Cooperation between interleukin-5 and the chemokine eotaxin to induce eosinophil accumulation in vivo.

Collins, Paul; Marleau, Sylvie; Griffiths-Johnson, David A.; Jose, Peter J.; Williams, Timothy J.

doi:10.1084/jem.182.4.1169

Cited by 601 publications

(380 citation statements)

References 36 publications

(39 reference statements)

Supporting

Mentioning

359

Contrasting

Unclassified

Order By: Relevance

“…The first event seen when exogenous IL-5 is given by i.v. administration is that the number of eosinophils in the bone marrow is reduced, and the number of eosinophils in the circulation is increased (54). A similar effect is also seen with a single-day allergen exposure (4,19).…”

Section: Discussionsupporting

confidence: 58%

Eosinophilopoiesis in A Murine Model of Allergic Airway Eosinophilia: Involvement of Bone Marrow IL-5 and IL-5 Receptor α

Tomaki

Zhao

Lundahl

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

The airway inflammation in asthma is dominated by eosinophils. The aim of this study was to elucidate the contribution of newly produced eosinophils in airway allergic inflammation and to determine mechanisms of any enhanced eosinophilopoiesis. OVA-sensitized BALB/c mice were repeatedly exposed to allergen via airway route. Newly produced cells were identified using a thymidine analog, 5-bromo-2′-deoxyuridine, which is incorporated into DNA during mitosis. Identification of IL-5-producing cells in the bone marrow was performed using FACS. Bone marrow CD3+ cells were enriched to evaluate IL-5-protein release in vitro. Anti-IL-5-treatment (TRFK-5) was given either systemically or directly to the airways. IL-5R-bearing cells were localized by immunocytochemistry. Repeated airway allergen exposure caused prominent airway eosinophilia after three to five exposures, and increased the number of immature eosinophils in the bone marrow. Up to 78% of bronchoalveolar lavage (BAL) granulocytes were 5-bromo-2′-deoxyuridine positive. After three allergen exposures, both CD3+ and non-CD3 cells acquired from the bone marrow expressed and released IL-5-protein. Anti-IL-5 given i.p. inhibited both bone marrow and airway eosinophilia. Intranasal administration of anti-IL-5 also reduced BAL eosinophilia, partly via local effects in the airways. Bone marrow cells, but not BAL eosinophils, displayed stainable amounts of the IL-5R α-chain. We conclude that the bone marrow is activated by airway allergen exposure, and that newly produced eosinophils contribute to a substantial degree to the airway eosinophilia induced by allergen. Airway allergen exposure increases the number of cells expressing IL-5-protein in the bone marrow. The bone marrow, as well as the lung, are possible targets for anti-IL-5-treatment.

show abstract

Section: Discussionsupporting

confidence: 58%

Eosinophilopoiesis in A Murine Model of Allergic Airway Eosinophilia: Involvement of Bone Marrow IL-5 and IL-5 Receptor α

Tomaki

Zhao

Lundahl

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…It has also been demonstrated that anti-IL-5 mAb treatment inhibits eosinophilia in mice infected with Toxocara canis, Nippostrongylus brasiliensis and Schistosoma mansoni (14)(15)(16). In addition, IL-5 plays an important role in mobilizing eosinophils from bone marrow to peripheral blood and in priming eosinophils to respond easily to other chemotactic stimuli such as chemokines and lipid mediators (7,17). When a low dose of IL-5 is administered intravenously, it rapidly and dramatically enhances the eosinophil accumulation induced by intradermally injected eotaxin and leukotriene B 4 (17), suggesting a link between chemoattractant factors and IL-5.…”

mentioning

confidence: 99%

“…In addition, IL-5 plays an important role in mobilizing eosinophils from bone marrow to peripheral blood and in priming eosinophils to respond easily to other chemotactic stimuli such as chemokines and lipid mediators (7,17). When a low dose of IL-5 is administered intravenously, it rapidly and dramatically enhances the eosinophil accumulation induced by intradermally injected eotaxin and leukotriene B 4 (17), suggesting a link between chemoattractant factors and IL-5. It has been demonstrated that the chemotactic activity of eosinophils in bronchoalveolar lavage fluid obtained from rats infected with T. canis was significantly reduced after treatment with either a specific leukotriene B 4 receptor antagonist (ONO-4057), a platelet aggregating factor receptor antagonist (TCV-309), and an anti-IL-5 mAb (TB13) (18).…”

mentioning

confidence: 99%

Interleukin-5 mediates peritoneal eosinophilia induced by the F1 cell wall fraction of Histoplasma capsulatum

