Fundamental and Distinct Roles of P-Selectin and LFA-1 in Ischemia/Reperfusion-Induced Leukocyte-Endothelium Interactions in the Mouse Colon

Riaz, Amjid; Wan, Ming; Schaefer, Thilo; Schramm, René; Ekberg, Henrik; Menger, Michael D.; Jeppsson, Bengt; Thorlacius, Henrik

doi:10.1097/00000658-200212000-00010

Cited by 37 publications

(50 citation statements)

References 44 publications

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“…Thus, it was found that inhibition of P-selectin, but not E-selectin reduced reperfusion-induced leukocyte rolling and adhesion in the colon, which is in agreement with previous fi ndings [29]. Nonetheless, we observed, herein, that inhibition of PSGL-1 decreased leukocyte rolling by nearly 90 % in colonic I/R.…”

Section: Discussionsupporting

confidence: 93%

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

et al. 2007

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Section: Discussionsupporting

confidence: 93%

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

et al. 2007

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“…Histones have been reported to bind and activate TLR2, TLR4 and TLR9 on immune cells [10,34,35], whereas others have shown that histones mainly cause toxic effects on different cell types, such as endothelial and epithelial cells [3,4]. Nonetheless, histone-dependent inflammatory reactions are frequently associated with increased tissue accumulation of leukocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Extracellular histones have also been shown to increase thrombin generation, which could cause dysfunctional coagulation in systemic inflammation [6]. In this context, it is important to note that leukocyte recruitment is a rate-limiting step in mediating tissue damage in many inflammatory diseases, including sepsis, acute pancreatitis [7] and colitis [8] as well as cholestatic liver injury [9] and ischemia reperfusion [10]. Interestingly, inhibition of histone function has been associated with reduced levels of tissue accumulation of leukocytes in disease models, such as endotoxemia and acute kidney injury [5,11,12].…”

Section: Introductionmentioning

confidence: 99%

Adhesive Mechanisms of Histone-Induced Neutrophil-Endothelium Interactions in the Muscle Microcirculation

Puegge

Wang²,

Roller³

et al. 2015

Eur Surg Res

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Background: Extracellular histones released during cell damage have the capacity to cause tissue injury associated with increased leukocyte accumulation. However, the molecular mechanisms regulating histone-induced leukocyte recruitment remain elusive. The objective of this study was to examine the role of adhesion molecules in histone-dependent leukocyte accumulation by use of intravital microscopy of the mouse cremaster microcirculation. Methods: Histone 3 and TNF-α were intrascrotally administered, and anti-P-selectin, anti-P-selectin glycoprotein ligand-1 (PSGL-1), anti-membrane-activated complex-1 (Mac-1), anti-lymphocyte function antigen-1 (LFA-1) antibody and neutrophil depletion antibody were injected intravenously or intraperitoneally. Results: Intrascrotal injection of histone 3 dose-dependently increased leukocyte recruitment. Neutrophil depletion abolished intravascular and extravascular leukocytes after histone 3 challenge, suggesting that neutrophils were the dominating leukocyte subtype responding to histone stimulation. Pretreatment with an anti-P-selectin and an anti-PSGL-1 antibody abolished histone-stimulated neutrophil rolling, adhesion and emigration. When the anti-P-selectin or the anti-PSGL-1 antibody was administrated after histone 3 stimulation, neutrophil rolling was reduced, whereas the number of firmly adherent and emigrated neutrophils were unchanged, suggesting that the inhibitory effect of blocking P-selectin and PSGL-1 on neutrophil adhesion and recruitment was due to the reduction in neutrophil rolling. Moreover, pretreatment with antibodies against Mac-1 and LFA-1 had no effect of neutrophil rolling but abolished adhesion and emigration evoked by histone 3. Thus, our data demonstrate that P-selectin and PSGL-1 play an important role in histone-induced inflammatory cell recruitment by mediating neutrophil rolling as a precondition for histone-provoked firm adhesion and emigration in vivo. Moreover, we conclude that both Mac-1 and LFA-1 are critical in supporting histone-provoked firm adhesion of neutrophils to endothelial cells. Conclusion: These novel findings define specific selectins and integrins as potential targets for pharmacological intervention in histone-dependent inflammatory diseases.

