Periostin, a matrix protein, is a novel biomarker for idiopathic interstitial pneumonias

Okamoto, Masaki; Hoshino, Tomoaki; Kitasato, Yasuhiko; Sakazaki, Yuki; Kawayama, Tomotaka; Fujimoto, Kiminori; Ohshima, Koichi; Shiraishi, Hiroshi; Uchida, Masataka; Ono, Junya; Ohta, Shoichiro; Kato, Seiya; Izuhara, Kenji; Aizawa, Hisamichi

doi:10.1183/09031936.00059810

Cited by 201 publications

(196 citation statements)

References 30 publications

(41 reference statements)

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“…However, periostin, an-other IL-13 target gene, is strongly induced by IL-13 stimulation in stromal cells. Periostin is highly expressed in lung tissue and peripheral blood of IPF patients and, similar to CCL18, has been shown to be associated with decreased lung function and poor prognosis in IPF (35). Under conditions in which IL-13Ra2 is highly expressed, fibroblasts have decreased sensitivity to IL-13, which can be overcome by increasing doses of IL-13.…”

Section: Implications Of Il-13ra2 Expression In Ipfmentioning

confidence: 98%

Endogenously Expressed IL-13Rα2 Attenuates IL-13–Mediated Responses but Does Not Activate Signaling in Human Lung Fibroblasts

Chandriani¹,

DePianto²,

N'Diaye³

et al. 2014

The Journal of Immunology

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IL-13 can bind to two distinct receptors: a heterodimer of IL-13Rα1/IL-4Rα and IL-13Rα2. Whereas IL-13Rα1/IL-4Rα engagement by IL-13 leads to the activation of STAT6, the molecular events triggered by IL-13 binding to IL-13Rα2 remain incompletely understood. IL-4 can bind to and signal through the IL-13Rα1/IL-4Rα complex but does not interact with IL-13Rα2. Idiopathic pulmonary fibrosis is a progressive and generally fatal parenchymal lung disease of unknown etiology with no current pharmacologic treatment options that substantially prolong survival. Preclinical models of fibrotic diseases have implicated IL-13 activity on multiple cell types, including macrophages and fibroblasts, in initiating and perpetuating pathological fibrosis. In this study, we show that IL-13, IL-4, IL-13Rα2, and IL-13–inducible target genes are expressed at significantly elevated levels in lung tissue from patients with idiopathic pulmonary fibrosis compared with control lung tissue. IL-4 and IL-13 induce virtually identical transcriptional responses in human monocytes, macrophages, and lung fibroblasts. IL-13Rα2 expression can be induced in lung fibroblasts by IL-4 or IL-13 via a STAT6-dependent mechanism, or by TNF-α via a STAT6-independent mechanism. Endogenously expressed IL-13Rα2 decreases, but does not abolish, sensitivity of lung fibroblasts to IL-13 and does not affect sensitivity to IL-4. Genome-wide transcriptional analyses of lung fibroblasts stimulated with IL-13 in the presence of Abs that selectively block interactions of IL-13 with IL-13Rα1/IL-4Rα or IL-13Rα2 show that endogenously expressed IL-13Rα2 does not activate any unique IL-13–mediated gene expression patterns, confirming its role as a decoy receptor for IL-13 signaling.

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Section: Implications Of Il-13ra2 Expression In Ipfmentioning

confidence: 98%

Endogenously Expressed IL-13Rα2 Attenuates IL-13–Mediated Responses but Does Not Activate Signaling in Human Lung Fibroblasts

Chandriani¹,

DePianto²,

N'Diaye³

et al. 2014

The Journal of Immunology

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“…Future studies should also consider whether sLOXL2, along with other promising prognostic IPF biomarkers (e.g. matrix metalloproteinase (MMP)1, MMP7, KL-6, periostin, surfactant protein-A and D, CC chemokine ligand 18, vascular endothelial growth factor and YKL-40) [19][20][21][22][23][24][25][26][27][28][29], as well as prognostic scores [30,31] and radiological modalities [32], might have prognostic value for helping physicians and patients anticipate the patient's IPF disease progression. This might include evaluation of serially collected sLOXL2 levels and their relationship to IPF acute exacerbations, which represent a terminal event for many IPF patients [33].…”

Section: Discussionmentioning

confidence: 99%

Serum lysyl oxidase-like 2 levels and idiopathic pulmonary fibrosis disease progression

Chien¹,

Richards

Gibson

et al. 2013

European Respiratory Journal

131

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We evaluated whether lysyl oxidase-like 2 (LOXL2), which promotes cross-linking of collagen in pathological stroma, was detectable in serum from idiopathic pulmonary fibrosis (IPF) patients, and assessed its relationship with IPF disease progression.Patients from the ARTEMIS-IPF (n569) and the Genomic and Proteomic Analysis of Disease Progression in IPF (GAP) (n5104) studies were analysed. Baseline serum LOXL2 (sLOXL2) levels were compared with baseline clinical and physiological surrogates of disease severity, and the association with IPF disease progression was assessed using a classification and regression tree (CART) method. sLOXL2 correlated weakly with forced vital capacity and carbon monoxide diffusion capacity (r -0.24-0.05) in both cohorts. CART-determined thresholds were similar: ARTEMIS-IPF 800 pg?mL -1 and GAP 700 pg?mL -1. In ARTEMIS-IPF, higher sLOXL2 (.800 pg?mL -1 ) was associated with increased risk for disease progression (hazard ratio (HR) 5.41, 95% CI 1.65-17.73). Among GAP subjects with baseline spirometric data (n570), higher sLOXL2 levels (.700 pg?mL -1 ) were associated with more disease progression events (HR 1.78, 95% CI 1.01-3.11). Among all GAP subjects, higher sLOXL2 levels were associated with increased risk for mortality (HR 2.28, 95% CI 1.18-4.38).These results suggest that higher sLOXL2 levels are associated with increased risk for IPF disease progression. However, due to multiple limitations, these results require validation. Clinical trial: This study is registered at www.ClinicalTrials.gov with identifier number NCT00768300 and NCT 00373841.

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“…A recent study (31) found that serum levels of periostin were significantly higher in patients with IPF than in healthy volunteers and patients with cryptogenic organizing pneumonia (COP). Furthermore, periostin levels were inversely correlated with patients' pulmonary function.…”

Section: Periostinmentioning

confidence: 99%

Advances in the study of biomarkers of idiopathic pulmonary fibrosis in Japan

2013

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Periostin, a matrix protein, is a novel biomarker for idiopathic interstitial pneumonias

Cited by 201 publications

References 30 publications

Endogenously Expressed IL-13Rα2 Attenuates IL-13–Mediated Responses but Does Not Activate Signaling in Human Lung Fibroblasts

Endogenously Expressed IL-13Rα2 Attenuates IL-13–Mediated Responses but Does Not Activate Signaling in Human Lung Fibroblasts

Serum lysyl oxidase-like 2 levels and idiopathic pulmonary fibrosis disease progression

Advances in the study of biomarkers of idiopathic pulmonary fibrosis in Japan

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