Regular ArticleIL-12p40−/− Mice Treated with Intratracheal Bleomycin Exhibit Decreased Pulmonary Inflammation and Increased Fibrosis
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Treg depletion attenuates irradiation-induced pulmonary fibrosis by reducing fibrocyte accumulation, inducing Th17 response, and shifting IFN-γ, IL-12/IL-4, IL-5 balance
2015, ImmunobiologyCitation Excerpt :Besides direct effects, Tregs may affect fibrocytes by tipping the Th1/Th2 cytokine balance. Th1 cytokines such as IL-12 and IFN-γ inhibit fibrocyte differentiation (Herzog and Bucala 2010; Shao et al. 2008) and promote normal tissue repair by limiting fibroblast proliferation, differentiation and collagen synthesis (Sakamoto et al. 2002; Keane et al. 2001). Th2 cytokines like IL-4, on the other hand, promote fibrocyte differentiation (Sun et al. 2011) and regulate fibrotic tissue repair by augmenting fibroblast proliferation and collagen production (Westermann et al. 1999; Gharaee-Kermani et al. 2001; Lakos et al. 2006).
Transforming growth factor β3 attenuates the development of radiation-induced pulmonary fibrosis in mice by decreasing fibrocyte recruitment and regulating IFN-γ/IL-4 balance
2014, Immunology LettersCitation Excerpt :Among them, an inflammatory phenotype (Th1 or Th2) is regarded as a vital factor to mediate tissue repair and fibrosis. Recent research showed that Th1 cytokines such as IL-12 and IFN-γ inhibit fibrocyte differentiation [33,34] and promote normal tissue repair by limiting fibroblasts proliferation, differentiation and collagen synthesis [35,36], whereas Th2 cytokines like IL-4 and IL-10 promote fibrocyte differentiation [37] and regulate fibrotic tissue repair by augmenting fibroblasts proliferation and collagen production [38,39]. The imbalance in Th1/Th2 cytokine production was involved in the pathogenesis of pulmonary fibrosis [40].
Inhaled tacrolimus modulates pulmonary fibrosis without promoting inflammation in bleomycin-injured mice
2014, Journal of Drug Delivery Science and TechnologyPulmonary functional and morphological damage after exposure to tripoli dust
2014, Respiratory Physiology and NeurobiologyCitation Excerpt :Despite the important role of inflammation in fibrogenesis, some evidence suggests that inflammation is not necessarily related to the fibrotic response and that additional pathogenic pathways may be responsible for development of the fibrotic response in the lung. Some studies show that lung inflammation is not always followed by fibrotic disease (Adamson et al., 1992; Huaux et al., 1998; Munger et al., 1999), whereas other works reveal that control of inflammation is not always associated with reduced fibrosis (Tanino et al., 2002; Sakamoto et al., 2002). Chronic exposure to silica particles is histologically characterized by the presence of granulomas, alveolar septal thickening and accumulation of inflammatory cells such as macrophages (Delgado et al., 2006).
Distinct from its canonical effects, deletion of IL-12p40 induces cholangitis and fibrosis in interleukin-2Rα<sup>-/-</sup> mice
2014, Journal of AutoimmunityCitation Excerpt :We observed splenomegaly in p40−/−IL-2Rα−/− mice, and in PBC patients splenomegaly are found in the setting of portal hypertension [55]. IL-12p40 can promote silica-induced pulmonary fibrosis [39], but limit bleomycin-induced pulmonary fibrosis [56]. IL-12p40 can suppress liver fibrosis in mice following infection with S mansoni [57].
Cytokine-like factor 1 gene expression is enriched in idiopathic pulmonary fibrosis and drives the accumulation of CD4 <sup>+</sup> T cells in murine lungs: Evidence for an antifibrotic role in bleomycin injury
2012, American Journal of PathologyCitation Excerpt :How is this apparently antifibrotic effect of CLF-1 explained? Enhanced inflammation in the mouse lung is often associated with increased fibrosis,20,65–69 although in certain contexts increased inflammation may be associated with decreased fibrosis.48,70,71 We hypothesize that the increased representation of CD4+Tbet+ T cells in the CLF-1/CLC-treated mice enriches Th1 tone in the lung and leads to an antifibrotic microenvironment in the bleomycin-injured lung.72
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