Daintain/AIF-1 (Allograft Inflammatory Factor-1) accelerates type 1 diabetes in NOD mice

Zhao, Yanying; Huang, Xuhua; Chen, Zhengwang

doi:10.1016/j.bbrc.2012.09.087

Cited by 18 publications

(13 citation statements)

References 22 publications

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“…Then, the cells were maintained in DMEM containing 10% FBS and 10 µg/mL insulin for another 2 days, and replenished with DMEM containing 10% FBS until full differentiation into adipocytes. Thereafter, the medium was replaced with macrophage-conditioned medium or 0, 0.1, 1, 10 nmol/L AIF-1 [16] in DMEM supplemented with 10% FBS for 2 days. The cells were harvested by centrifuging at 500 g for 5 min and lysed.…”

Section: Methodsmentioning

confidence: 99%

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Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes

Ren¹,

Lin²,

Tang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Allograft inflammatory factor-1 (AIF-1) is an inflammatory cytokine produced mainly by macrophages within human white adipose tissue. Its expression is increased in obese subjects and positively correlated with insulin resistance. The purpose of this study is to characterize the regulatory role of AIF-1 in insulin signaling of adipocyte. Methods: AIF-1 was over-expressed via transfection of AIF-1 cDNA into murine RAW 264.7 macrophages, and the constitutive expression of AIF-1 was decreased via transfection of targeting siRNA. Murine 3T3L1 adipocytes were treated with macrophage-conditioned medium or AIF-1 protein. Intracellular lipid accumulation was assayed by oil red O stain. Reactive oxygen species production was determinated by a flow cytometer and adipokine secretion was measured with ELISA. Glucose uptake was detected using the glucose oxidase method and insulin-signal-transduction related molecules were analyzed by Western blot. Results: Short term (48 h) AIF-1 treatment slightly promoted intracellular lipid storage in differentiating 3T3L1 cells. The protein stimulated reactive oxygen species production, provoked TNFα, IL6, resistin, but suppressed adiponectin release and insulin-stimulated glucose uptake both under normal basal and insulin resistance conditions. Furthermore, AIF-1 induced NF-κB activation, inhibited PPARγ expression, GLUT4 translocation to plasma membrane and Akt phosphorylation. Conclusion: Macrophage-derived AIF-1 up-regulated reactive oxygen species production, adipokine TNFα, IL6, resistin release, and inhibited adiponectin secretion. Moreover, it suppressed insulin-stimulated glucose uptake by down-regulating insulin signaling. Thus, AIF-1 could be related to obesity-related diseases.

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Section: Methodsmentioning

confidence: 99%

“…AIF-1 has been recognized as a crucial molecular for the survival and pro-inflammatory activity of macrophages [13, 14]. Thus, it is involved in inflammation and immune responses associated with vasculopathy [15], autoimmune diseases [16], and central nervous system (CNS) injury [17] et al…”

Section: Introductionmentioning

confidence: 99%

Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes

Ren¹,

Lin²,

Tang³

et al. 2018

Cell Physiol Biochem

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“…The current study also demonstrated that inflammation and oxidative stress were enhanced using exogenous AIF-1 treatment in primary peritoneal mesothelial cells. In addition, it also played an important role in a vast array of inflammatory diseases, for example, autoimmune diseases (Zhao et al, 2012), vasculopathy (Sommerville et al, 2012), central nervous system (CNS) injury (Deininger et al, 2003) and human gliomas (Deininger et al, 2000). However, the effect of AIF-1 on NF-kB pathway and inflammation can be alleviated by the BAY 11-7082, a NF-kB signaling inhibitor.…”

Section: Discussionmentioning

confidence: 99%

“…AIF-1 was crucial for the survival and pro-inflammatory activity in macrophages (Watano et al, 2001;Kohler, 2007) and it increased the IL-6, IL-10, and IL-12 levels (Watano et al, 2001;Yamamoto and Kawahito, 2014). In addition, it also played an important role in a vast array of inflammatory diseases, for example, autoimmune diseases (Zhao et al, 2012), vasculopathy (Sommerville et al, 2012), central nervous system (CNS) injury (Deininger et al, 2003) and human gliomas (Deininger et al, 2000). Likewise, our study showed that exogenous AIF-1 protein supplementation stimulates inflammatory factors IL-6 and TNF-a secretion in primary peritoneal mesothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Role of allograft inflammatory factor‐1 in the regulation of inflammation and oxidative stress in primary peritoneal mesothelial cells