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“…Indeed, numerous studies have shown that P-, E-, and L-selectin support early interactions between leukocytes and endothelial cells at sites of inflammation (13,19,21,28). Selectins bind to complex carbohydrates expressed on specific glycoproteins.…”

Section: Discussionmentioning

confidence: 99%

“…Upon activation, neutrophil stiffness increases, promoting mechanical sequestration of neutrophils in lung capillaries (20,34). It is widely held that leukocyte rolling is mediated by the selectin family of adhesion molecules, including P-, E-and L-selectins although their relative roles appear to be both tissue-and stimulus-dependent (2,28). Selectin ligands are complex glycoproteins and, in terms of selectin specificity and function, are poorly understood.…”

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confidence: 99%

Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury

Zhang

Song

Wang

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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Zhang S, Song L, Wang Y, Herwald H, Thorlacius H. Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury. Am J Physiol Lung Cell Mol Physiol 305: L756 -L763, 2013. First published September 13, 2013 doi:10.1152/ajplung.00220.2013.-Streptococcus pyogenes of the M1 serotype can cause streptococcal toxic shock syndrome and acute lung damage. CD162 is an adhesion molecule that has been reported to mediate neutrophil recruitment in acute inflammatory reactions. In this study, the purpose was to investigate the role of CD162 in M1 protein-provoked lung injury. Male C57BL/6 mice were treated with monoclonal antibody directed against CD162 or a control antibody before M1 protein challenge. Edema, neutrophil infiltration, and CXC chemokines were determined in the lung, 4 h after M1 protein administration. Fluorescence intravital microscopy was used to analyze leukocyte-endothelium interactions in the pulmonary microcirculation. Inhibition of CD162 reduced M1 proteinprovoked accumulation of neutrophils, edema, and CXC chemokine formation in the lung by Ͼ54%. Moreover, immunoneutralization of CD162 abolished leukocyte rolling and firm adhesion in pulmonary venules of M1 protein-treated animals. In addition, inhibition of CD162 decreased M1 protein-induced capillary trapping of leukocytes in the lung microvasculature and improved microvascular perfusion in the lungs of M1 protein-treated animals. Our findings suggest that CD162 plays an important role in M1 protein-induced lung damage by regulating leukocyte rolling in pulmonary venules. Consequently, inhibition of CD162 attenuates M1 protein-evoked leukocyte adhesion and extravasation in the lung. Thus, our results suggest that targeting the CD162 might pave the way for novel opportunities to protect against pulmonary damage in streptococcal infections. adhesion; chemokines; inflammation and leukocyte CLINICAL MANIFESTATIONS OF Streptococcus pyogenes infections vary from uncomplicated cases to severe and fatal conditions, such as streptococcal toxic shock syndrome (STSS), which is associated with a mortality exceeding 50% (7, 15). Despite significant investigative efforts, management of patients with STSS is largely restricted to antibiotics and supportive care, which is partly due to an incomplete understanding of the basic pathophysiology in STSS. S. pyogenes express several different virulence factors, including M proteins, of which there are more than 80 different serotypes described in the literature (15,26). The M1 serotype of Streptococcus pyogenes is most commonly linked to STSS (7). Numerous studies have documented that M1 protein is a powerful stimulator of innate immune cells, such as monocytes (26) and neutrophils (15). In addition, the M1 protein has the capacity to induce formation of cytokines (26), chemokines (9), and tissue factor (25), which all contribute to M1 protein-induced edema formation and tissue damage in the lung. Several studies have shown that lung failure is an insidious feature in STSS patie...

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Fundamental and Distinct Roles of P-Selectin and LFA-1 in Ischemia/Reperfusion-Induced Leukocyte-Endothelium Interactions in the Mouse Colon

Cited by 37 publications

References 44 publications

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

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

Adhesive Mechanisms of Histone-Induced Neutrophil-Endothelium Interactions in the Muscle Microcirculation

Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury

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