Original articleRelevance of Tissue Factor and Tissue Factor Pathway Inhibitor for Hypercoagulable State in the Lungs of Patients with Idiopathic Pulmonary Fibrosis
Section snippets
Patients
A total of 22 patients with IPF were included in this study after giving their informed consent. All patients exhibited findings commonly seen in IPF, and usual interstitial pneumonia (UIP) findings were confirmed by either video-thoracoscopic or open-lung biopsy.
The clinical and laboratory findings of the patients are summarized in Table 1. Patients were divided into two groups according to the severity of pulmonary impairment: Patients with respiratory failure [PaO2 level less than 55 torr
TF and TFPI Antigen Levels in BAL Fluid Supernatant
Both TFPI and TF antigen levels were significantly higher in IPF patients than in controls. In addition, both TF and TFPI antigen levels were significantly higher in “advanced” patients than in “nonadvanced” patients (Table 2).
Regression analysis revealed a significant positive correlation between the TF and TFPI antigen levels in IPF patients (Figure 1).
PC Activity and TF Activity in BAL Fluid Supernatant
Both PC activity and TF activity were significantly higher in IPF patients than in normal controls (Table 2). However, there was no
Discussion
Our study showed that both TF and TFPI antigens were mainly positive in hyperplastic cuboidal alveolar epithelial cells in the lungs of IPF patients. The distribution of TF was quite consistent with previous observations by Imokawa et al. [4]. Regarding TFPI, the present study is the first report showing its localization in alveolar epithelial cells. Previous studies have indicated that TFPI is exclusively expressed in endothelial cells under physiologic conditions [10], and limited information
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2023, Respiratory Medicine and ResearchThe impaired proteases and anti-proteases balance in Idiopathic Pulmonary Fibrosis
2018, Matrix BiologyCitation Excerpt :Excessive or smouldering pro-coagulant activity in the alveolar space results from the disruption of the balance between the pro- and anti-coagulant factors, and this imbalance may occur as a result of an on-going stimulus to coagulation or a defect of the natural anti-coagulant or fibrinolytic system. Thus, TF pathway activity is increased in the alveolar compartment of IPF patients [97,98] and its inhibition using overexpression of the endogenous inhibitor ‘Tissue factor pathway inhibitor’ (TFPI) limited pulmonary fibrosis in the bleomycin model [99]. Thrombin is also detected within the lung and intra-alveolar spaces in diverse pulmonary fibrotic conditions [100] and its inhibition reduced lung inflammation and fibrosis in a bleomycin model of pulmonary fibrosis [101,102].
The fibrogenic actions of the coagulant and plasminogen activation systems in pulmonary fibrosis
2018, International Journal of Biochemistry and Cell BiologyCitation Excerpt :FXa combined with FV then activates thrombin, which in turn converts fibrinogen into fibrin. Increased levels of TF detected within the airspaces and on the outer surface of lung alveolar epithelial cells, macrophages and fibroblasts of IPF patients support a role of extravascular coagulation in pulmonary fibrosis (Fujii et al., 2000; Wygrecka et al., 2011). Furthermore, there is a net increase in the levels of other coagulant factors in both the serum and broncho-alveolar lavage fluid (BALF) of patients with IPF, particularly during acute exacerbations (Kotani et al., 1995; Collard et al., 2010; Bargagli et al., 2014).