Viruses and idiopathic pulmonary fibrosis

European Respiratory Journal (Impact Factor: 7.64). 08/1997; 10(7):1433-7. DOI: 10.1183/09031936.97.10071433
Source: PubMed
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    • "PF results as a consequence of many types of severe lung injury and is almost always associated with an inflammatory reaction [12,13]. Some virus infections, such as severe acute respiratory syndrome (SARS) caused by a novel coronavirus, can induce the typical ARDS and PF, and most patients eventually die [14,15]. Also, it is possible that patients infected with H5N1 viruses may suffer from PF as a result of ARDS. "
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    ABSTRACT: Inflammatory process results in lung injury that may lead to pulmonary fibrosis (PF). Here, we described PF in mice infected with H5N1 virus. Eight-week-old BALB/c mice were inoculated intranasally with 1 x 101 MID50 of A/Chicken/Hebei/108/2002(H5N1) viruses. Lung injury/fibrosis was evaluated by observation of hydroxyproline concentrations, lung indexes, and histopathology on days 7, 14, and 30 postinoculation. H5N1-inoculated mice presented two stages of pulmonary disease over a 30-d period after infection. At acute stage, infected-mice showed typical diffuse pneumonia with inflammatory cellular infiltration, alveolar and interstitial edema and hemorrhage on day 7 postinoculation. At restoration stage, most infected-mice developed PF of different severities on day 30 postinoculation, and 18% of the survived mice underwent severe interstitial and intra-alveolar fibrosis with thickened alveolar walls, collapsed alveoli and large fibrotic areas. The dramatically elevated hydroxyproline levels in H5N1-infected mice showed deposition of collagen in lungs, and confirmed fibrosis of lungs. The dry lung-to-body weight ratio was significantly increased in infected group, which might be associated with the formation of PF in H5N1-infected mice. Our findings show that H5N1-infected mice develop the typical PF during restoration period, which will contribute to the investigation of fibrogenesis and potential therapeutic intervention in human H5N1 disease.
    Respiratory research 11/2009; 10(1):107. DOI:10.1186/1465-9921-10-107 · 3.09 Impact Factor
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    • "Potential aetiological risk factors for CFA include cigarette smoking, and exposure to metal and wood dust [5,6,7]. Infectious agents, in particular Epstein–Barr virus, have been implicated in case referent data that demonstrated increased antibody titres to Epstein–Barr virus in CFA as compared with pulmonary fibrosis of known causes [8], although recent gene amplification studies [9,10] have been equivocal. There is some evidence for hereditary factors in descriptions of familial cases of CFA, although these are infrequent, and there has been no clear demonstration of an association with the major histocompatibility complex loci or other candidate genes. "
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    ABSTRACT: The pathogenesis of cryptogenic fibrosing alveolitis (CFA) involves injury, an immune/inflammatory response and fibrosis. The cause of the injury is unknown, but the identification of serum autoantibodies makes an autoimmune aetiology attractive. The core study on which this commentary is based used novel cloning and serum screening technologies in order to identify new public and private autoantibodies in sera from 12 patients with CFA. Largely negative conclusions were drawn from that study. However, we suggest that the prevalence of autoantibodies may have been underestimated, that the study was timely and that this approach is worth pursuing further.
    Respiratory Research 02/2001; 2(2):61-3. DOI:10.1186/rr38 · 3.09 Impact Factor
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