The earlier, the better: Impact of early diagnosis on clinical outcome in idiopathic pulmonary fibrosis

Aiello, Marina; Bertorelli, Giuseppina; Bocchino, Marialuisa; Chetta, Alfredo; Fiore-Donati, Alfeo; Fois, Alessandro Giuseppe; Marinari, Stefano; Oggionni, Tiberio; Polla, Biagio; Rosi, Elisabetta; Stanziola, Anna Agnese; Varone, Francesco; Sanduzzi, Alessandro

doi:10.1016/j.pupt.2017.02.005

Cited by 31 publications

(26 citation statements)

References 55 publications

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“…Given the irreversibility of pulmonary fibrosis, it appears logical that identifying and treating horses earlier in the disease course to prevent further fibrosis would be more likely to produce a favorable outcome. A similar correlation has been noted in human cases of IPF with improved response to treatment generally noted in younger patients with less marked disease . The combination of strains or genotypes of EHV‐5 present in a horse with EMPF might have clinical importance; however, further work is necessary to determine whether strain variability is an important component of pathogenicity .…”

Section: Discussionsupporting

confidence: 63%

Effect of valacyclovir on EHV‐5 viral kinetics in horses with equine multinodular pulmonary fibrosis

Easton-Jones

Madigan

Barnum

et al. 2018

Veterinary Internal Medicne

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BackgroundEquine herpesvirus‐5 is commonly isolated from the lungs of horses with EMPF, suggesting an etiological link. Valacyclovir is used empirically to treat EMPF; however, no data is available concerning its impact on EHV‐5 viral kinetics.ObjectivesTo determine the effect of oral administration of valacyclovir on EHV‐5 viral load measured by qPCR in blood, nasal secretions (NS) and BALF in horses with EMPF.AnimalsSix horses diagnosed with EMPF.MethodsA prospective clinical trial was performed. Horses received 10 days of PO administered valacyclovir (loading dose 30 mg/kg, maintenance dose 20 mg/kg). Blood, NS, and BALF were collected for EHV‐5 viral kinetics analyses during treatment. Blood and NS were collected every other day. BALF was collected on day 0 and day 10.ResultsThere was no statistical difference in median EHV‐5 viral load between day 0 and day 10 for all samples tested. In blood median EHV‐5 viral load was 7676 (range 575‐39 781) on day 0 and 6822 (range 1136‐18 635) glycoprotein B (gB) gene copies per million cells on day 10. For NS median EHV‐5 viral load was 2.944 × 106 (range 184 691‐3.394 × 109) on day 0 and 8.803 × 106 (range 251 186‐9.868 × 108) gB gene copies per million cells on day 10. For BALF median EHV‐5 viral load was 59,842 (range 61‐315 655) on day 0 and 185 083 (range 3562‐542 417) gB gene copies per million cells on day 10.Conclusions and Clinical ImportanceValacyclovir might not be an effective short‐term antiviral treatment but efficacy in treatment of EMPF is unknown.

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Section: Discussionsupporting

confidence: 63%

Effect of valacyclovir on EHV‐5 viral kinetics in horses with equine multinodular pulmonary fibrosis

Easton-Jones

Madigan

Barnum

et al. 2018

Veterinary Internal Medicne

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“…Idiopathic pulmonary fibrosis (IPF) is a progressive lung-scarring disorder with difficult early diagnosis ( 1 ) and diagnosing IPF requires multidisciplinary clinical approaches ( 2 ). Serological evaluation for pulmonary fibrosis is recommended but the signs are so far not specific enough ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

S100A4+ Macrophages Are Necessary for Pulmonary Fibrosis by Activating Lung Fibroblasts

Bao

Bian

et al. 2018

Front. Immunol.

