Elevated levels of periostin and TGF-β1 in the bronchoalveolar lavage fluid of patients with idiopathic eosinophilic pneumonia

Katoh, Shigeki; Matsumoto, Nobuhiro; Tanaka, Hitomi; Yasokawa, Naoya; Kittaka, Makoto; Kurose, Kouji; Abe, Masaaki; Yoshioka, Daisuke; Shirai, Ryo; Nakazato, Masamitsu; Kobashi, Yoshihiro

doi:10.12932/ap-111018-0414

Cited by 7 publications

(5 citation statements)

References 23 publications

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“…It was found that the value of periostin positively correlated with the IL-13 and TGF- β 1. The finding was similar to the research of patients with idiopathic eosinophilic pneumonia, Katoh et al, demonstrating that periostin was induced by IL-13 and TGF- β 1, which accounted for an important role in tissue remodeling and fibrosis [ 44 ]. Moreover, the LVEF was negatively correlated with the IL-13, TGF- β 1, and periostin, which might be caused by the elevated periostin that mediates the progress of myocardial fibrosis, leading to cardiac remodeling.…”

Section: Discussionsupporting

confidence: 88%

Circulating Levels of IL-13, TGF-β1, and Periostin as Potential Biomarker for Coronary Artery Disease with Acute Heart Failure

Qiu

Fengyi

Zhang

2021

Evidence-Based Complementary and Alternative Medicine

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Objective. Coronary artery disease (CAD) and associated comorbidities such as heart failure (HF) remain the leading cause of morbidity and mortality worldwide, attributed to, at least partially, the lack of biomarkers for efficient disease diagnosis. The study intended to explore potential biomarkers for predicting the presence of HF in CAD patients. Methods. According to the presence of HF, 83 CAD patients with HF were assigned to the AHF group and 52 CAD patients without HF to the CAD group. Additionally, healthy controls (n = 52) were those who had received physical examinations at the same period. The serum levels of IL-13, TGF-β1, and periostin were detected by the enzyme-linked immunosorbent assay (ELISA). Left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDD), left ventricle-end diastolic volume (LVEDV), and left ventricular mass index (LVMI) were detected 3 times by color Doppler ultrasound. The predictive values of IL-13, TGF-β1, and periostin methods were compared by receiver-operating characteristic (ROC) analysis and the area under the curve (AUC). Results. Increased levels of IL-13, TGF-β1, and periostin were noted in the AHF group than in the control and CAD groups ( p < 0.001 ); the CAD group showed higher levels of IL-13, TGF-β1, and periostin than the control group ( p < 0.001 ). Based on the NYHA classification, there were 33 cases with grade II, 28 cases with grade III, and 22 cases with grade IV among 83 CAD patients with HF. It was found that the serum levels of IL-13, TGF-β1, and periostin were higher in the AHF-IV group than in the AHF-III and AHF-II groups ( p < 0.001 ); these levels were also higher in the AHF-III group than in the AHF-II group ( p < 0.001 ). The periostin level was positively correlated with the levels of IL-13 (r = 0.458) and TGF-β1 (r = 0.569) in CAD patients with AHF. Besides, the serum levels of periostin (r = -0.425), IL-13 (r = -0.341), and TGF-β1 (r = -0.435) were negatively correlated with the LVEF of CAD patients with AHF, respectively. When IL-13, TGF-β1, and periostin levels were used to predict the presence of AHF in CAD patients in combination, the sensitivity and specificity were 75.9% and 90.38%, respectively, with the AUC of 0.906 (95% CI: 0.912–0.996). Conclusion. These data reveal that IL-13, TGF-β1, and periostin levels might be associated with the occurrence of AHF in CAD patients and their combination shows the predictive value for the presence of AHF in CAD patients.

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Section: Discussionsupporting

confidence: 88%

Circulating Levels of IL-13, TGF-β1, and Periostin as Potential Biomarker for Coronary Artery Disease with Acute Heart Failure

Qiu

Fengyi

Zhang

2021

Evidence-Based Complementary and Alternative Medicine

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“…In other words, miR-216a-5p other researches showed that the TGF-β1 signaling participated in the regulation of pulmonary inflammation, 22 and its expression was elevated in the bronchoalveolar lavage fluid of patients with idiopathic eosinophilic pneumonia. 28 Thus, this study inferred that miR-216a-5p might also suppressed the TGF-β1 signaling pathway through modulating TGFBR2. Furthermore, the investigation of the underlying mechanism of miR-216a-5p on LPS-induced inflammation in the human bronchial epithelial cell revealed that miR-216a-5p suppressed LPS-induced inflammation in BEAS-2B cells via regulating TGFBR2.…”

