scholarly journals Tumor Necrosis Factor-α-Induced Protein 8-Like 2 Negatively Regulates Innate Immunity Against RNA Virus by Targeting RIG-I in Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Ziqi Zou ◽  
Mengyao Li ◽  
Yunlian Zhou ◽  
Jiaying Li ◽  
Ting Pan ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Retinoic Acid ◽  
Viral Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Rna Virus ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor ◽  
Inducible Gene

A systematic and flexible immunoregulatory network is required to ensure the proper outcome of antiviral immune signaling and maintain homeostasis during viral infection. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2), a novel immunoregulatory protein, has been extensively studied in inflammatory response, apoptosis, and cancer. However, the function of TIPE2 in antiviral innate immunity is poorly clarified. In this study, we reported that the expression of TIPE2 declined at the early period and then climbed up in macrophages under RNA virus stimulation. Knockout of TIPE2 in the macrophages enhanced the antiviral capacity and facilitated type I interferon (IFN) signaling after RNA viral infection both in vitro and in vivo. Consistently, overexpression of TIPE2 inhibited the production of type I IFNs and pro-inflammatory cytokines, and thus promoted the viral infection. Moreover, TIPE2 restrained the activation of TBK1 and IRF3 in the retinoic acid inducible gene-I (RIG-I)-like receptors (RLR) signaling pathway by directly interacting with retinoic acid inducible gene-I (RIG-I). Taken together, our results suggested that TIPE2 suppresses the type I IFN response induced by RNA virus by targeting RIG-I and blocking the activation of downstream signaling. These findings will provide new insights to reveal the immunological function of TIPE2 and may help to develop new strategies for the clinical treatment of RNA viral infections.

Tumor-necrosis factor-α induces retinoic acid-inducible gene-I in rheumatoid fibroblast-like synoviocytes

2009 ◽  
Vol 122 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Tadaatsu Imaizumi ◽  
Tomoh Matsumiya ◽  
Hidemi Yoshida ◽  
Takuya Naraoka ◽  
Ryoko Uesato ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Fibroblast Like Synoviocytes ◽  
Inducible Gene

scholarly journals Cannabinoid Reduces Inflammatory Cytokines, Tumor Necrosis Factor-α, and Type I Interferons in Dermatomyositis In Vitro

2017 ◽  
Vol 137 (11) ◽  
pp. 2445-2447 ◽  
Author(s):  
Elizabeth S. Robinson ◽  
Paul Alves ◽  
Muhammad M. Bashir ◽  
Majid Zeidi ◽  
Rui Feng ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Type I Interferons ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Virulence factor p60 ofListeria monocytogenesmodulates innate immunity by inducing tumor necrosis factor α

2010 ◽  
Vol 59 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Hiroshi Sashinami ◽  
Dong-Liang Hu ◽  
Sheng-Jun Li ◽  
Toshihito Mitsui ◽  
Ken-Ichi Hakamada ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Tumor Necrosis Factor ◽  
Virulence Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

254 9-cis RETINOIC ACID INHIBITS CUMULUS CELL APOPTOSIS DURING IN VITRO MATURATION OF BOVINE OOCYTES THROUGH INHIBITION OF AP-1 PATHWAY

2011 ◽  
Vol 23 (1) ◽  
pp. 225
Author(s):  
G. K. Deb ◽  
S. R. Dey ◽  
J. I. Bang ◽  
S. J. Cho ◽  
T. H. Kwon ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Tumor Necrosis Factor ◽  
Oocyte Maturation ◽  
Tumor Necrosis ◽  
In Vitro Maturation ◽  
Tumor Necrosis Factor Α ◽  
Cumulus Cell ◽  
Factor Α ◽  
Necrosis Factor

