Elevated Levels of Thymus- and Activation-regulated Chemokine in Bronchoalveolar Lavage Fluid from Patients with Eosinophilic Pneumonia

Miyazaki, Eishi; Nureki, Shin-ichi; Fukami, Tetsujiro; Shigenaga, Takehiko; Ando, Masayuki; Ito, Kota; Ando, Hiroaki; Sugisaki, Katsunori; Kumamoto, Toshihide; Tsuda, Toshihide

doi:10.1164/ajrccm.165.8.2106110

Cited by 71 publications

(69 citation statements)

References 41 publications

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“…As in CEP, the chemokine CCL17 has been detected in high levels in AEP, potentially consistent with a role for recruited T cells in the pathogenesis of AEP (114). An array of both Th2 and Th1 cytokines are elevated in the BAL fluid in AEP, including IL-1ra, IL-2, IL-5, IL-10, IL-12, IL-13, and IL-18, perhaps reflecting the known pluripotent secretory potential of eosinophils (3,76,180).…”

Section: Aepmentioning

confidence: 55%

“…BAL fluid in CEP contains the cytokines IL-4, IL-5, IL-6, IL-10, IL-13, and IL-18, which is largely consistent with local Th2 inflammation, though the Th1 cytokines IL-2 and IL-12 are present as well (76,85,114). Several chemokines are also present in BAL fluid samples, including CCL17 and CCL22, the chemokine ligands of the receptor CCR4, suggesting that T cell recruitment may be an important factor in the pathophysiology of CEP (74,114). In addition, CXCL9, CXCL10, CCL5 (RANTES), CCL11 (eotaxin-1), CCL2, and CCL4 have also been observed to be elevated in CEP (73,75,89,186).…”

Section: Cepmentioning

confidence: 89%

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Eosinophilic Pneumonias

2012

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SUMMARY This review starts with discussions of several infectious causes of eosinophilic pneumonia, which are almost exclusively parasitic in nature. Pulmonary infections due specifically to Ascaris , hookworms, Strongyloides , Paragonimus , filariasis, and Toxocara are considered in detail. The discussion then moves to noninfectious causes of eosinophilic pulmonary infiltration, including allergic sensitization to Aspergillus , acute and chronic eosinophilic pneumonias, Churg-Strauss syndrome, hypereosinophilic syndromes, and pulmonary eosinophilia due to exposure to specific medications or toxins.

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Section: Aepmentioning

confidence: 55%

Section: Cepmentioning

confidence: 89%

Eosinophilic Pneumonias

2012

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“…This supports a role for these CC chemokines in the development of fibrosis. Previous researchers have shown that CCL17 is elevated in BAL fluid of patients with eosinophilic pneumonia that correlated with the presence of IL-4, IL-5, and IL-13 in BAL fluid (33). Similarly Katoh et al (34) have shown that CCR4 ϩ CD4 ϩ T cells in BAL fluid from patients with eosinophilic pneumonia correlated with BAL fluid levels of CCL17, CCL22, and IL-5.…”

Section: Discussionmentioning

confidence: 75%

The Role of the Th2 CC Chemokine Ligand CCL17 in Pulmonary Fibrosis

Belperio

Murray

et al. 2004

The Journal of Immunology

161

132

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Increasing evidence suggests that the development of pulmonary fibrosis is a Th2-mediated process. We hypothesized that the CC chemokines that are associated with a Th2 profile (CCL17 and CCL22) have an important role in the development of pulmonary fibrosis. We measured CCL17 and CCL22 during the pathogenesis of bleomycin-induced pulmonary fibrosis. We found that both CCL17 and CCL22 were significantly elevated through day 20 as compared with control mice. Peak expression of CCL22 preceded the peak levels of CCL17, as measured by real-time quantitative PCR. CCR4 is the receptor for CCL17 and CCL22 therefore, to further characterize the role of CCL17 and CCL22, we measured CCR4 mRNA in lung tissue of bleomycin-treated mice by real-time quantitative PCR. CCR4 was significantly elevated in bleomycin-treated mice as compared with control mice. Immunolocalization demonstrated that CCR4 was expressed predominantly on macrophages. Neutralization of CCL17, but not CCL22, led to a reduction in pulmonary fibrosis. Immunolocalization of bleomycin-treated lung tissue and human idiopathic pulmonary fibrosis tissue specimens showed that epithelial cells expressed CCL17. These findings demonstrate a central role for Th2 chemokines and the macrophage in the pathogenesis of pulmonary fibrosis and are further support for the role of a Th2 phenotype in the pathogenesis of pulmonary fibrosis.

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“…CCL22 and CCL17 belong to a CC chemokine family and are involved in several Th2-dominant diseases, such as bronchial asthma, atopic dermatitis and eosinophilic pneumonia [22][23][24][25]. These two chemokines are the specific ligands of CCR4 [10] and are pivotal in recruiting Th2 to sites of inflammation under Th2-dominant conditions.…”

Section: Discussionmentioning

confidence: 99%

CCL22 and CCL17 in rat radiation pneumonitis and in human idiopathic pulmonary fibrosis

Inoue¹,

Fujishima²,

Ikeda³

et al. 2004

Eur Respir J

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Pulmonary fibrosis is caused by various known and unknown aetiologies, but the key pathogenic mechanisms are still ill-defined. Chemokines are a large family of chemotactic cytokines that play pivotal roles in various inflammatory diseases.In the present study, the roles of chemokines in a rat model of radiation pneumonitis/ pulmonary fibrosis were examined.Accumulation of inflammatory cells and pneumonitis were observed on day 28, and diffuse alveolar wall thickening with extensive fibrosis was observed on day 56. In addition to the previously reported CCL2 (macrophage chemoattractant protein-1) induction, selective upregulation of CCL22 (macrophage-derived chemokine) and CCL17 (thymus and activation-regulated chemokine) were demonstrated for the first time in the irradiated lung tissues. Immunohistochemically, it was demonstrated that CCL22 and CCL17 were localised primarily to alveolar macrophages, whereas their receptor CC chemokine receptor 4 (CCR4) was detected on alveolar lymphocytes and macrophages. On further analysis of bronchoalveolar lavage fluid from patients with idiopathic pulmonary fibrosis and sarcoidosis, elevated levels of CCL22, but not of CCL17, were observed in the idiopathic pulmonary fibrosis patients.Since these two chemokines play pivotal roles in various type-2 T-helper celldominant diseases, it was speculated that CCL22, and probably CCL17, are involved in the pathophysiology of radiation pneumonitis/pulmonary fibrosis and idiopathic pulmonary fibrosis through the recruitment of CC chemokine receptor 4-positive type-2 T-helper cells and alveolar macrophages.

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Elevated Levels of Thymus- and Activation-regulated Chemokine in Bronchoalveolar Lavage Fluid from Patients with Eosinophilic Pneumonia

Cited by 71 publications

References 41 publications

Eosinophilic Pneumonias

Eosinophilic Pneumonias

The Role of the Th2 CC Chemokine Ligand CCL17 in Pulmonary Fibrosis

CCL22 and CCL17 in rat radiation pneumonitis and in human idiopathic pulmonary fibrosis

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