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• W2017723770 abstract "Idiopathic pulmonary fibrosis (IPF) is a chronic diffuse interstitial lung disease that is associated with the histologic appearance of usual interstitial pneumonitis (UIP).1American Thoracic Society Idiopathic pulmonary fibrosis: diagnosis and treatment. International Consensus Statement. American Thoracic Society and the European Respiratory Society.Am J Respir Crit Care Med. 2000; 161: 646-664Crossref PubMed Scopus (994) Google ScholarIPF, which is the most common idiopathic interstitial lung disease, has the worse prognosis, with a median survival of only 3 to 4 years.1American Thoracic Society Idiopathic pulmonary fibrosis: diagnosis and treatment. International Consensus Statement. American Thoracic Society and the European Respiratory Society.Am J Respir Crit Care Med. 2000; 161: 646-664Crossref PubMed Scopus (994) Google Scholar2Gross TJ Hunninghake GW Idiopathic pulmonary fibrosis.N Engl J Med. 2001; 345: 517-525Crossref PubMed Scopus (885) Google Scholar3Bjoraker JA Ryu JH Edwin MK et al.Prognostic significance of histopathologic subsets in idiopathic pulmonary fibrosis.Am J Respir Crit Care Med. 1998; 157: 199-203Crossref PubMed Scopus (982) Google ScholarThis grim prognosis rivals many cancers or disease due to HIV. IPF typically affects people between the age of 50 years and 70 years, and is noted worldwide without any clear ethnic predisposition. The estimated incidence of IPF in the United States is 7 to 11 cases per 100,000 each year.1American Thoracic Society Idiopathic pulmonary fibrosis: diagnosis and treatment. International Consensus Statement. American Thoracic Society and the European Respiratory Society.Am J Respir Crit Care Med. 2000; 161: 646-664Crossref PubMed Scopus (994) Google ScholarThe characteristic histologic features of IPF include the following: (1) injury and activation of alveolar epithelial cells in an inhomogeneous subpleural distribution, (2) the distinctive presence of fibroblastic foci, and (3) exuberant extracellular matrix deposition. Although much has been learned recently about the pathogenesis of IPF, the etiology and precise cellular and molecular mechanisms involved are not established. Notably, no specific therapy has been proven unequivocally effective in IPF.4Douglas WW Ryu JH Schroeder DR Idiopathic pulmonary fibrosis: impact of oxygen and colchicine, prednisone, or no therapy on survival.Am J Respir Crit Care Med. 2000; 161: 1172-1178Crossref PubMed Scopus (244) Google ScholarAccordingly, it is not surprising that there is considerable controversy regarding various aspects of this disease. Early theories on the pathogenesis of IPF focused on the role of chronic inflammation triggered by unknown stimuli that subsequently leads to lung injury and pulmonary fibrosis.5Keogh BA Crystal RG Alveolitis: the key to the interstitial lung disorders.Thorax. 1982; 37: 1-10Crossref PubMed Scopus (124) Google ScholarSupport for this hypothesis was suggested by the presence of interstitial and alveolar inflammatory cells as well as the expression of proinflammatory cytokines, especially interleukin (IL)-1β, transforming growth factor (TGF)-β, and tumor necrosis factor (TNF)-α, in the lungs of patients with IPF.6Keane MP Strieter RM The importance of balanced pro-inflammatory and anti-inflammatory mechanisms in diffuse lung disease.Respir Res. 2002; 3: 5-13Crossref PubMed Scopus (86) Google Scholar7Piguet PF Ribaux C Karpuz V et al.Expression and localization of tumor necrosis factor-α and its mRNA in idiopathic pulmonary fibrosis.Am J Pathol. 1993; 143: 651-655PubMed Google ScholarA key role for proinflammatory cytokines is suggested by detecting, blocking, or augmenting cytokine expression in various experimental models of pulmonary fibrosis.8Kolb M Margetts PJ Anthony DC et al.Transient expression of IL-1β induces acute lung injury and chronic repair leading to pulmonary fibrosis.J Clin Invest. 2001; 107: 1529-1536Crossref PubMed Scopus (613) Google Scholar9Sime PJ Xing Z Graham FL et al.Adenovector-mediated gene transfer of active transforming growth factor β1 induces prolonged severe fibrosis in rat lung.J Clin Invest. 