scholarly journals Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Lisa T. C. Vogelpoel ◽  
Ivo S. Hansen ◽  
Theo Rispens ◽  
Femke J. M. Muller ◽  
Toni M. M. van Capel ◽  
...  
Keyword(s):  
Cross Talk ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
M2 Macrophages ◽  
Fc Gamma Receptor ◽  
Inflammatory Cytokine Production ◽  
Gamma Receptor

Dendritic cells sub-sets are associated with inflammatory cytokine production in progressive vitiligo disease

2021 ◽  
Author(s):  
Niharika Srivastava ◽  
Anuradha Bishnoi ◽  
Davinder Parsad ◽  
Muthu Sendhil Kumaran ◽  
Keshavamurthy Vinay ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

scholarly journals Prominent Indomethacin-Induced Enteropathy in Fcgriib Defi-cient lupus Mice: An Impact of Macrophage Responses and Immune Deposition in Gut

2021 ◽  
Vol 22 (3) ◽  
pp. 1377
Author(s):  
Thansita Bhunyakarnjanarat ◽  
Kanyarat Udompornpitak ◽  
Wilasinee Saisorn ◽  
Bhumdhanin Chantraprapawat ◽  
Peerapat Visitchanakun ◽  
...  
Keyword(s):  
Cytokine Production ◽  
High Dose ◽  
Flux Analysis ◽  
Wild Type ◽  
Fc Gamma Receptor ◽  
Serum Cytokines ◽  
Extracellular Flux ◽  
Gamma Receptor ◽  
Gut Leakage ◽  
Gastrointestinal Permeability

A high dose of NSAIDs, a common analgesic, might induce lupus activity through several NSAIDs adverse effects including gastrointestinal permeability defect (gut leakage) and endotoxemia. Indomethacin (25 mg/day) was orally administered for 7 days in 24-wk-old Fc gamma receptor IIb deficient (FcgRIIb-/-) mice, an asymptomatic lupus model (increased anti-dsDNA without lupus nephritis), and age-matched wild-type (WT) mice. Severity of indomethacin-induced enteropathy in FcgRIIb-/- mice was higher than WT mice as demonstrated by survival analysis, intestinal injury (histology, immune-deposition, and intestinal cytokines), gut leakage (FITC-dextran assay and endotoxemia), serum cytokines, and lupus characteristics (anti-dsDNA, renal injury, and proteinuria). Prominent responses of FcgRIIb-/- macrophages toward lipopolysaccharide (LPS) compared to WT cells due to the expression of only activating-FcgRs without inhibitory-FcgRIIb were demonstrated. Extracellular flux analysis indicated the greater mitochondria activity (increased respiratory capacity and respiratory reserve) in FcgRIIb-/- macrophages with a concordant decrease in glycolysis activity when compared to WT cells. In conclusion, gut leakage-induced endotoxemia is more severe in indomethacin-administered FcgRIIb-/- mice than WT, possibly due to the enhanced indomethacin toxicity from lupus-induced intestinal immune-deposition. Due to a lack of inhibitory-FcgRIIb expression, mitochondrial function, and cytokine production of FcgRIIb-/- macrophages were more prominent than WT cells. Hence, lupus disease-activation from NSAIDs-enteropathy-induced gut leakage is possible.

Long non-coding RNA SNHG14 aggravates LPS-induced acute kidney injury through regulating miR-495-3p/HIPK1

2021 ◽  
Author(s):  
Ni Yang ◽  
Hai Wang ◽  
Li Zhang ◽  
Junhua Lv ◽  
Zequn Niu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Kidney Injury ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Kidney Injury ◽  
Interaction Network ◽  
High Morbidity ◽  
Abrupt Decrease ◽  
Inflammatory Cytokine Production ◽  
Non Coding Rna

Abstract Acute kidney injury (AKI) is a complex syndrome with an abrupt decrease of kidney function, which is associated with high morbidity and mortality. Sepsis is the common cause of AKI. Mounting evidence has demonstrated that long non-coding RNAs (lncRNAs) play critical roles in the development and progression of sepsis-induced AKI. In this study, we aimed to illustrate the function and mechanism of lncRNA SNHG14 in lipopolysaccharide (LPS)-induced AKI. We found that SNHG14 was highly expressed in the plasma of sepsis patients with AKI. SNHG14 inhibited cell proliferation and autophagy and promoted cell apoptosis and inflammatory cytokine production in LPS-stimulated HK-2 cells. Functionally, SNHG14 acted as a competing endogenous RNA (ceRNA) to negatively regulate miR-495-3p expression in HK-2 cells. Furthermore, we identified that HIPK1 is a direct target of miR-495-3p in HK-2 cells. We also revealed that the SNHG14/miR-495-3p/HIPK1 interaction network regulated HK-2 cell proliferation, apoptosis, autophagy, and inflammatory cytokine production upon LPS stimulation. In addition, we demonstrated that the SNHG14/miR-495-3p/HIPK1 interaction network regulated the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) via modulating NF-κB/p65 signaling in LPS-challenged HK-2 cells. In conclusion, our findings suggested a novel therapeutic axis of SNHG14/miR-495-3p/HIPK1 to treat sepsis-induced AKI.

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