CXCL1-Triggered Interaction of LFA1 and ICAM1 Control Glucose-Induced Leukocyte Recruitment during Inflammation<i>In Vivo</i>

Buschmann, Kirsten; Koch, Lutz; Braach, Natascha; Mueller, Hanna; Frommhold, David; Poeschl, Johannes; Ruef, Peter

doi:10.1155/2012/739176

Cited by 11 publications

(15 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Different coating of flow chambers allowed a functional analysis of the used or omitted molecules. As reported previously [ 37 , 43 ], we first used a combination of P-selectin, IL-8 and ICAM-1, which triggers significant adhesion of adult neutrophils when compared to uncoated controls (Figure 2 A). This molecular coating also led to a relevant adhesion of neutrophils of neonates or premature infants compared to their respective controls.…”

Section: Resultsmentioning

confidence: 99%

RAGE controls leukocyte adhesion in preterm and term infants

et al. 2014

Self Cite

View full text Add to dashboard Cite

BackgroundInsufficient leukocyte recruitment may be one reason for the high incidence of life-threatening infections in preterm infants. Since the receptor of advanced glycation end products (RAGE) is a known leukocyte adhesion molecule and highly expressed during early development, we asked whether RAGE plays a role for leukocyte recruitment in preterm and term infants.MethodsLeukocyte adhesion was analyzed in dynamic flow chamber experiments using isolated leukocytes of cord blood from extremely premature (<30 weeks of gestation), moderately premature (30–35 weeks of gestation) and mature neonates (>35 weeks of gestation) and compared to the results of adults. For fluorescent microscopy leukocytes were labeled with rhodamine 6G. In the respective age groups we also measured the plasma concentration of soluble RAGE (sRAGE) by ELISA and Mac-1 and LFA-1 expression on neutrophils by flow cytometry.ResultsThe adhesive functions of fetal leukocytes significantly increase with gestational age. In all age groups, leukocyte adhesion was crucially dependent on RAGE. In particular, RAGE was equally effective to mediate leukocyte adhesion when compared to ICAM-1. The plasma levels of sRAGE were high in extremely premature infants and decreased with increasing gestational age. In contrast, expression of β2-Integrins Mac-1 and LFA-1 which are known ligands for RAGE and ICAM-1 did not change during fetal development.ConclusionWe conclude that RAGE is a crucial leukocyte adhesion molecule in both preterm and term infants.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-014-0053-0) contains supplementary material, which is available to authorized users.

show abstract

Section: Resultsmentioning

confidence: 99%

RAGE controls leukocyte adhesion in preterm and term infants

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…The expression of Mac-1 was determined using a previously described method with slight modifications [28]. Following lysis of red blood cells, bone-marrow-derived neutrophils were incubated at 37°C for 30 min in the presence or absence of 10 μ M SB203580 in vitro .…”

Section: Methodsmentioning

confidence: 99%

Pharmacological Inhibition of p38 Mitogen-Activated Protein Kinases Affects KC/CXCL1-Induced Intraluminal Crawling, Transendothelial Migration, and Chemotaxis of NeutrophilsIn Vivo

Hossain

Liu

2013

Mediators of Inflammation

View full text Add to dashboard Cite

p38 mitogen-activated protein kinase (MAPK) signalling is critical in the pathophysiology of a variety of inflammatory processes. Leukocyte recruitment to the site of inflammation is a multistep process governed by specific signalling cascades. After adhesion in the lumen, many leukocytes crawl to optimal sites at endothelial junctions and transmigrate to extravascular tissue in a Mac-1-dependent manner. The signalling mechanisms that regulate postadhesion steps of intraluminal crawling, transmigration, and chemotaxis in tissue remain incompletely understood. The present study explored the effect of p38 MAPK inhibitor SB203580 on various parameters of neutrophil recruitment triggered by chemokine KC (CXCL1) gradient. Neutrophil-endothelial interactions in microvasculature of murine cremaster muscle were determined using intravital microscopy and time-lapsed video analysis. SB203580 (100 nM) did not change leukocyte rolling but significantly attenuated neutrophil adhesion, emigration, and transmigration and impaired the initiation of neutrophil crawling and transmigration. In response to KC chemotactic gradient, SB203580 significantly reduced the velocity of migration and chemotaxis index of neutrophils in tissue. The upregulation of Mac-1 expression in neutrophils stimulated by KC was significantly blunted by SB203580 in vitro. Collectively, our findings demonstrate that pharmacological suppression of p38 MAPK significantly impairs multiple steps of neutrophil recruitment in vivo.

show abstract

“…Thus, the findings of this study could stimulate the development of course-specific therapeutic approaches to treat inflammatory diseases involving ICAM-1 and RAGE [15, 16, 33, 40]. …”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Functions of Protein C Require RAGE and ICAM-1 in a Stimulus-Dependent Manner

Braach

Buschmann

Pflaum

et al. 2014

Mediators of Inflammation

Self Cite

View full text Add to dashboard Cite

By binding β 2-integrins both ICAM-1 and the receptor for advanced glycation end products (RAGE) mediate leukocyte recruitment in a stimulus-dependent manner. Using different inflammatory mouse models we investigated how RAGE and ICAM-1 are involved in anti-inflammatory functions of protein C (PC; Ceprotin, 100 U/kg). We found that, depending on the stimulus, RAGE and ICAM-1 are cooperatively involved in PC-induced inhibition of leukocyte recruitment in cremaster models of inflammation. During short-term proinflammatory stimulation (trauma, fMLP, and CXCL1), ICAM-1 is more important for mediation of anti-inflammatory effects of PC, whereas RAGE plays a major role after longer proinflammatory stimulation (TNFα). In contrast to WT and Icam-1−/− mice, PC had no effect on bronchoalveolar neutrophil emigration in RAGE−/− mice during LPS-induced acute lung injury, suggesting that RAGE critically mediates PC effects during acute lung inflammation. In parallel, PC treatment effectively blocked leukocyte recruitment and improved survival of WT mice and Icam-1-deficient mice in LPS-induced endotoxemia, but failed to do so in RAGE-deficient mice. Exploring underlying mechanisms, we found that PC is capable of downregulating intracellular RAGE and extracellular ICAM-1 in endothelial cells. Taken together, our data show that RAGE and ICAM-1 are required for the anti-inflammatory functions of PC.

show abstract

CXCL1-Triggered Interaction of LFA1 and ICAM1 Control Glucose-Induced Leukocyte Recruitment during InflammationIn Vivo

Cited by 11 publications

References 34 publications

RAGE controls leukocyte adhesion in preterm and term infants

RAGE controls leukocyte adhesion in preterm and term infants

Pharmacological Inhibition of p38 Mitogen-Activated Protein Kinases Affects KC/CXCL1-Induced Intraluminal Crawling, Transendothelial Migration, and Chemotaxis of NeutrophilsIn Vivo

Anti-Inflammatory Functions of Protein C Require RAGE and ICAM-1 in a Stimulus-Dependent Manner

Contact Info

Product

Resources

About