P-selectin glycoprotein ligand-1 regulates chemokine-dependent leukocyte recruitment in colonic ischemia-reperfusion

Santén, Stefan; Schramm, René; Menger, Michael D.; Wang, Yusheng; Jeppsson, Bengt; Thorlacius, Henrik

doi:10.1007/s00011-007-7071-9

Cited by 22 publications

(12 citation statements)

References 31 publications

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“…This view is further supported by the fact that an antibody directed against the ligand of P-selectin, i.e. Pselectin glycoprotein ligand-1 also abrogates I/R-induced leukocyte recruitment in the gut [58]. Intestinal I/R-induced firm leukocyte adhesion is mainly dependent on beta2-integrins and immunoglobulins on the leukocytic and endothelial site, respectively.…”

Section: Mechanisms Of Acute Intestinal I/r Injurymentioning

confidence: 92%

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

Vollmar

Menger

2010

Langenbecks Arch Surg

228

153

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Section: Mechanisms Of Acute Intestinal I/r Injurymentioning

confidence: 92%

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

Vollmar

Menger

2010

Langenbecks Arch Surg

228

153

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“…It seems that the relative level of L-selectin function is dependent on the model investigated, suggesting that expression or participation of selectin molecules is dependent not only on the type of inflammatory stimulus, but also on the anatomic compartment analyzed. Interestingly, administration of an anti-Eselectin antibody had a profound effect in the LPS model (P Ͻ 0.001), but had no effect in the peritonitis model, as shown in other mouse models (7,14,16,34,40). Not all data in the literature, however, agree with the notion that exclusive blockade of E-selectin has no effect on neutrophil recruitment.…”

mentioning

confidence: 87%

Circulating platelet-neutrophil complexes are important for subsequent neutrophil activation and migration

Kornerup

Salmon

Pitchford

et al. 2010

Journal of Applied Physiology

145

137

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Previous studies in our laboratory have shown that platelets are essential for the migration of eosinophils into the lungs of allergic mice, and that this is dependent on the functional expression of platelet P-selectin. We sought to investigate whether the same is true for nonallergic, acute inflammatory stimuli administered to distinct anatomic compartments. Neutrophil trafficking was induced in two models, namely zymosan-induced peritonitis and LPS-induced lung inflammation, and the platelet dependence of these responses investigated utilizing mice rendered thrombocytopenic. The relative contribution of selectins was also investigated. The results presented herein clearly show that platelet depletion (>90%) significantly inhibits neutrophil recruitment in both models. In addition, we show that P-selectin glycoprotein ligand-1, but not P-selectin, is essential for neutrophil recruitment in mice in vivo, thus suggesting the existence of different regulatory mechanisms for the recruitment of leukocyte subsets in response to allergic and nonallergic stimuli. Further studies in human blood demonstrate that low-dose prothrombotic and pro-inflammatory stimuli (CCL17 or CCL22) synergize to induce platelet and neutrophil activation, as well as the formation of platelet-neutrophil conjugates. We conclude that adhesion between platelets and neutrophils in vivo is an important event in acute inflammatory responses. Targeting this interaction may be a successful strategy for inflammatory conditions where current therapy fails to provide adequate treatment.

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“…PSGL-1 is the bestcharacterized selectin counter-receptor, which preferentially binds to P-selectin but can also bind to E-selectin with low affinity [11]. It is well-documented that inhibition of PSGL-1 effectively inhibits leukocyte recruitment in different models of inflammation [12][13][14][15][16], including septic lung damage [5]. However, the recruitment process of leukocytes in the lung is more complex and less studied than in other organs.…”

Section: Introductionmentioning

confidence: 99%

Direct in vivo observations of P-selectin glycoprotein ligand-1-mediated leukocyte–endothelial cell interactions in the pulmonary microvasculature in abdominal sepsis in mice

et al. 2012

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Thorlacius, H. (2013). Direct in vivo observations of P-selectin glycoprotein ligand-1-mediated leukocyte-endothelial cell interactions in the pulmonary microvasculature in abdominal sepsis in mice. Inflammation Research, 62(3), 275-282. DOI: 10.1007/s00011-012-0575-y General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal AbstractObjective P-selectin glycoprotein ligand-1 (PSGL-1) has been shown to play a significant role in septic lung injury. However, the detailed role of PSGL-1 in the pulmonary leukocyte recruitment remains elusive. We have developed a method based on intravital fluorescence microscopy of the lung microcirculation to examine the role of PSGL-1 in the extravasation process of leukocytes in septic lung damage.Methods Male C57BL/6 mice were treated with a control antibody or an anti-PSGL-1 antibody prior to cecal ligation and puncture (CLP). Leukocyte-endothelium interactions and microvascular hemodynamics were studied in pulmonary arterioles, capillaries and venules 4 hours after CLP.Results Immunoneutralization of PSGL-1 decreased CLP-induced leukocyte rolling in pulmonary arterioles and venules significantly. Inhibition of PSGL-1 had no effect on leukocyte adhesion in venules, whereas the number of adherent leukocytes in lung arterioles and the number of trapped leukocytes in capillaries were markedly decreased. Moreover, immunoneutralization of PSGL-1 improved microvascular perfusion in the lung of septic animals.Conclusions Taken together, these results document that PSGL-1 mediates leukocyte rolling in arterioles and venules. However, inhibition of PSGL-1 only decreases leukocyte adhesion in arterioles, suggesting that leukocyte rolling is not a prerequisite for pulmonary venular adhesion of leukocytes in sepsis. In addition, our data show that capillary trapping of leukocytes is dependent on PSGL-1 function.

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P-selectin glycoprotein ligand-1 regulates chemokine-dependent leukocyte recruitment in colonic ischemia-reperfusion

Cited by 22 publications

References 31 publications

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

Circulating platelet-neutrophil complexes are important for subsequent neutrophil activation and migration

Direct in vivo observations of P-selectin glycoprotein ligand-1-mediated leukocyte–endothelial cell interactions in the pulmonary microvasculature in abdominal sepsis in mice

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