P-selectin glycoprotein ligand-1 (PSGL-1) is up-regulated on leucocytes from patients with chronic obstructive pulmonary disease

Schumacher, Axel; Liebers, Uta; Morser, John; Gerl, Velia; Meyer, Michael C.; Witt, Christian; Wolff, Gerhard

doi:10.1111/j.1365-2249.2005.02920.x

Cited by 24 publications

(16 citation statements)

References 26 publications

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“…We found that PSGL-1 expression itself was up-regulated following the activation of CLA + CD4 + T cells. Others have also shown that surface expression of PSGL-1 can be up-regulated upon T cell stimulation in an antigen specific manner using TCR transgenic mice [44,45]. Moreover, we found that CHO-131 directly recognized PSGL-1 and the expression of C2-O-sLe X -modified PSGL-1 significantly increased following the activation of CLA + CD4 + T cells.…”

Section: Discussionsupporting

confidence: 68%

Cutaneous lymphocyte-associated antigen (CLA) T cells up-regulate P-selectin ligand expression upon their activation

Ni¹,

Walcheck²

2009

Clinical Immunology

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Memory T cells expressing CLA occur in humans and accumulate in normal and inflamed skin. These cells uniformly bind to the vascular adhesion molecule E-selectin, yet only a subset bind to P-selectin. The latter cells are distinguished by the mAb CHO-131, and are enriched in psoriasis lesions. Activated T cells up-regulate CLA expression, but little is currently known about their binding to P-selectin. We observed that CLA + CD4 + T cells derived from stimulated naïve T cells uniformly express the CHO-131 epitope. This occurred as well upon the restimulation of memory CLA + CD4 + T cells. The latter cells also expressed higher levels of PSGL-1 modified by P-selectin glycan ligands; C2GlcNAcT-1 mRNA, a glycosyltransferase critical for such glycan synthesis; and more uniformly bound to P-selectin. Our findings thus indicate that unlike memory CLA + CD4 + T cells, when activated these cells can broadly bind to P-selectin, suggesting a more diverse tissue trafficking capacity.

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Section: Discussionsupporting

confidence: 68%

Cutaneous lymphocyte-associated antigen (CLA) T cells up-regulate P-selectin ligand expression upon their activation

Ni¹,

Walcheck²

2009

Clinical Immunology

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“…Contradictory to this finding, a small study of subjects with varying stages of COPD (GOLD I-IV) found increased CD162 expression on circulating neutrophils in the COPD group [28]. The ligand of CD162, P-selectin, has received attention as a marker of platelet activation and systemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Adhesion molecules in subjects with COPD and healthy non-smokers: a cross sectional parallel group study

Blidberg¹,

Palmberg²,

James³

et al. 2013

Respiratory Research

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BackgroundThe aim of the study was to investigate how the expression of adhesion molecules changes as neutrophils migrate from the circulation to the lung and if these changes differ between non-smoking subjects and smokers with and without COPD.MethodsNon-smoking healthy subjects (n=22), smokers without (n=21) and with COPD (n=18) were included. Neutrophils from peripheral blood, sputum and bronchial biopsies were analysed for cell surface expression of adhesion molecules (CD11b, CD62L, CD162). Serum, sputum supernatant and BAL-fluid were analysed for soluble adhesion molecules (ICAM-1, -3, E-selectin, P-selectin, VCAM-1, PECAM-1).ResultsExpression of CD11b was increased on circulating neutrophils from smokers with COPD. It was also increased on sputum neutrophils in both smokers groups, but not in non-smokers, as compared to circulating neutrophils.Serum ICAM-1 was higher in the COPD group compared to the other two groups (p<0.05) and PECAM-1 was lower in smokers without COPD than in non-smoking controls and the COPD group (p<0.05). In BAL-fluid ICAM-1 was lower in the COPD group than in the other groups (p<0.05).ConclusionsThus, our data strongly support the involvement of a systemic component in COPD and demonstrate that in smokers neutrophils are activated to a greater extent at the point of transition from the circulation into the lungs than in non-smokers.

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“…Previous studies have reported increased CD162 [11], no differences in CD11a and CD62L [12-15] and both increased [12,14,16,17] and unchanged [14,15] CD11b on neutrophils in COPD. These discrepant results are likely due to variations between studies in severity of COPD, different control groups and different methods of neutrophil isolation.…”

Section: Discussionmentioning

confidence: 95%

Neutrophil adhesion molecules in experimental rhinovirus infection in COPD

et al. 2013

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BackgroundCOPD exacerbations are associated with neutrophilic airway inflammation. Adhesion molecules on the surface of neutrophils may play a key role in their movement from blood to the airways. We analysed adhesion molecule expression on blood and sputum neutrophils from COPD subjects and non-obstructed smokers during experimental rhinovirus infections.MethodsBlood and sputum were collected from 9 COPD subjects and 10 smoking and age-matched control subjects at baseline, and neutrophil expression of the adhesion molecules and activation markers measured using flow cytometry. The markers examined were CD62L and CD162 (mediating initial steps of neutrophil rolling and capture), CD11a and CD11b (required for firm neutrophil adhesion), CD31 and CD54 (involved in neutrophil transmigration through the endothelial monolayer) and CD63 and CD66b (neutrophil activation markers). Subjects were then experimentally infected with rhinovirus-16 and repeat samples collected for neutrophil analysis at post-infection time points.ResultsAt baseline there were no differences in adhesion molecule expression between the COPD and non-COPD subjects. Expression of CD11a, CD31, CD62L and CD162 was reduced on sputum neutrophils compared to blood neutrophils. Following rhinovirus infection expression of CD11a expression on blood neutrophils was significantly reduced in both subject groups. CD11b, CD62L and CD162 expression was significantly reduced only in the COPD subjects. Blood neutrophil CD11b expression correlated inversely with inflammatory markers and symptom scores in COPD subjects.ConclusionFollowing rhinovirus infection neutrophils with higher surface expression of adhesion molecules are likely preferentially recruited to the lungs. CD11b may be a key molecule involved in neutrophil trafficking in COPD exacerbations.

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P-selectin glycoprotein ligand-1 (PSGL-1) is up-regulated on leucocytes from patients with chronic obstructive pulmonary disease

Cited by 24 publications

References 26 publications

Cutaneous lymphocyte-associated antigen (CLA) T cells up-regulate P-selectin ligand expression upon their activation

Cutaneous lymphocyte-associated antigen (CLA) T cells up-regulate P-selectin ligand expression upon their activation

Adhesion molecules in subjects with COPD and healthy non-smokers: a cross sectional parallel group study

Neutrophil adhesion molecules in experimental rhinovirus infection in COPD

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