IL-33 regulates M1/M2 chemokine expression via mitochondrial redox-related mitophagy in human monocytes

Lin, Yi; Lin, Yu-Chih; Tsai, Mei-Lan; Tsai, Yu-Chen; Kuo, Chao-Hung; Hung, Chih‐Hsing

doi:10.1016/j.cbi.2022.109915

Cited by 20 publications

(13 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Currently, we found that MLT ameliorated neurological de cits via IL-33-mediated inhibition of cerebral edema and ferroptosis. IL-33 is a potent anti-in ammatory and antioxidant cytokine that not only increases the expression of IL-13 and IL-10 24 but also inhibits the expression of TNF-α and IL-6 34 . IL-13 and IL-10 are derived from M2 phenotype macrophages and protect the blood-brain barrier from damage, thereby reducing cerebral edema and neurological dysfunction 15,16 .…”

Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates neurological deficits through MT2/IL-33/ferritin H signaling-mediated inhibition of neuroinflammation and ferroptosis after traumatic brain injury

Gao¹,

Wang²,

Cheng³

et al. 2023

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates neurological deficits through MT2/IL-33/ferritin H signaling-mediated inhibition of neuroinflammation and ferroptosis after traumatic brain injury

Gao¹,

Wang²,

Cheng³

et al. 2023

Free Radical Biology and Medicine

View full text Add to dashboard Cite

“…On the other hand, previous literature showed that IL-33 induced an increase in p-AMPK expression in group 2 innate lymphoid cells (ILC2) in a short period of time, but the negative feedback would decrease p-AMPK expression due to the prolonged induction of IL-33 [ 60 ]. In addition, IL-33 induced p-AMPK expression in monocytes to promote mitophagy [ 61 ]. However, in our experiment, the intervention of IL-33 did not significantly change the expression of p-AMPK.…”

Section: Discussionmentioning

confidence: 99%

Quercetin Ameliorates Renal Injury and Pyroptosis in Lupus Nephritis through Inhibiting IL-33/ST2 Pathway In Vitro and In Vivo

et al. 2022

View full text Add to dashboard Cite

Lupus nephritis (LN) is a common and serious symptom in patients with systemic lupus erythematosus (SLE). Tubular interstitial fibrosis is a common underlying mechanism in the development of lupus nephritis to end-stage renal failure (ESRD). Quercetin is widely proven to prevent tissue fibrosis. Therefore, the purpose of this study is to investigate the beneficial effects of quercetin on the inhibition of fibrosis and inflammation pathways in in vitro and in vivo lupus nephritis models. In the current study, MRL/lpr mice as animal models, and HK-2 human renal tubular epithelial cells were stimulated by interleukin-33 (IL-33) to mimic the cellular model of lupus nephritis. Immunohistochemical staining, immunoblotting assay, immunofluorescence staining, and quantitative real-time polymerase chain reaction assay were used. The in vivo results showed that quercetin improved the renal function and inhibited both fibrosis- and inflammation-related markers in MRL/lpr mice animal models. The in vitro results indicated that quercetin ameliorated the accumulation of fibrosis- and inflammation-related proteins in IL-33-induced HK-2 cells and improved renal cell pyroptosis via the IL33/ST2 pathway. Overall, quercetin can improve LN-related renal fibrosis and inflammation, which may offer an effective potential therapeutic strategy for lupus nephritis.

show abstract

“…To date, some research on airway inf lammation, M1/M2 macrophage polarization and secretion of TNF-α have been reported in asthmatic and COPD animal models and in vitro (37)(38)(39). Some in vitro M1/M2 research is also performed in human primary monocyte-derived macrophages (40) and RAW264.7 cells (35,41).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from in vitro and in silico studies

et al. 2022

View full text Add to dashboard Cite

Budesonide (Bud), one of the most widely used lung medicines, is currently used as a repurposing medicine for immunoglobulin A nephropathy (IgAN) treatment. The progression of IgAN is related to inflammation involving macrophages and podocytes. The present study aimed to explore the effects of Bud on classically activated (M1)/alternatively activated (M2) macrophage polarization and podocyte injury under lipopolysaccharide (LPS)-induced inflammatory stress in vitro. Anti-inflammatory bioinformation of Bud was identified based on the Gene Expression Omnibus database. RAW264.7 cells were treated with normal medium, LPS, curcumin (Cur, positive control), or Bud 5, 10, or 20 µM. The expression levels of inducible nitric oxide synthase (iNOS), TNF-α, mannose receptor (CD206) and arginase (Arg)-1 were quantified by western blotting. The collected supernatants from macrophages were termed (Nor)MS, (LPS)MS, (Cur)MS and (Bud)MS. The TNF-α, IL-1β and nitric oxide (NO) levels in the supernatants were evaluated by ELISA and Griess assay. The podocytes were cultured in different supernatants and their survival rates were assessed by bromodeoxyuridine assay. TNF signaling is an important pathway by which Bud exerts anti-inflammatory activities. Compared with the LPS group, 5, 10 and 20 µM Bud significantly increased Arg-1 and decreased iNOS expression (Six: P<0.05) and 20 µM Bud significantly increased Arg-1 and CD206 and decreased iNOS and TNF-α expression (Four: P<0.05). Cur significantly decreased iNOS and TNF-α expression (Two: P<0.05). Compared with LPS, 5, 10 and 20 µM Bud and Cur significantly decreased TNF-α, IL-1β and NO levels (All: P<0.05). The podocyte survival rates of (Bud)MS and (Cur)MS were significantly higher than those of (LPS)MS (Four: P<0.05). The protective effect of Bud on podocyte injury is related to its modulation of M1/M2 polarization.

show abstract

IL-33 regulates M1/M2 chemokine expression via mitochondrial redox-related mitophagy in human monocytes

Cited by 20 publications

References 56 publications

Melatonin ameliorates neurological deficits through MT2/IL-33/ferritin H signaling-mediated inhibition of neuroinflammation and ferroptosis after traumatic brain injury

Melatonin ameliorates neurological deficits through MT2/IL-33/ferritin H signaling-mediated inhibition of neuroinflammation and ferroptosis after traumatic brain injury

Quercetin Ameliorates Renal Injury and Pyroptosis in Lupus Nephritis through Inhibiting IL-33/ST2 Pathway In Vitro and In Vivo

Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from in vitro and in silico studies

Contact Info

Product

Resources

About