The role of selectins in VLA-4 and CD18-independent neutrophil migration to joints of rats with adjuvant arthritis

Birner, Ulrieke; Issekutz, Thomas B.; Issekutz, Andrew C.

doi:10.1002/(sici)1521-4141(199904)29:04<1094::aid-immu1094>3.0.co;2-6

Cited by 13 publications

(10 citation statements)

References 34 publications

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“…Studies in rodents have implicated P-selectin up-regulation in rheumatoid arthritis, 30 atherosclerosis, 31,32 and allergy, 33 however the mediator responsible remains unknown. This is intriguing in light of the fact that in these chronic human diseases, bursts of neutrophil recruitment are a common feature.…”

Section: Discussionmentioning

confidence: 99%

Exclusive Neutrophil Recruitment with Oncostatin M in a Human System

Kerfoot

Raharjo

et al. 2001

The American Journal of Pathology

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Oncostatin M (OSM), a member of the IL-6 family has been postulated to be a potent recruiter of leukocytes, however information regarding the molecular mechanism(s) underlying this event is extremely limited. Therefore, the aim of this study was to investigate the role of OSM-mediated leukocyte recruitment in a human system in vitro under flow conditions. A parallelplate flow chamber assay was used to examine leukocyte recruitment from whole blood by human umbilical vein endothelium treated for 24 hours with OSM. OSM in a dose-response manner revealed very significant leukocyte rolling and adhesion reaching optimal levels at a very low concentration of OSM (10 ng/ml). The OSM-induced leukocyte rolling and adhesion was comparable to levels seen with tumor necrosis factor. OSM was extremely selective for neutrophil recruitment (96%) with <3% lymphocyte recruitment. By contrast, tumor necrosis factor-␣ revealed no such selectivity, recruiting 70% neutrophils and at least 25% lymphocytes and detectable levels of eosinophils at 24 hours. The molecular mechanism underlying the leukocyte recruitment seemed to be entirely dependent on P-selectin as leukocyte recruitment could be completely blocked by the addition of a P-selectin-blocking antibody. An elevation in both Pselectin message and protein was observed with 24 hours of OSM stimulation of endothelium. By contrast, E-selectin and VCAM-1 were not detectable after OSM stimulation. Similar results were seen with passaged dermal microvascular endothelium that does not have a prestored pool of P-selectin. Based on these results, we conclude that OSM may be a very selective potent recruiter of neutrophils in more prolonged inflammatory conditions, an event exclusively dependent on P-selectin. Leukocytes are recruited to sites of inflammation through a well-defined series of interactions with activated endothelium. Cytokines induce endothelium to express various adhesion molecules that mediate this cascade of events.1-3 Initially, selectins on endothelium mediate transient interactions with their leukocyte ligands, resulting in leukocyte tethering and rolling along the vessel wall. Activation of leukocytes by chemoattractants leads to functional up-regulation of integrins, resulting in firm adhesion to their immunoglobulin superfamily ligands on endothelium and permitting extravasion into the surrounding tissue.

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Section: Discussionmentioning

confidence: 99%

Exclusive Neutrophil Recruitment with Oncostatin M in a Human System

Kerfoot

Raharjo

et al. 2001

The American Journal of Pathology

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“…Adhesion molecules on neutrophils and on vascula endothelium mediate neutrophil migration from blood into inflamed tissues. Birne et al demonstrated that Pselectin and E-selectin are required for the VLA-4-and CD18-integrin independent migration of neutrophils to sites of chronic arthritis in the rat [24]. Prednisolone administration prevents reduction in bone mass and strength of the lumbar trabecular bone in AIA rats by reducing the disease-associated increase in bone resorption and decrease in bone formation at both the local and systemic levels [25].…”

Section: Mycobacteria-adjuvant-induced Arthritis In Ratsmentioning

confidence: 99%

Animal models of rheumatoid arthritis and related inflammation

et al. 1999

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The major, extensively studied, experimentally-induced rat and mouse models of arthritis with features resembling rheumatoid arthritis are reviewed here. Etiopathogenetic studies that were recently published are emphasized. In summary, multiple triggering stimuli can induce disease in genetically-prone strains of inbred rats and mice. Multiple genetic loci, including both MHC and non-MHC, regulate disease expression in these animals. By comparison with other models of autoimmune disease, clustering of regulatory loci within and among species is increasingly becoming evident. At the cellular level, both innate and acquired immune systems are involved in the disease manifestations. At the molecular level, unbalanced chronic production of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1, IL-6 and IL-12, as opposed to IL-4 and IL-10, is correlated with arthritis disease susceptibility and severity.

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“…However, recent investigations have suggested that neutrophil accumulation may be more complex than previously considered. For example, some studies have shown that neutrophil infiltration may be CD18-independent in the lung [6] and joints [7] but the alternative adhesive mechanism remains elusive. Nonetheless, these findings indicate that the contribution of CD18 may vary in microvascular beds of different organs.…”

Section: Introductionmentioning

confidence: 99%

Important role of CD18 in TNF- α -induced leukocyte adhesion in muscle and skin venules in vivo

Zhang

Schramm²,

Liu

et al. 2000

Inflammation Research

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These findings suggest that CD18 is a dominant mediator of firm neutrophil adhesion to venular endothelial cells in the muscle and skin stimulated by TNF-alpha in vivo. In addition, this decreased adhesion in CD18-mutants attenuates leukocyte extravasation in response to TNF-alpha activation. Thus, inhibition of CD 18-function may provide an important strategy to inhibit leukocyte recruitment in cytokine-dependent diseases.

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The role of selectins in VLA-4 and CD18-independent neutrophil migration to joints of rats with adjuvant arthritis

Cited by 13 publications

References 34 publications

Exclusive Neutrophil Recruitment with Oncostatin M in a Human System

Exclusive Neutrophil Recruitment with Oncostatin M in a Human System

Animal models of rheumatoid arthritis and related inflammation

Important role of CD18 in TNF- α -induced leukocyte adhesion in muscle and skin venules in vivo

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