Sá-Nunes

Medeiros

Faccioli

2004

Braz J Med Biol Res

View full text Add to dashboard Cite

An alkali-insoluble fraction 1 (F1), which contains mainly ß-glucan isolated from the cell wall of Histoplasma capsulatum, induces eosinophil recruitment into the peritoneal cavity of mice. The present study was carried out to determine the participation of interleukin-5 (IL-5) in this process. Inbred C57BL/6 male mice weighing 15-20 g were treated ip with 100 µg of anti-IL-5 monoclonal antibody (TRFK-5, N = 7) or an isotype-matched antibody (N = 7), followed by 300 µg F1 in 1 ml PBS ip 24 h later. Controls (N = 5) received only 1 ml PBS. Two days later, cells from the peritoneal cavity were harvested by injection of 3 ml PBS and total cell counts were determined using diluting fluid in a Neubauer chamber. Differential counts were performed using Rosenfeld-stained cytospin preparations. The F1 injection induced significant (P < 0.01) leukocyte recruitment into the peritoneal cavity (8.4 x 10 6 cells/ml) when compared with PBS alone (5.5 x 10 6 cells/ ml). Moreover, F1 selectively (P < 0.01) induced eosinophil recruitment (1 x 10 6 cells/ml) when compared to the control group (0.07 x 10 6 cells/ml). Treatment with TRFK-5 significantly (P < 0.01) inhibited eosinophil recruitment (0.18 x 10 6 cells/ml) by F1 without affecting recruitment of mononuclear cells or neutrophils. We conclude that the F1 fraction of the cell wall of H. capsulatum induces peritoneal eosinophilia by an IL-5-dependent mechanism. Depletion of this cytokine does not have effect on the recruitment of other cell types induced by F1.

show abstract

“…Eotaxin acts through the receptor CCR3, which is expressed on cell types prominent in allergic inflammation, i.e., eosinophils, Th2 cells, mast cells, and basophils (11)(12)(13)(14). Eotaxin acts systemically, in concert with IL-5, to stimulate the release of eosinophils from the bone marrow, and locally, to mediate their selective recruitment to sites of inflammation (15,16). Disruption of the eotaxin gene in mice suggests that eotaxin is not only an important mediator of eosinophil recruitment during inflammatory responses in the lung, but is also required for maintenance of basal levels of eosinophils in the mucosal tissue of the gut (17,18).…”

mentioning

confidence: 99%

Eotaxin Is Specifically Cleaved by Hookworm Metalloproteases Preventing Its Action In Vitro and In Vivo

Culley

Brown

Conroy

et al. 2000

The Journal of Immunology

132

View full text Add to dashboard Cite

Eotaxin is a potent eosinophil chemoattractant that acts selectively through CCR3, which is expressed on eosinophils, basophils, mast cells, and Th2-type T cells. This arm of the immune system is believed to have evolved to control helminthic parasites. We hypothesized that helminths may employ mechanisms to inhibit eosinophil recruitment, to prolong worm survival in the host. We observed that the excretory/secretory products of the hookworm Necator americanus inhibited eosinophil recruitment in vivo in response to eotaxin, but not leukotriene B4, a phenomenon that could be prevented by the addition of protease inhibitors. Using Western blotting, N. americanus supernatant was shown to cause rapid proteolysis of eotaxin, but not IL-8 or eotaxin-2. N. americanus homogenate was fractionated by gel filtration chromatography, and a FACS-based bioassay measured the ability of each fraction to inhibit the activity of a variety of chemokines. This resulted in two peaks of eotaxin-degrading activity, corresponding to ∼15 and 50 kDa molecular mass. This activity was specific for eotaxin, as responses to other agonists tested were unaffected. Proteolysis of eotaxin was prevented by EDTA and phenanthroline, indicating that metalloprotease activity was involved. Production of enzymes inactivating eotaxin may be a strategy employed by helminths to prevent recruitment and activation of eosinophils at the site of infection. As such this represents a novel mechanism of regulation of chemokine function in vivo. The existence of CCR3 ligands other than eotaxin (e.g., eotaxin-2) may reflect the evolution of host counter measures to parasite defense systems.

show abstract

Cooperation between interleukin-5 and the chemokine eotaxin to induce eosinophil accumulation in vivo.

Cited by 601 publications

References 36 publications

Eosinophilopoiesis in A Murine Model of Allergic Airway Eosinophilia: Involvement of Bone Marrow IL-5 and IL-5 Receptor α

Eosinophilopoiesis in A Murine Model of Allergic Airway Eosinophilia: Involvement of Bone Marrow IL-5 and IL-5 Receptor α

Interleukin-5 mediates peritoneal eosinophilia induced by the F1 cell wall fraction of Histoplasma capsulatum

Eotaxin Is Specifically Cleaved by Hookworm Metalloproteases Preventing Its Action In Vitro and In Vivo

Contact Info

Product

Resources

About