Th1/Th2 cytokine gene polymorphisms in patients with idiopathic pulmonary fibrosis

Vašáková, Martina; Striz, Ilja; Slavčev, Antonij; Jandova, Sarka; Kolesár, Libor; Šulc, Jan

doi:10.1111/j.1399-0039.2006.00560.x

Cited by 41 publications

(54 citation statements)

References 23 publications

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“…In rats, the response to injury is characterized by Th2 response following which these rats are susceptible to pulmonary fibrosis (Kunkel et al, 1996). Adults with activation of IL-4 gene are susceptible to pulmonary fibrosis (Vasakova et al, 2006). In the present study, the IL-4 level in the GC group, TR groups and BLM group was increased and IFNdecreased accompanied by decrease of IL-4/IFN-, which suggests that rats with pulmonary fibrosis were characterized by Th2 response in immune function.…”

Section: Discussionsupporting

confidence: 53%

Effect of tranilast on bleomycin induced pulmonary fibrosis in a rat model

Tang¹,

Jiang²,

Han³

et al. 2011

Afr. J. Pharm. Pharmacol.

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This study aimed to investigate the effect and mechanism of tranilast (TR) on bleomycin (BLM) induced pulmonary fibrosis in a rat model, pulmonary fibrosis was induced in rats by using intratracheal bleomycin and the serum and lungs were collected 28 days later. The serum levels of IL-4 and IFNwere determined by ELISA and IL-4/IFN-was calculated. Reverse transcription polymerase chain reaction (RT-PCR) was employed to measure the mRNA expression of TGF-1. Immunohistochemistry was employed to detect the protein expression of TGF-1 followed by evaluation of alveolitis and fibrosis. When compared with BLM group and glucocorticoid (GC) group, the INF-level was markedly increased and IL-4 level dramatically decreased in the TR group with a significant decrease of IL-4/INFratio. The mean optical density and mRNA expression of TGF-1 were markedly decreased accompanied by low scores of alveolitis and fibrosis. Significant differences were observed between TR groups (medium and high dose) and BLM group as well as control group (P < 0.05) in the aforementioned parameters. Moreover, marked difference was also observed among TR groups (P < 0.05) in the aforementioned parameters. Both TR and GC can affect the Th1/Th2 lymphocyte balance and inhibit the TGF-1 expression improving the BLM induced pulmonary fibrosis.

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Section: Discussionsupporting

confidence: 53%

Effect of tranilast on bleomycin induced pulmonary fibrosis in a rat model

Tang¹,

Jiang²,

Han³

et al. 2011

Afr. J. Pharm. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…The critical role of IL-13 was confirmed in IL-13-blocking studies (5,6). Chronic bouts of Th2-associated inflammation in idiopathic pulmonary fibrosis (12), ulcerative colitis (13), or helminth infection (14,15) are also associated with IL-13-mediated pathologies. Given that IL-13 is the foremost Th2 cytokine mediating Th2-dependent disease, it is important to understand how IL-13 effector function is regulated in distinct tissues and in acute and chronic Th2-driven disorders.…”

Section: Introductionmentioning

confidence: 74%

IL-13Rα2 and IL-10 coordinately suppress airway inflammation, airway-hyperreactivity, and fibrosis in mice

Wilson¹,

Elnekave²,

et al. 2007

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Development of persistent Th2 responses in asthma and chronic helminth infections are a major health concern. IL-10 has been identified as a critical regulator of Th2 immunity, but mechanisms for controlling Th2 effector function remain unclear. IL-10 also has paradoxical effects on Th2-associated pathology, with IL-10 deficiency resulting in increased Th2-driven inflammation but also reduced airway hyperreactivity (AHR), mucus hypersecretion, and fibrosis. We demonstrate that increased IL-13 receptor α 2 (IL-13Rα2) expression is responsible for the reduced AHR, mucus production, and fibrosis in BALB/c IL-10 -/-mice. Using models of allergic asthma and chronic helminth infection, we demonstrate that IL-10 and IL-13Rα2 coordinately suppress Th2-mediated inflammation and pathology, respectively. Although IL-10 was identified as the dominant antiinflammatory mediator, studies with double IL-10/IL-13Rα2-deficient mice illustrate an indispensable role for IL-13Rα2 in the suppression of AHR, mucus production, and fibrosis. Thus, IL-10 and IL-13Rα2 are both required to control chronic Th2-driven pathological responses.

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“…Polymorphisms of genes encoding for cytokines (interleukin [IL]-1 a, tumor necrosis factor-a, lymphotoxin a, IL-4, IL-6, IL-8, IL-10, and IL-12 [79][80][81][82][83][84][85][86][87][88]), enzymes (a 1 -antitrypsin [89,90] and angiotensinconverting enzyme [91]), profibrotic molecules (transforming growth factor-b1 [92]), coagulation pathway genes (plasminogen activator inhibitors-1 and -2), genes for surfactant protein-A and -B (70), immunomodulatory genes (complement receptor 1, NOD2/CARD15 [93]), and matrix metalloproteinase (MMP)-1 (94) have been reported to have increased frequencies in patients with sporadic IPF. Many of these have also been related to disease progression.…”

Section: Genetic Factorsmentioning

confidence: 99%