1997; 100: 768-776Crossref PubMed Scopus (906) Google ScholarMore recently, an imbalance in the expression of T-helper type 1 (Th1) [including interferon (IFN)-γ and others] and T-helper type 2 (Th2) [including IL-4, IL-5, and others] cytokines have been implicated in having an important role in the pathogenesis of pulmonary fibrosis.6Keane MP Strieter RM The importance of balanced pro-inflammatory and anti-inflammatory mechanisms in diffuse lung disease.Respir Res. 2002; 3: 5-13Crossref PubMed Scopus (86) Google Scholar10Ziesche R Hofbauer E Wittmann K et al.A preliminary study of long-term treatment with interferon γ-1b and low-dose prednisolone in patients with idiopathic pulmonary fibrosis.N Engl J Med. 1999; 341: 1264-1269Crossref PubMed Scopus (585) Google ScholarThe Th1 and Th2 cytokines are expressed in a wide variety of cells besides lymphocytes. These data plus a limited number of treatment trials formed the scientific basis on which the American Thoracic Society recommended combined anti-inflammatory therapy (corticosteroids and either azathioprine or cyclophosphamide) in the management of IPF.1American Thoracic Society Idiopathic pulmonary fibrosis: diagnosis and treatment. International Consensus Statement. American Thoracic Society and the European Respiratory Society.Am J Respir Crit Care Med. 2000; 161: 646-664Crossref PubMed Scopus (994) Google Scholar Additional support for the inflammation hypothesis was suggested by the findings of a large prospective study11Flaherty KR Travis WD Colby TV et al.Histopathologic variability in usual and nonspecific interstitial pneumonias.Am J Respir Crit Care Med. 2001; 164: 1722-1727Crossref PubMed Scopus (573) Google Scholarexamining the histopathologic variability of surgical lung biopsies in 109 patients with idiopathic interstitial pneumonia. In 47% of the patients, UIP was the only finding in all the lobes that were sampled (concordant) [mean age, 63 years; fibrosis score (FS), 2.13]. Notably, UIP was intermixed with nonspecific interstitial pneumonitis (NSIP) in 26% (discordant) [mean age, 57 years; FS, 1.42], while NSIP alone was present in 27% (mean age, 55 years; FS, 0.8). The biopsy findings combined with the progressive age and fibrosis score going from NSIP to UIP/NSIP (discordant) to UIP (concordant) suggested to these investigators and others of an evolving disease process from NSIP to UIP with a pathogenic role for chronic inflammation.11Flaherty KR Travis WD Colby TV et al.Histopathologic variability in usual and nonspecific interstitial pneumonias.Am J Respir Crit Care Med. 2001; 164: 1722-1727Crossref PubMed Scopus (573) Google Scholar12Strieter RM Inflammatory mechanisms are not a minor component of the pathogenesis of idiopathic pulmonary fibrosis.Am J Respir Crit Care Med. 2002; 165: 1206-1207Crossref PubMed Scopus (68) Google ScholarSince NSIP has not been fully characterized and the cellular and fibrotic forms of NSIP may not necessarily be related,11Flaherty KR Travis WD Colby TV et al.Histopathologic variability in usual and nonspecific interstitial pneumonias.Am J Respir Crit Care Med. 2001; 164: 1722-1727Crossref PubMed Scopus (573) Google Scholar13Travis WD Matsui K Moss J et al.Idiopathic nonspecific interstitial pneumonia: prognostic significance of cellular and fibrosing patterns.Am J Surg Pathol. 2000; 24: 19-33Crossref PubMed Scopus (524) Google ScholarFlaherty and associates11Flaherty KR Travis WD Colby TV et al.Histopathologic variability in usual and nonspecific interstitial pneumonias.Am J Respir Crit Care Med. 2001; 164: 1722-1727Crossref PubMed Scopus (573) Google Scholarcautioned that additional prospective studies are required to assess the longitudinal changes in pulmonary physiology and high-resolution CT in these patients. Several groups2Gross TJ Hunninghake GW Idiopathic pulmonary fibrosis.N Engl J Med. 2001; 345: 517-525Crossref PubMed Scopus (885) Google Scholar14Selman M King TE Pardo A Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy.Ann Intern Med. 2001; 134: 136-151Crossref PubMed Scopus (1551) Google Scholar15Sheppard D Pulmonary fibrosis: a cellular overreaction or a failure of communication?.J Clin Invest. 