Overexpression of macrophage inducible C-type lectin Mincle aggravates proinflammatory responses to Streptococcus pneumoniae with fatal outcome in mice

Hollwedel, Femke; Maus, Regina; Stolper, Jennifer; Khan, Ayesha; Stocker, Bridget L.; Pich, Andreas; Welte, Tobias; Yamasaki, Satoshi; Maus, Ulrich A.

doi:10.1183/13993003.congress-2020.2324

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Macrophage inducible C‐type lectin (Mincle) is a pattern recognition receptor, which can recognize damage‐associated molecular patterns (DAMPs) and pathogen‐associated molecular patterns (PAMPS), and mainly expressed on membrane of monocyte, macrophage and dendritic cell 14 . At first, Mincle was considered to be an active receptor for a variety of pathogenic bacteria, 15 even it is currently believed to enhance the response to Streptococcus pneumoniae in mice and aggravate inflammation 16 . However, more and more studies have shown that Mincle is also involved in various other pathological and physiological activities, including promoting fibrosis, 17 tumour formation 18 and infection 19 .…”

Section: Introductionmentioning

confidence: 99%

“… 14 At first, Mincle was considered to be an active receptor for a variety of pathogenic bacteria, 15 even it is currently believed to enhance the response to Streptococcus pneumoniae in mice and aggravate inflammation. 16 However, more and more studies have shown that Mincle is also involved in various other pathological and physiological activities, including promoting fibrosis, 17 tumour formation 18 and infection. 19 A recent study demonstrated that Mincle is essential for maintaining the M1 phenotype of macrophage in kidney of AKI, and down‐regulation of Mincle in macrophage relieved the renal injury, suggesting that Mincle is a key promotor for macrophagic inflammation in AKI.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle‐mediated necroptosis and inflammation to tubular epithelial cell

Xin

Tan

Jia

et al. 2021

J Cellular Molecular Medi

View full text Add to dashboard Cite

Artesunate is a widely used derivative of artemisinin for malaria. Recent researches have shown that artesunate has a significant anti‐inflammatory effect on many diseases. However, its effect on acute kidney injury with a significant inflammatory response is not clear. In this study, we established a cisplatin‐induced AKI mouse model and a co‐culture system of BMDM and tubular epithelial cells (mTEC) to verify the renoprotective and anti‐inflammatory effects of artesunate on AKI, and explored the underlying mechanism. We found that artesunate strongly down‐regulated the serum creatinine and BUN levels in AKI mice, reduced the necroptosis of tubular cells and down‐regulated the expression of the tubular injury molecule Tim‐1. On the other hand, artesunate strongly inhibited the mRNA expression of inflammatory cytokines (IL‐1β, IL‐6 and TNF‐α), protein levels of inflammatory signals (iNOS and NF‐κB) and necroptosis signals (RIPK1, RIPK3 and MLKL) in kidney of AKI mouse. Notably, the co‐culture system proved that Mincle in macrophage can aggravate the inflammation and necroptosis of mTEC induced by LPS, and artesunate suppressed the expression of Mincle in macrophage of kidney in AKI mouse. Overexpression of Mincle in BMDM restored the damage and necroptosis inhibited by artesunate in mTEC, indicating Mincle in macrophage is the target of artesunate to protect tubule cells in AKI. Our findings demonstrated that artesunate can significantly improve renal function in AKI, which may be related to the inhibition of Mincle‐mediated macrophage inflammation, thereby reducing the damage and necroptosis to tubular cells that provide new option for the treatment of AKI.

show abstract