Highly purified murine interleukin 5 (IL-5) stimulates eosinophil function and prolongs in vitro survival. IL-5 as an eosinophil chemotactic factor.

Yamaguchi, Yuji; Hayashi, Yukinori; Sugama, Yasuo; Miura, Yasusada; Kimura, Tadashi; Kitamura, Satoshi; Torisu, Motomichi; Mita, Seiji; Tominaga, Akira; Takatsu, Kiyoshi

doi:10.1084/jem.167.5.1737

Cited by 598 publications

(296 citation statements)

References 17 publications

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“…IL-5 is mainly produced by Th2 cells and mast cells. As an eosinophil differentiation and maturation factor (40,41), it is widely studied for its role in asthma and allergies, as well as in host defense from intestinal parasites. Interestingly, patients with asthma have been reported to have decreased atherosclerotic disease (42).…”

Section: Discussionmentioning

confidence: 99%

IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis

Binder

Hartvigsen²,

Chang³

et al. 2004

J. Clin. Invest.

253

242

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Section: Discussionmentioning

confidence: 99%

IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis

Binder

Hartvigsen²,

Chang³

et al. 2004

J. Clin. Invest.

253

242

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“…Both granulocyte-macrophage colonystimulation factor and IL-3 stimulate the recruitment of eosinophils as well as other leukocytes, whereas IL-5 specifically supports the terminal differentiation and proliferation of eosinophil precursors as well as the eosinophil activation effect (11)(12)(13). Several chemoattractants are involved in both in vitro and in vivo eosinophil migration.…”

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

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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.

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“…The demonstration of eosinophil major basic protein and eosinophil derived neurotoxin indicating degranulation at sites of injury are an important part of the evidence that eosinophils are producing tissue damage in the asthmatic lung (Sur et al 1995). Hence, the current evidence suggests that the local production of IL-5 in asthmatic airways may play an important role in the priming of eosinophils for subsequent activation, and in enhancing their survival at sites of allergic inflammation (Lopez et al 1988, Yamaguchi et al 1988, all of which is likely to be important in asthma.…”

Section: Asthma and Il-5 Human Studies: Il5 Mrna And Proteinmentioning

confidence: 99%

“…It activates mature eosinophils and prolongs their survival in culture (Yamaguchi et al 1988)-possibly via its ability to delay apoptosis , as well as selectively enhancing eosinophil degranulation, antibody-dependent cytotoxicity and adhesion to vascular endothelium (Lopez et al 1988, Fujisawa et al 1990). IL-5 enhances the capacity of eosinophils to release LTC4 (Weller et al 1992) and also primes basophils, leading to increased histamine and LTC4 generation (Bischoff et al 1990, Laviollette et al 1995 and increases synthesis of IgM, IgA, IgE by B cells costimulated with IL-4 (Pene et al 1988, Purkerson & Isakson 1992.…”

Section: Il-5 T Cells and Eosinophilsmentioning

confidence: 99%

IL-5 and IL-5 receptor in asthma

Kotsimbos

Hamid

1997

Mem. Inst. Oswaldo Cruz

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and a soluble isoform (αIL-5Rs). Cytokines such as IL-5 produce specific and non-specific cellular responses through specific cell membrane receptor mediated activation of intracellular signal transduction pathways which, to a large part, regulate gene expression. The major intracellular signal transduction mechanism is activation of non-receptor associated tyrosine kinases including JAK and MAP kinases which can then transduce signals via a novel family of transcriptional factors named signal transducers and activators of transcription (STATS). JAK2, STAT1 and STAT 5 appear to be particularly important in IL-5 mediated eosinophil responses. Asthma is characterized by episodic airways obstruction, increased bronchial responsiveness, and airway inflammation. Several studies have shown an association between the number of activated T cells and eosinophils in the airways and abnormalities in FEV1, airway reactivity and clinical severity in asthma. It has now been well documented that IL-5 is highly expressed in the bronchial mucosa of atopic and intrinsic asthmatics and that the increased IL-5 mRNA present in airway tissues is predominantly T cell derived. Immunocytochemical staining of bronchial biopsy sections has confirmed that IL-5 mRNA transcripts are translated into protein in asthmatic subjects. Furthermore, the number of activated CD 4 + T cells and IL-5 mRNA positive cells are increased in asthmatic airways following antigen challenge and studies that have examined IL-5 expression in asthmatic subjects before and after steroids have shown significantly decreased expression following oral corticosteroid treatment in steroid-sensitive asthma but not in steroid resistant and chronic severe steroid dependent asthma. The link between T cell derived IL-5 and eosinophil activation in asthmatic airways is further strengthened by the demonstration that there is an increased number of αIL-5R mRNA positive cells in the bronchial biopsies of atopic and non-atopic asthmatic subjects and that the eosinophil is the predominant site of this increased

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Highly purified murine interleukin 5 (IL-5) stimulates eosinophil function and prolongs in vitro survival. IL-5 as an eosinophil chemotactic factor.

Cited by 598 publications

References 17 publications

IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis

IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis

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

IL-5 and IL-5 receptor in asthma

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