2001; 107: 1501-1502Crossref PubMed Scopus (70) Google Scholar16Gauldie J Inflammatory mechanisms are a minor component of the pathogenesis of idiopathic pulmonary fibrosis.Am J Respir Crit Care Med. 2002; 165: 1205-1208Crossref PubMed Scopus (96) Google Scholarhave challenged the inflammation hypothesis; their rationale centers on four lines of evidence. First, inflammation is a not a major histopathologic feature in IPF; rather, the distinctive feature is the predominance of fibroblastic foci. Second, studies in animals have been able to dissociate the extent of pulmonary inflammation from fibrosis. Although no ideal animal model of IPF exists, bleomycin has been widely used to study the mechanisms underlying the formation of pulmonary fibrosis with the understanding of its limitation. It is now clear that bleomycin-induced inflammation can ensue in the absence of fibrosis in mice deficient in either the epithelial cell integrin αvβ6 (β6−/−), which activates latent TGF-β, or CD44, a transmembrane adhesion receptor that is involved in T-cell recruitment.17Munger JS Huang X Kawakatsu H et al.The integrin αvβ6 binds and activates latent TGFβ1: a mechanism for regulating pulmonary inflammation and fibrosis.Cell. 1999; 96: 319-328Abstract Full Text Full Text PDF PubMed Scopus (1657) Google Scholar18Teder P Vandivier RW Jiang D et al.Resolution of lung inflammation by CD44.Science. 2002; 296: 155-158Crossref PubMed Scopus (577) Google ScholarAlternatively, pulmonary fibrosis can occur in the absence of inflammation in areas of ongoing alveolar epithelial injury.8Kolb M Margetts PJ Anthony DC et al.Transient expression of IL-1β induces acute lung injury and chronic repair leading to pulmonary fibrosis.J Clin Invest. 2001; 107: 1529-1536Crossref PubMed Scopus (613) Google Scholar19Adamson IY Young L Bowden DH Relationship of alveolar epithelial injury and repair to the induction of pulmonary fibrosis.Am J Pathol. 1988; 130: 377-383PubMed Google ScholarThird, inflammatory markers are not associated with IPF outcome. The number of fibroblastic foci directly correlates with mortality as well as greater declines in the FVC and measures of gas transfer (diffusion capacity of the lung for carbon monoxide), whereas the level of interstitial inflammation is less predictive.20King Jr, TE Schwartz MI Brown K et al.Idiopathic pulmonary fibrosis: relationship between histopathologic features and mortality.Am J Respir Crit Care Med. 2001; 164: 1025-1032Crossref PubMed Scopus (539) Google Scholar21Nicholson AG Fulford LG Colby TV et al.The relationship between individual histologic features and disease progression in idiopathic pulmonary fibrosis.Am J Respir Crit Care Med. 2002; 166: 173-177Crossref PubMed Scopus (249) Google ScholarFinally, perhaps most troublesome for the inflammation hypothesis, is that anti-inflammatory therapy has never been definitively shown to alter the course of IPF. These observations have led opponents of the inflammation hypothesis to reason that IPF results from abnormal wound healing arising from altered signaling mechanisms derived from areas of activated epithelial and mesenchymal cells in a milieu of abnormal extracellular matrix.2Gross TJ Hunninghake GW Idiopathic pulmonary fibrosis.N Engl J Med. 2001; 345: 517-525Crossref PubMed Scopus (885) Google Scholar14Selman M King TE Pardo A Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy.Ann Intern Med. 2001; 134: 136-151Crossref PubMed Scopus (1551) Google Scholar15Sheppard D Pulmonary fibrosis: a cellular overreaction or a failure of communication?.J Clin Invest. 2001; 107: 1501-1502Crossref PubMed Scopus (70) Google Scholar16Gauldie J Inflammatory mechanisms are a minor component of the pathogenesis of idiopathic pulmonary fibrosis.Am J Respir Crit Care Med. 2002; 165: 1205-1208Crossref PubMed Scopus (96) Google Scholar In this issue of CHEST (see page 1206), Tajima and colleagues add another piece of the puzzle to the IPF inflammation hypothesis. These investigators show that serum soluble ST2 protein, which is preferentially expressed in Th2 cells, increases during an acute exacerbation of IPF. In this retrospective study involving 49 patients, serum ST2 levels in control patients and stable IPF patients were comparable; however, during an acute exacerbation of IPF, which was defined clinically after excluding infection and heart failure, the serum ST2 levels were increased sixfold. Furthermore, serum ST2 levels were directly correlated with other nonspecific serum markers of inflammation, such as C-reactive protein or lactate dehydrogenase levels, and inversely correlated with oxygenation and the percentage of predicted vital capacity. The authors speculate that the increased serum ST2 levels during an acute exacerbation of IPF reflects the severity of inflammation and Th2 activity in the lungs. To better understand the findings of Tajima and colleagues, one must