner and Nielsen, {O. H.}",
year = "2004",
month = sep,
day = "1",
doi = "10.1007/s00011-004-1280-2",
language = "English",
volume = "53",
pages = "458--461",
journal = "Inflammation Research",
issn = "1023-3830",
publisher = "Springer Basel AG",
number = "9",

}

RIS

TY - JOUR

T1 - Spontaneous aggregation of leukocytes in active ulcerative colitis might be ICAM-1 dependent

AU - Vainer, B.

AU - Berliner, S.

AU - Nielsen, O. H.

PY - 2004/9/1

Y1 - 2004/9/1

N2 - Objective: In active stages of ulcerative colitis (UC), a tendency for neutrophils to aggregate in the colonic lamina propria is mediated by yet unidentified surface receptors. The aim was to assess the spontaneous leukocyte aggregation and the aggregation induced by bacteria-derived products in UC and to evaluate the involvement of ICAM-1 and β2-integrins in this aggregation. Materials and methods: Blood was drawn from 10 patients with quiescent UC, 10 patients with active UC, and 10 healthy volunteers. The blood was stimulated with LPS or fMLP with subsequent blocking of CD11b or ICAM-1 with specific antibodies. The aggregation was assessed on glass slides with an automated image analyzer (Inflamet™). Results: The spontaneous leukocyte aggregation was increased in quiescent and active UC as compared to healthy controls (p < 0.05). Although not statistically significant, LPS and fMLP seemed to increase the leukocyte adhesiveness, and also a tendency towards inhibition of the leukocyte aggregation was observed by blocking ICAM-1. Conclusions: Increased adhesiveness of circulating leukocytes seems to be involved in the pathogenesis of UC, and ICAM-1 is suggested to be a part of this phenomenon. The results indicate an altered basic neutrophil response in UC.

AB - Objective: In active stages of ulcerative colitis (UC), a tendency for neutrophils to aggregate in the colonic lamina propria is mediated by yet unidentified surface receptors. The aim was to assess the spontaneous leukocyte aggregation and the aggregation induced by bacteria-derived products in UC and to evaluate the involvement of ICAM-1 and β2-integrins in this aggregation. Materials and methods: Blood was drawn from 10 patients with quiescent UC, 10 patients with active UC, and 10 healthy volunteers. The blood was stimulated with LPS or fMLP with subsequent blocking of CD11b or ICAM-1 with specific antibodies. The aggregation was assessed on glass slides with an automated image analyzer (Inflamet™). Results: The spontaneous leukocyte aggregation was increased in quiescent and active UC as compared to healthy controls (p < 0.05). Although not statistically significant, LPS and fMLP seemed to increase the leukocyte adhesiveness, and also a tendency towards inhibition of the leukocyte aggregation was observed by blocking ICAM-1. Conclusions: Increased adhesiveness of circulating leukocytes seems to be involved in the pathogenesis of UC, and ICAM-1 is suggested to be a part of this phenomenon. The results indicate an altered basic neutrophil response in UC.

KW - Colitis

KW - ICAM-1

KW - Integrins

KW - Leukocyte aggregation

KW - Ulcerative

UR - http://www.scopus.com/inward/record.url?scp=6044253490&partnerID=8YFLogxK

U2 - 10.1007/s00011-004-1280-2

DO - 10.1007/s00011-004-1280-2

M3 - Journal article

C2 - 15550998

AN - SCOPUS:6044253490

VL - 53

SP - 458

EP - 461

JO - Inflammation Research

JF - Inflammation Research

SN - 1023-3830

IS - 9

ER -

ID: 218708324