Interleukin 5 synthesis by eosinophils: association with granules and immunoglobulin-dependent secretion.

Dubucquoi, Sylvain; Desreumaux, Pierre; Janin, Anne; Klein, Olivier; Goldman, Michel; Tavernier, Jan; Caprón, A; Capron, Moníque

doi:10.1084/jem.179.2.703

Cited by 272 publications

(170 citation statements)

References 19 publications

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“…7 c). IL-5 plays an important role in eosinophil activation which may also serve as producers of this cytokine [46] . It is likely that the ability of PM exposure to provoke IL-5 secretion is in part responsible for the mobilization and accumulation of eosinophils in the lung, as we reported here.…”

Section: Discussionmentioning

confidence: 99%

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

et al. 2010

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The biological effects of acute particulate air pollution exposure in host innate immunity remain obscure and have relied largely on in vitro models. We hypothesized that single acute exposure to ambient or engineered particulate matter (PM) in the absence of other secondary stimuli would activate lung dendritic cells (DC) in vivo and provide information on the early immunological events of PM exposure and DC activation in a mouse model naïve to prior PM exposure. Activation of purified lung DC was studied following oropharyngeal instillation of ambient particulate matter (APM). We compared the effects of APM exposure with that of diesel-enriched PM (DEP), carbon black particles (CBP) and silver nanoparticles (AgP). We found that PM species induced variable cellular infiltration in the lungs and only APM exposure induced eosinophilic infiltration. Both APM and DEP activated pulmonary DC and promoted a Th2-type cytokine response from naïve CD4+ T cells ex vivo. Cultures of primary peribronchial lymph node cells from mice exposed to APM and DEP also displayed a Th2-type immune response ex vivo. We conclude that exposure of the lower airway to various PM species induces differential immunological responses and immunomodulation of DC subsets. Environmental APM and DEP activated DC in vivo and provoked a Th2 response ex vivo. By contrast, CBP and AgP induced altered lung tissue barrier integrity but failed to stimulate CD4+ T cells as effectively. Our work suggests that respirable pollutants activate the innate immune response with enhanced DC activation, pulmonary inflammation and Th2-immune responsiveness.

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Section: Discussionmentioning

confidence: 99%

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

et al. 2010

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“…The eosinophil lineage appears to be specifically regulated by interleukin 5 (IL-5), a cytokine produced by the T helper 2 subset (Th2) as well as by eosinophils and mast cells. 2 Although earlier studies suggested additional activities of IL-5 in regulating mouse B cells and antibody production 3 recent studies with an IL-5 deficient mouse strain indicate that the regulation of eosinophilia may be the only obligatory role for IL-5 in the adult mouse. 4 IL-5 deficient mice, produced by gene targeting of embryonal stem cells, 4 appear to be normal in appearance and do not develop any obvious disease.…”

Section: Introductionmentioning

confidence: 99%

Eosinophilia is attenuated in experimental colitis induced in IL-5 deficient mice

Stevceva

Pavli²,

Husband

et al. 2000

Genes Immun

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Tissue eosinophilia is a feature of idiopathic inflammatory bowel disease and other forms of colonic inflammation but it is not clear whether the role of eosinophils in the disease process is to contribute to tissue damage. Interleukin 5 (IL-5) stimulates production and activation of eosinophils in vitro and enhances immunoglobulin A (IgA) production. As very little is known about the function of IL-5 in the colon, the aim of this study was to assess its role in colonic inflammation. IL-5 deficient mice were studied using the dextran sulphate sodium (DSS)-induced colitis model and the results compared to a congenic IL-5+/+ strain. The absence of IL-5 resulted in reduction of tissue eosinophilia (P Ͻ 0.0001) but was not reflected in differences in the severity of the disease (P Ͼ 0.5) or in the extent of tissue damage in this model of colitis. Numbers of immunoglobulin-containing cells in IL-5 deficient mice were similar to those in the IL-5+ mice. We conclude that the main role of IL-5 in DSS-induced colonic inflammation is to attract a population of eosinophils which do not appear to contribute significantly to the initiation or development of tissue damage in this model of colitis. Genes and Immunity (2000) 1, 213-218.

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“…In particular, eosinophils may mediate enhanced bronchial reactivity and damage to the respiratory epithelium by the secretion of major basic protein (MBP) (8 -10). In asthma, eosinophils may also localize to the airways mucosa, where they have the potential to prime and amplify the underlying immune responses that predispose to allergic inflammation by the secretion of cytokines (11)(12)(13)(14)(15)(16). Although there is accumulating evidence that eosinophils drive the pathogenesis of allergic disease under some circumstances, the mechanisms regulating their selective trafficking and degranulation in the airways have not been fully delineated.…”

mentioning

confidence: 99%

The Effect of IL-5 and Eotaxin Expression in the Lung on Eosinophil Trafficking and Degranulation and the Induction of Bronchial Hyperreactivity

Mould

Ramsay

Matthaei³

et al. 2000

The Journal of Immunology

170

119

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The mechanisms regulating the selective migration and degranulation of eosinophils in the asthmatic lung and the subsequent development of airways hyperreactivity (AHR) have not been fully delineated. In this investigation, we have employed a novel transgene model to facilitate the dissection of the contributions of IL-5 and/or eotaxin to eosinophil function in the absence of complex tissue signals derived from the allergic lung. Gene transfer of IL-5 and/or eotaxin to the lungs of naive mice induced a pronounced and selective airways eosinophilia, but did not result in eosinophil degranulation or AHR. Airways eosinophilia occurred independently of the induction of a blood eosinophilia, but was markedly augmented by the coexpression of both cytokines and/or by the transient mobilization of eosinophils from the bone marrow by the administration of i.v. IL-5. However, for eosinophil degranulation and AHR to occur, the inhalation of Ag was required in association with IL-5 and eotaxin expression. Investigations in IL-5-deficient mice linked eosinophilia, and not solely IL-5 and eotaxin, with the induction of AHR. Furthermore, eosinophil degranulation and AHR were dependent on CD4+ T cells. Importantly, this investigation shows that IL-5 regulates eosinophilia within the lung as well as in the circulation and also amplifies eotaxin-induced chemotaxis in the airway compartment. Moreover, the interplay between these cytokines, CD4+ T cells, and factors generated by Ag inhalation provides fundamental signals for eosinophil degranulation and the induction of AHR.

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Interleukin 5 synthesis by eosinophils: association with granules and immunoglobulin-dependent secretion.

Cited by 272 publications

References 19 publications

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

Eosinophilia is attenuated in experimental colitis induced in IL-5 deficient mice

The Effect of IL-5 and Eotaxin Expression in the Lung on Eosinophil Trafficking and Degranulation and the Induction of Bronchial Hyperreactivity

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