Zhou

Yuan

et al. 2019

Cell Biology International

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Peritoneal dialysis (PD) is often used to treat patients with end stage renal disease, and its long-term complications include excessive inflammation and oxidative stress. Allograft inflammatory factor 1 (AIF-1), as a cytoplasmic protein, is originally identified from infiltrating macrophages, and it was associated with inflammation in the cells other than macrophages, such as endothelial cells and vascular smooth muscle cells. To clarify the molecular mechanisms of AIF-1-modulated pathological changes in the peritoneum during PD, we first detected the AIF-1 expression in peritoneal tissues from PD mice. Results revealed that the pro-fibrotic stimulation caused AIF-1 upregulation and triggered inflammation in peritoneal tissues, and that AIF-1 co-expressed with pancytokeratin (a marker of peritoneal mesothelial cells). We next treated primary mouse peritoneal mesothelial cells (pan-cytokeratin and intercellular adhesion molecule 1 positive cells) with 50 or 100 ng/mL recombinant AIF-1, and evaluated the direct effects of AIF-1 on these cells in vitro. We found that exogenous AIF-1 treatment induced inflammation and oxidative stress in mesothelial cells. Apart from the augmented IL-6 and TNF-a secretion, the level of ROS was upregulated and the activity of anti-oxidative SOD was reduced in cells exposed to AIF-1. Moreover, AIF-1 simulation triggered the activation of NF-kB pathway-enhanced the conversion of IkB to phosphorylated IkB and promoted the translocation of NF-kB p65 from cytoplasm into nucleus. Additionally, AIF-1-evoked inflammation in peritoneal mesothelial cells was attenuated by the addition of NF-kB inhibitor . In brief, this study provides us novel information to understand the molecular regulation mechanisms of AIF-1 in peritoneal fibrosis.

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“…In ammatory processes, especially bacterial infection, increased AIF-1 expression [13]. Our previous study also revealed higher level of AIF-1 secreted into serum of mice suffering from insulitis than that in healthy mice and the antibody against AIF-1 prevented insulitis [14]. Furthermore, AIF-1 plays a central role in in ammation by in uencing multiple key events such as activation of immune cells and the production of cytokines, chemokines and in ammatory mediators.…”

Section: Introductionmentioning

confidence: 97%

Allograft inflammatory factor-1 (AIF-1) induces inflammatory mediator production via NF-κB signaling and impairs bovine mammary epithelial cells via mitochondrial pathway

Yang¹,

Wu²,

Zhao³

2020

Preprint

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Background Bovine mastitis is the inflammatory response of the mammary gland with an utmost threat to the dairy industry worldwide. Cytokine networks fuel inflammation. The sensitive and subtle changes of the inflammatory cytokine network in healthy and mastitic bovine mammary gland may encourage the use of cytokines in the diagnosis and prognosis of bovine mastitis. Allograft inflammatory factor-1 (AIF-1) is a proinflammatory cytokine mainly secreted by immune cells and it plays a central role in the complex signaling network of inflammation activation. Therefore, we explored the possible role of bovine AIF-1 related to bovine mastitis in the present study. Results The average concentration of AIF-1 in milks suffering from mastitis was 2.5 fold of that in the healthy cows, while its value decreased in cows recovered from mastitis. Furthermore, recombinant bovine AIF-1 up-regulated TNF-α, IL-6, and monocyte chemoattractant protein 1 secretion from bovine mammary epithelial cells with NF-κB activating, then NF-κB signaling inhibitor BAY 11-7085 abolished the increase of these inflammatory cytokines secretion induced by AIF-1. Thereafter, AIF-1 impaired bovine mammary epithelial cell viability, induced cell membrane permeability and cell apoptosis with exacerbated nitric oxide and oxidative stress, activated caspase 3, decreased mitochondrial membrane potential and intracellular ATP concentration. Conclusion These results indicated that AIF-1 prompted inflammation mediator production of bovine mammary epithelial cells via NF-κB signaling. Moreover, it damaged epithelial cells by depressing cell viability, inducing cell membrane permeability and cell apoptosis, which might be related to bovine mastitis.

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Daintain/AIF-1 (Allograft Inflammatory Factor-1) accelerates type 1 diabetes in NOD mice

Cited by 18 publications

References 22 publications

Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes

Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes

Role of allograft inflammatory factor‐1 in the regulation of inflammation and oxidative stress in primary peritoneal mesothelial cells

Allograft inflammatory factor-1 (AIF-1) induces inflammatory mediator production via NF-κB signaling and impairs bovine mammary epithelial cells via mitochondrial pathway

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