understand the biology of ST2. The ST2 gene was originally identified as an oncogene and serum-responsive gene expressed in fibroblasts22Tominaga S A putative protein of a growth specific cDNA from BALB/c-3T3 cells is highly similar to the extracellular portion of mouse interleukin 1 receptor.FEBS Lett. 1989; 258: 301-304Abstract Full Text PDF PubMed Scopus (324) Google Scholarand subsequently found to be expressed by Th2, but not Th1, cells.23Xu D Chan WL Leung BP et al.Selective expression of a stable cell surface molecule on type 2 but not type 1 helper T cells.J Exp Med. 1998; 187: 787-794Crossref PubMed Scopus (451) Google ScholarIt encodes a membrane receptor of the IL-1 receptor family and a truncated soluble receptor that can be detected in the serum of patients with an exacerbation of asthma or heart failure.24Oshikawa K Kuroiwa K Tago K et al.Elevated soluble ST2 protein levels in sera of patients with asthma with an acute exacerbation.Am J Respir Crit Care Med. 2001; 164: 277-281Crossref PubMed Scopus (254) Google Scholar25Weinberg EO Shimpo M Hurwitz S et al.Identification of serum soluble ST2 receptor as a novel heart failure biomarker.Circulation. 2003; 107: 721-726Crossref PubMed Scopus (426) Google ScholarAlthough ST2 is an IL-1 receptor family member, it does not bind IL-1 and no ligand or function has yet been ascribed to either the soluble or membrane form of ST2. A role for ST2 in modulating Th2 function was suggested by studies26Coyle AJ Lloyd C Tian J et al.Critical role of the interleukin 1 receptor family member T1/ST2 in T helper cell type 2-mediated lung mucosal immune responses.J Exp Med. 1999; 190: 895-902Crossref PubMed Scopus (327) Google Scholar27Townsend MJ Fallon PG Matthews DJ et al.T1/ST2 deficient mice demonstrate the importance of T1/ST2 in developing primary T helper cell type 2 responses.J Exp Med. 2000; 191: 1069-1076Crossref PubMed Scopus (418) Google Scholarusing neutralizing antibodies against ST2 as well as in ST2-deficient mice. The messenger RNA encoding ST2 has also been found in a rapidly expanding list of cells including a variety human lung cells such as pulmonary epithelial cells.28Oshikawa K Yanagisawa K Tominaga S et al.ST2 protein induced by inflammatory stimuli can modulate acute lung inflammation.Biochem Biophys Res Comm. 2002; 299: 18-24Crossref PubMed Scopus (86) Google ScholarThere is accumulating evidence that ST2 has anti-inflammatory properties that function in part by inhibiting Toll-like receptor 4 expression which subsequently prevents inflammatory stimuli-induced IL-1β and TNF-α release.28Oshikawa K Yanagisawa K Tominaga S et al.ST2 protein induced by inflammatory stimuli can modulate acute lung inflammation.Biochem Biophys Res Comm. 2002; 299: 18-24Crossref PubMed Scopus (86) Google Scholar29Sweet MJ Leung BP Kang D et al.A novel pathway regulating lipopolysaccharide-induced shock by ST2/T1 via inhibition of Toll-like receptor 4 expression.J Immunol. 2001; 166: 6633-6639Crossref PubMed Scopus (225) Google Scholar Collectively, these data suggest that soluble ST2 protein can reduce the severity and pathology of acute inflammatory conditions that may occur in the setting of an acute exacerbation of IPF as well as other diverse conditions. Although the findings of Tajima et al may stimulate a renewed interest in the role of acute inflammation in IPF, caution is warranted. Further studies are necessary to better understand the biology of ST2 in the lungs. It will be important to determine the cellular origin of ST2 in the lungs, since fibroblasts, epithelial cells, endothelial cells, macrophages, as well as Th2 cells may all be involved. Also, the precise cellular and molecular mechanisms regulating ST2 gene expression, the identity of the ST2 receptor, as well as down-stream signaling mechanisms that lead to inhibition of the Toll-like receptor 4 expression must be identified. In the broader context, we need a better understanding of the mechanisms by which the principal proinflammatory and anti-inflammatory mediators in IPF alter epithelial barrier function and wound healing in the lung. These are important scientific goals for not only resolving the IPF inflammation controversy but for developing novel therapeutic targets for this challenging disease. The author is grateful for the helpful comments of Jacob I. Sznajder and Peter Sporn." @default.
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