Selectins mediate eosinophil recruitment in vivo: a comparison with their role in neutrophil influx

Henriques, GM; Miotla, JM; Cordeiro, SB; Wolitzky, Barry A.; Woolley, ST; Hellewell, PG

doi:10.1182/blood.v87.12.5297.bloodjournal87125297

Cited by 37 publications

(12 citation statements)

References 42 publications

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“…These results mirror the findings reported in arthritic rats in which integrin blockade was not used and where Eselectin was found to play a statistically significant role only in concert with P-selectin [14]. Our findings are consistent with the findings of others employing E-and Pselectin blockade or E-and P-selectin double-deficient mice, indicating that these selectins in combination are more efficient for neutrophil recruitment to inflamed tissues than either alone [14,15,19,20].…”

Section: Discussionsupporting

confidence: 92%

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

Birner

Issekutz

1999

Eur. J. Immunol.

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Neutrophil migration from blood into inflamed tissues is mediated by adhesion molecules on neutrophils and on vascular endothelium. It was previously shown that the integrins VLA-4 and CD11/CD18 in combination mediate 70-80% of neutrophil recruitment to arthritic joints of rats. To investigate if the remaining recruitment involves the selectins, the effect of adhesion-blocking monoclonal antibodies (mAb) to each of the selectins (E-, P and L-), in combination with mAb to VLA-4 and CD18, on the migration of radiolabeled neutrophils to joints of rats with adjuvant arthritis was examined. Blocking P-selectin inhibited neutrophil accumulation in hindlimb joints by 40% whereas mAb to P- and E-selectin together inhibited the accumulation in all joints by 60% relative to anti-VLA-4 plus anti-CD18 treatment alone. Overall there was 90% inhibition relative to arthritic controls. Blocking E- or L-selectin alone or together had no effect. Our results demonstrate that P-selectin in particular and in concert with E-selectin are required for the VLA-4- and CD18-independent migration of neutrophils to sites of chronic arthritis in the rat.

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Section: Discussionsupporting

confidence: 92%

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

Birner

Issekutz

1999

Eur. J. Immunol.

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“…Also surprising was the finding that P‐selectin played no role in eosinophil recruitment, because numerous studies have demonstrated reduced rolling, adhesion, and/or recruitment of eosinophils in mice lacking P‐selectin or in animals treated with selectin‐blocking antibodies 25–29. In fact, it has been suggested that P‐selectin antagonists may be effective in inhibiting eosinophil accumulation at sites of allergic inflammation 30–33. Nonetheless, the current study clearly demonstrated that the blocking of P‐selectin/PSGL‐1 interactions alone may be insufficient.…”

Section: Discussionmentioning

confidence: 62%

P-selectin suppresses hepatic inflammation and fibrosis in mice by regulating interferon ? and the IL-13 decoy receptor

et al. 2004

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The selectin family of cell adhesion molecules is widely thought to promote inflammatory reactions by facilitating leukocyte recruitment. However, it was unexpectedly found that mice with targeted deletion of the P-selectin gene (PsKO mice) developed unpolarized type 1/type 2 cytokine responses and severely aggravated liver pathology following infection with the type 2-promoting pathogen Schistosoma mansoni. In fact, liver fibrosis, which is dependent on interleukin 13 (IL-13), increased by a factor of more than 6, despite simultaneous induction of the antifibrotic cytokine interferon gamma (IFN-␥). Inflammation, as measured by granuloma size, also increased significantly in the absence of P-selectin. When infected PsKO mice were treated with neutralizing anti-IFN-␥ monoclonal antibodies, however, granuloma size was restored to wild-type levels; this finding revealed the potent proinflammatory role of IFN-␥ when expressed concomitantly with IL-13. Untreated PsKO mice also exhibited a significant (sixfold) reduction in decoy IL-13 receptor (IL-13 receptor alpha-2) expression when compared with infected wild-type animals. It is noteworthy, however, that when decoy receptor activity was restored in PsKO mice by treatment with soluble IL-13 receptor alpha-2-Fc, the exacerbated fibrotic response was completely inhibited. Thus, reduced expression of the decoy IL-13 receptor mediated by the elevated type 1 cytokine response probably accounts for the enhanced activity of IL-13 in PsKO mice and for the resultant increase in collagen deposition. In conclusion, the current study has revealed the critical role of P-selectin in the progression of chronic liver disease caused by schistosome parasites. By suppressing IFN-␥ and up-regulating the decoy IL-13 receptor, P-selectin dramatically inhibits the pathologic tissue remodeling that results from chronic type 2 cytokine-mediated inflammation. (HEPATOLOGY 2004;39:676 -687.)

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“…Our previous work showed that LPS-induced neutrophil accumulation in the mouse pleural cavity was dependent on all three selectins, although inhibition of either endothelial selectin alone was not inhibitory (Henriques et al, 1996). LPS induces expression of P-and E-selectin in vivo (Gotsch et al, 1994) and therefore the requirement for these molecules in mediating neutrophil migration was not unexpected.…”

Section: Discussionmentioning

confidence: 97%

Dominant role of L‐ and P‐selectin in mediating CXC chemokine‐induced neutrophil migration in vivo

Miotla

Ridger

Hellewell

2001

British J Pharmacology

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1 The role of selectins in neutrophil emigration in response to the CXC chemokines KC and MIP-2 was investigated in wild type and P-selectin de®cient mice. 2 Intrapleural injection of KC or MIP-2 induced a rapid and speci®c neutrophil accumulation. Emigration 2 h after KC or MIP-2 was reduced 83 ± 88% by anti-L-selectin mAb and 53 ± 63% by anti-P-selectin mAb. Co-administration of anti-L-and P-selectin mAbs abolished neutrophil migration induced by either chemokine. 3 An anti-E-selectin mAb tested alone did not aect KC-induced neutrophil migration after 2 or 4 h. Moreover, anti-E-selectin did not have an additive inhibitory eect on KC-induced neutrophil migration compared with P-selectin blockade alone. This was found when neutrophil migration was measured at 2 and 4 h after KC. 4 Despite a blood neutrophilia, neutrophil migration at 2 and 4 h after KC was markedly smaller (by approximately 90%) in P-selectin de®cient mice compared with wild type animals. Responses at both time points were not decreased further in animals given E-selectin mAb but were reduced to the PBS control level in the presence of anti-L-selectin. 5 In vitro study of cultured murine endothelial cells demonstrated that KC can directly increase cell surface P-selectin expression. 6 These data suggest that CXC chemokine-induced neutrophil accumulation is dependent on both neutrophil L-selectin and a rapid upregulation of endothelial P-selectin but there is no evidence for E-selectin induction.

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Selectins mediate eosinophil recruitment in vivo: a comparison with their role in neutrophil influx

Cited by 37 publications

References 42 publications

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

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

P-selectin suppresses hepatic inflammation and fibrosis in mice by regulating interferon ? and the IL-13 decoy receptor

Dominant role of L‐ and P‐selectin in mediating CXC chemokine‐induced neutrophil migration in vivo

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