Section: Discussionmentioning

confidence: 66%

MiR-216a-5p alleviates LPS-induced inflammation in the human bronchial epithelial cell by inhibition of TGF-β1 signaling via down-regulating TGFBR2

Liu

2021

aei

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Objective: Bronchopneumonia is a common respiratory infection disease and is the leading cause of hospitalization in children under 5 years of age. Inflammation is the primary response caused by bronchopneumonia. But the detailed underlying mechanism of inflammation in bronchopneumonia remains unclear. Therefore, this study focused on studying the effect of miR-216a-5p on inflammation induced by bronchopneumonia and investigate the potential mechanism underlying it.Methods: Human bronchial epithelial cells (BEAS-2B) were stimulated using lipopolysaccha-rides (LPS) to trigger bronchopneumonia in vitro. The production of interleukin (IL)-1β, IL-6, and Tumor necrosis factor (TNF)-α was measured using the enzyme-linked immunosorbent assay. The luciferase assay was conducted to explore the relationship between miR-216a-5p and TGFBR2. Quantitative real-time polymerase chain reaction and western blot were used to detect the gene expression.Results: miR-216a-5p gene expression decreased in BEAS-2B cells stimulated by LPS. Overexpression of miR-216a-5p suppressed the elevated levels of IL-1β, IL-6, and TNF-α induced by LPS. Transforming growth factor-beta receptor 2 (TGFBR2) proved to be a direct target of miR-216a-5p, and they negatively modulated TGFBR2 expression. In addition, overexpression of miR-216a-5p inhibited LPS-induced protein levels of TGFBR2,transforming growth factor (TGF)-β1, and phosphorylation of SMAD family member 2 (smad2),. This ectopic expression of miR-216a-5p was restored by overexpressed TGFBR2.Conclusion: miR-216a-5p was decreased in LPS-stimulated BEAS-2B cells. Overexpressed miR-216a-5p suppressed LPS-induced inflammation in BEAS-2B cells by inhibition of TGF-β1 signal-ing via down-regulating TGFBR2. miR-216a-5p may be a valuable target for anti-inflammation treatment in bronchopneumonia.

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“…TGFβ was not significantly correlated with any other soluble markers, although it was grouped with type 2 cytokines. Given the functional role of TGF-β in mucosal immunity and eosinophilic pneumonia, 24,25 a significant elevation of TGF-β in respiratory specimens from severe COVID-19 patients can be indicative of eosinophilic and type 2 mucosal immune responses.…”

Section: Resultsmentioning

confidence: 99%

Enhanced eosinophilic inflammation associated with antibody and complement-mediated pneumonic insults in severe COVID-19

Kim

Seo

Kim

et al. 2020

Preprint

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Despite the worldwide effect of the Coronavirus disease 2019 (COVID-19) pandemic, the underlying mechanisms of fatal viral pneumonia remain elusive. Here, we conducted kinetic profiling of respiratory leukocytes and associated inflammatory mediators to show that severe COVID-19 is associated with delayed but enhanced eosinophilic inflammation when compared to mild cases. In addition, we confirmed increased Th2-biased adaptive immune responses, accompanying overt complement activation, in the severe group. Moreover, enhanced antibody responses and complement activation was associated with disease pathogenesis as evidenced by formation of immune complexes and membrane attack complexes in airways and vasculature of lung biopsies from a fatal case, as well as by enhanced hallmark gene set signatures of FcgR signaling and complement activation in myeloid cells of respiratory specimens from severe COVID-19 patients. We also observed expression of viral antigen in lung epithelial and endothelial cells without producing viruses during late stage of COVID-19, indicating abortive viral infection which may further fuel antibody responses and aggravate immune-complex-mediated inflammation. These results suggest that SARS-CoV-2 infection may drive scripted specific innate immune responses, including eosinophilic inflammation, and subsequent pulmonary pathogenesis via enhanced Th2-biased immune responses, which might be crucial drivers of severe pneumonia in COVID-19 patients.

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Elevated levels of periostin and TGF-β1 in the bronchoalveolar lavage fluid of patients with idiopathic eosinophilic pneumonia

Cited by 7 publications

References 23 publications

Circulating Levels of IL-13, TGF-β1, and Periostin as Potential Biomarker for Coronary Artery Disease with Acute Heart Failure

Circulating Levels of IL-13, TGF-β1, and Periostin as Potential Biomarker for Coronary Artery Disease with Acute Heart Failure

MiR-216a-5p alleviates LPS-induced inflammation in the human bronchial epithelial cell by inhibition of TGF-β1 signaling via down-regulating TGFBR2

Enhanced eosinophilic inflammation associated with antibody and complement-mediated pneumonic insults in severe COVID-19

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