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S100A4, a calcium-binding protein, can promote pulmonary fibrosis via fibroblast activation. Due partly to its various cellular origins, the exact role of S100A4 in the development of lung fibrosis remains elusive. Here, we show that in the bronchoalveolar lavage fluid, numbers of S100A4+ macrophages correlated well with S100A4 protein levels and occurrence of idiopathic pulmonary fibrosis (IPF) in patients. A mouse model of bleomycin-induced pulmonary fibrosis demonstrated S100A4+ macrophages as main source for extracellular S100A4 in the inflammatory phase. In vitro studies revealed that extracellular S100A4 could activate both mouse and human lung fibroblasts by upregulation of α-SMA and type I collagen, during which sphingosine-1-phosphate (S1P) increased. Inhibiting the S1P receptor subtypes S1P1/S1P3 abrogated fibroblast activation. Accordingly, absence or neutralization of S100A4 significantly attenuated bleomycin-induced lung fibrosis in vivo. Importantly, adoptive transfer of S100A4+ but not of S100A4− macrophages installed experimental lung injury in S100A4−/− mice that were otherwise not sensitive to fibrosis induction. Taken together, S100A4 released by macrophages promotes pulmonary fibrosis through activation of lung fibroblasts which is associated with S1P. This suggests that extracellular S100A4 or S100A4+ macrophages within the lung as promising targets for early clinical diagnosis or therapy of IPF.

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“…PF is a severe inflammatory interstitial lung disease with poor prognosis, high mortality, and increasing incidence and prevalence [16]. However, the treatments of PF still remain not promising.…”

Section: Discussionmentioning

confidence: 99%

Buyang Huanwu Tang inhibits cellular epithelial-to-mesenchymal transition by inhibiting TGF-β1 activation of PI3K/Akt signaling pathway in pulmonary fibrosis model in vitro

Yin

Wei

Wang

et al. 2020

BMC Complement Med Ther

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Background: Pulmonary fibrosis (PF) is a chronic and progressive interstitial lung disease. Buyang Huanwu Tang (BYHWT), a classical traditional Chinese medicine formula, has been widely utilized for the treatment of PF in China. This present study aimed to explore the mechanism of BYHWT in the treatment of PF in vitro. Methods: TGF-β1 stimulated human alveolar epithelial A549 cells were used as in vitro model for PF. Post the treatment of BYHWT, cell viability was measured by MTT assay, and cell morphology was observed under microscope. The epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, Vimentin) and collagen I (Col I) were detected by western blot, immunofluorescence staining and real-time quantitative polymerase chain reaction. With the co-administration of activators (IGF-1, SC79) and inhibitors (LY294002, MK2206), the effect of BYHWT on PI3K/Akt pathway was analyzed by western blot. Results: BYHWT inhibited cell growth, and prevented cell morphology changed from epithelial to fibroblasts in TGF-β1 induced A549 cells. BYHWT decreased Vimentin and Col I, while increased E-cadherin at both protein and mRNA levels. Moreover, phosphorylation of PI3K (p-PI3K) and phosphorylation of Akt (p-Akt) were significantly down-regulated by BYHWT in TGF-β1 stimulated A549 cells. Conclusion:These results indicate that BYHWT suppressed TGF-β1-induced collagen accumulation and EMT of A549 cells by inhibiting the PI3K/Akt signaling pathway. These findings suggest that BYHWT may have potential for the treatment of PF.

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The earlier, the better: Impact of early diagnosis on clinical outcome in idiopathic pulmonary fibrosis

Cited by 31 publications

References 55 publications

Effect of valacyclovir on EHV‐5 viral kinetics in horses with equine multinodular pulmonary fibrosis

Effect of valacyclovir on EHV‐5 viral kinetics in horses with equine multinodular pulmonary fibrosis

S100A4+ Macrophages Are Necessary for Pulmonary Fibrosis by Activating Lung Fibroblasts

Buyang Huanwu Tang inhibits cellular epithelial-to-mesenchymal transition by inhibiting TGF-β1 activation of PI3K/Akt signaling pathway in pulmonary fibrosis model in vitro

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