Profibrotic Effect of Interleukin-18 in HK-2 Cells Is Dependent on Stimulation of the Toll-like Receptor 4 (TLR4) Promoter and Increased TLR4 Expression

Abstract

Background: IL-18 induces profibrotic changes in TECs independent of TGF-␤1 activity. Results: IL-18 stimulates the TLR4 promoter via AP-1 activation to increase TLR4 expression in TECs and stimulates profibrotic changes in TECs through increased TLR4 expression/signaling. Conclusion: The profibrotic effect of IL-18 in TECs is mediated through stimulation of TLR4 expression via activation of AP-1. Significance: This represents a novel fibrotic signaling pathway in TECs independent of TGF-␤1.

Induction of a type I interferon signature in normal human monocytes by gadolinium-based contrast agents: comparison of linear and macrocyclic agents

“…7. These results are of relevance to other fibrotic disorders, such as systemic sclerosis (SSc), in which activation of a type I IFN pathway has been reported [35][36][37][38][39][40][41].…”

Toll-like receptor 7 involves the injury in acute kidney ischemia/reperfusion of STZ-induced diabetic rats

“…In the present time, the research of TLR7 has been at least partly successful in terms of liver, lungs, coronary artery and related disorder [9][10][11] . In hepatitis viruses, TLR7 stimulation mediates an endogenous type I interferon response, that may lead to development of protective immunity and eradication of hepatitis B.…”

“…In hepatitis viruses, TLR7 stimulation mediates an endogenous type I interferon response, that may lead to development of protective immunity and eradication of hepatitis B. However, TLR7 agonists result in the generation of proinflammatory cytokines, such as IL-2, IL-8, and TNF along with interferon α/β, which may result in development of undesirable adverse events 11 . TLR7 was overexpressed in lung cancer patients and have been implicated in contributing to inflammation, tumor growth, cell survival, and metastasis 12,13 .…”

Prokaryotic Expression and Anti-IBDV Activity of Chicken Interleukin-18 and Interferon-γ

“…IL-18 is also required for the activation of NK cells in response to infections with vaccinia virus and murine cytomegalovirus and plays a critical role in antiviral defense [Su et al, 2011]. IL-18 may also play an important role in the initiation of innate immune responses [Thompson et al, 2009;Zhang et al, 2011;Brandstadter et al, 2014] by mediating the severity of infections and inflammatory diseases [Meldrum et al, 2012].…”