NF-κB signaling in inflammation

Abstract

The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition.

The mycotoxin alternariol suppresses lipopolysaccharide-induced inflammation in THP-1 derived macrophages targeting the NF-κB signalling pathway

“…Gene expression of cytokines is closely related to the activation of nuclear factor kappa B (NF-κB), a transcription factor involved in inflammatory processes (Newton and Dixit 2012). Various endo- and exogenous stimuli including reactive oxygen species (ROS), viral and bacterial antigens such as lipopolysaccharide (LPS) induce a downstream signalling cascade through stimulation of various receptors [e.g., toll-like receptors (TLRs)] leading to the activation of NF-κB (Liu et al 2017; Morgan and Liu 2011). Once activated, NF-κB is translocated into the nucleus, where it binds to the promotor region of its target genes and finally induces transcription of several inflammatory mediators (Liu et al 2017).…”

“…Various endo- and exogenous stimuli including reactive oxygen species (ROS), viral and bacterial antigens such as lipopolysaccharide (LPS) induce a downstream signalling cascade through stimulation of various receptors [e.g., toll-like receptors (TLRs)] leading to the activation of NF-κB (Liu et al 2017; Morgan and Liu 2011). Once activated, NF-κB is translocated into the nucleus, where it binds to the promotor region of its target genes and finally induces transcription of several inflammatory mediators (Liu et al 2017). Cytokines, such as IL-8, IL-6 and TNF-α are expressed in a NF-κB-dependent manner and function primarily as proinflammatory signals (Tak and Firestein 2001).…”

4‐O‐carboxymethylascochlorin protected against microglial‐mediated neurotoxicity in SH‐SY5Y and BV2 cocultured cells from LPS–induced neuroinflammation and death by inhibiting MAPK, NF‐κB, and Akt pathways

“…It was therefore of interest to test whether AS‐6 could inhibit the expression of transcription factors associated with processes of inflammation. Gene expression of COX‐2 and iNOS, which are well‐known as important proinflammatory proteins, is regulated by downstream signaling of NF‐κB . Therefore, we evaluated the effects of AS‐6 on attenuating LPS‐stimulated NF‐κB nuclear translocation in BV2 cells.…”

Altered cord serum 25‐hydroxyvitamin D signaling and placental inflammation is associated with pre‐term birth

“…29,32,33 Earlier reports from our laboratory showed an altered expression of S100A8 in endometrial decidual tissue samples of recurrent pregnancy loss cases. 35 No studies till date showed the functional relevance of S100A8 and HMGB1 at maternal-fetal in- To further confirm, whether altered inflammatory and vitamin D signaling in PTB affect the histological architecture of placenta, 35 No studies till date showed the functional relevance of S100A8 and HMGB1 at maternal-fetal in- To further confirm, whether altered inflammatory and vitamin D signaling in PTB affect the histological architecture of placenta,…”