Interleukin-5 Preferentially Recruits Eosinophils from Vessels in Nasal Mucosa

Terada, Nobuhisa; Konno, Akiyoshi; Natori, Tsuneo; Tada, Hiroyuki; Togawa, Kiyoshi

doi:10.3109/00016489309130242

Cited by 18 publications

(20 citation statements)

References 9 publications

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“…A monoclonal antibody to IL-S inhibits eosinophil infiltration into the airways of animals sensitized to allergen (17,18) and also reduces airway hyperresponsiveness (7,19). Recently, Terada and co-workers demonstrated that IL-S preferentially recruits eosinophils from vessels into nasal mucosa in perennial allergic rhinitis patients (20). The purpose of the present study was to determine whether rhIL-S, applied topically to peripheral airway, mobilized eosinophils to infiltrate into the bronchial mucosa in asthmatics.…”

Section: Discussionmentioning

confidence: 97%

Infiltration of eosinophils into the asthmatic airways caused by interleukin 5.

Shi

Qin²,

Huang³

et al. 1997

Am J Respir Cell Mol Biol

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Interleukin (IL)-5 is thought to play an important role in asthmatic bronchial mucosal inflammation and is a potential therapeutic target. To investigate the effect of IL-5 on the infiltration of eosinophils in airway in vivo, we compared eosinophil counts and their activation status in airways without and after the topical instillation of recombinant human IL-5. Eight subjects with mild atopic asthma underwent initial bronchoscopy during which control bronchoalveolar lavage (BAL) fluid as well as bronchial mucosa were obtained, and at the same time, normal saline and IL-5 were administered to two sublobar segments separately. The second bronchoscopy were carried out and samples from challenged sites were taken 24 h later. It was found that the total eosinophils (BMK-13+ cells) and the activated eosinophils (EG2+ cells) in bronchial mucosa, the eosinophil numbers in BAL fluid, as well as eosinophil cationic protein (ECP) in BAL fluid from saline-challenged segments were not different from those in unchallenged segments. However, a significant eosinophilia was observed in bronchial mucosa and BAL fluid from IL-5-challenged sites. Eosinophil activation, as assessed by secretion of ECP, was also increased significantly in bronchial mucosa and BAL fluid. The results strongly suggested that IL-5 is capable of inducing eosinophil infiltration into the asthmatic airways, as well as the activation of infiltrating eosinophils.

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Section: Discussionmentioning

confidence: 97%

Infiltration of eosinophils into the asthmatic airways caused by interleukin 5.

Shi

Qin²,

Huang³

et al. 1997

Am J Respir Cell Mol Biol

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“…In patients with allergic rhinitis, it has been noted that hrIL-5 recruits eosinophils from vessels [7] and there is a correlation between the number of eosinophils and IL-5 mRNA expression in nasal mucosa [29]. Thus, it is strongly suggested that there may be a relationship between cytokines, especially IL-5, and eosinophils in patients with allergic rhinitis.…”

Section: Discussionmentioning

confidence: 99%

“…It has been recently noted that T-lymphocytes [5,6] and several cytokines [7][8][9] play a role in the pathogenesis of allergic rhinitis. CyA [10] inhibits transcription of signals from T-cell antigen receptor to cytokine genes [11], is used for inhibiting organ transplant rejective reaction [10] and it has been recently noted that CyA is effective for some patients with chronic severe asthma [12].…”

Section: Introductionmentioning

confidence: 99%

Effects of cyclosporin A and glucocorticosteroids on antigen-induced hypersensitivity to histamine in a guinea pig model of allergic rhinitis

Narita¹,

Asakura

Shiraski

et al. 1998

Inflamm. res.

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“…Indeed, IL-5 is not detectable in the BAL fluid of mild asthmatics at 12min after allergen provocation (129). IL-5 may also be important for the recruitment of eosinophils from blood vessels into tissues because topical administration of recombinant human IL-5 to the nasal airway in allergic rhinitis induced eosinophil accumulation in the nasal mucosa (130,131 ). IL-5 may also induce activation of eosinophils that are resident in inflamed tissue, but this effect may be secondary to activation of secretory IgA ( I 3 1 ).…”

Section: Huniun Asthmamentioning

confidence: 99%