Cumulus cells (CC) play a critical role in oocyte maturation and fertilization via gap junctions. The oocyte itself maintains CC health to favour oocyte maturation via the secretion of paracrine growth factors. However, the antiapoptotic effects of oocyte-secreted factors follow a gradient from the site of the oocytes. Moreover, degrees of CC apoptosis are inversely related to the in vitro embryo development. Therefore, inhibition of CC apoptosis is important for efficient in vitro embryo development. The beneficial effects of retinoic acid (RA) during in vitro embryo production are well known in different species. However, the effect of RA on CC apoptosis is yet to be elucidated. All-trans RA and 9-cis RA are the natural components of retinoids, and all-trans RA are metabolized to 9-cis RA for physiological function. Therefore, the objective of the present study was to evaluate the effect of 9-cis RA on the mechanism for inhibition of apoptosis in CC. Slaughterhouse cumulus–oocyte complexes (COC) were matured in vitro in TCM-199-based in vitro maturation medium containing 0 or 5 mM 9-cis RA for 23 to 24 h (15 COC/100 μL droplet) at 38.5°C and 5% CO2 in air with maximum humidity. Following in vitro maturation, COC of a droplet were fixed in 4% paraformaldehyde for TUNEL staining using In Situ Cell Death Detection Kit (Roche, Budapest, Hungary). The proportion of apoptotic cells was estimated using Olympus Soft Imaging Solutions GmBH (Olympus, Münster, Germany). The COC of the remaining droplet were denuded. The CC were frozen and stored at –80°C. The CC of 3 different cultures were pooled, and total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA, USA). Total RNA was reverse transcribed into cDNA using Omniscript Reverse Transcription kit (Qiagen). Relative expression of candidate genes was quantified using SYBER green real-time PCR with ΔΔ CT method. The expression was normalized against β-actin, glyceraldehyde 3-phosphate dehydrogenase, and 18s rRNA genes expression. The PCR efficiencies were calculated using relative calibration curves following 10-fold dilution series at 5 measuring points. Data were analysed for one-way ANOVA. The proportion of apoptotic cells was low in the 9-cis RA group (1.3 v. 3.3% of total CC; P < 0.05). Expression of tumor necrosis factor-α (11.1 v. 1.0; P < 0.001), caspase9 (2.0 v. 1.0; P < 0.01), and caspase3 (2.1 v. 1.0; P < 0.001) genes was down-regulated in the 9-cis RA group, whereas expression of Bcl2 gene was increased (1.0 v. 2.6 fold; P < 0.05). Moreover, the expression of c-fos gene of AP-1 pathway was down-regulated (1.9 v. 1 fold; P < 0.05) in the 9-cis RA group. Retinoic acid suppressed the expression of NF-kB, which in turn inhibits tumor necrosis factor-α-mediated caspase activity. However, the expression of NF-kB in CC was not affected by 9-cis RA (1.1 v. 1.0; P > 0.05). In conclusion, the present study indicated that 9-cis RA may inhibit cumulus cell apoptosis through suppression of AP-1 pathway. This work was partly supported by a scholarship from the BK21 program, the KRF (KRF-2008-211-F00011), the IPET (108068-03-1-SB010), and the KOSEF (10525010001-05N2501-00110).

Exercise pretraining attenuates endotoxin-induced hemodynamic alteration in type I diabetic rats

2008 ◽  
Vol 33 (5) ◽  
pp. 976-983 ◽  
Author(s):  
Ching-Hsia Hung ◽  
Yu-Wen Chen ◽  
Dong-Zi Shao ◽  
Che-Ning Chang ◽  
Yung-Yuh Tsai ◽  
...  
Keyword(s):  
Exercise Training ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Diabetic Rats ◽  
Type I ◽  
Cardiovascular Dysfunction ◽  
Factor Α ◽  
Hsp72 Expression ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

Higher expression of heat shock protein 72 (HSP72) reduces the mortality rate and organ damage in septic shock and prevents cardiac mitochondrial dysfunction due to lipopolysaccharide (LPS). Our hypothesis is that exercise preconditioning may increase the expression of HSP72 in heart and the nucleus tractus solitarii (NTS) of the brain to alleviate the cardiovascular dysfunction in type I diabetic rats receiving endotoxin. Wistar rats were randomly assigned to the following groups: sedentary normal, sedentary type I diabetic rats, and type I diabetic rats with exercise training. The trained rats ran on a treadmill 5 d·week–1, 30–60 min·d–1, at an intensity of 1.0 mile·h–1 (1 mile = 1.6 km) over a 3 week period. Twenty-four hours after the last training session, we compared the temporal profiles of mean arterial pressure, heart rate, cardiac output, stroke volume, and serum tumor necrosis factor α level in rats receiving an injection of LPS. In addition, HSP72 expression in heart and NTS from each group was determined. We found that HSP72 expression in the heart and NTS was significantly increased in diabetic rats with exercise training. After administration of LPS, the survival time was significantly longer in diabetic rats with exercise training. Additionaly, serum tumor necrosis factor α levels decreased as compared with those rats not receiving exercise training. Exercise training also diminished cardiovascular dysfunction in diabetic rats during endotoxemia. These data suggest that exercise may increase the expression of HSP72 in the heart and NTS to protect against the high mortality rate and attenuate cardiovascular dysfunction in diabetic rats during endotoxemia.

In vitro regulation of rat Sertoli cell transferrin expression by tumor necrosis factor α and retinoic acid

1999 ◽  
Vol 148 (1-2) ◽  
pp. 163-170 ◽  
Author(s):  
F. Sigillo ◽  
F. Guillou ◽  
I. Fontaine ◽  
M. Benahmed ◽  
B. Le Magueresse-Battistoni
Keyword(s):  
Retinoic Acid ◽  
Tumor Necrosis Factor ◽  
Sertoli Cell ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Anti-inflammatory Effects of Clostridial Collagenase

2015 ◽  
Vol 105 (6) ◽  
pp. 509-519 ◽  
Author(s):  
Richard C. Galperin ◽  
Darrell L. Lange ◽  
Sarah J. Ramsay ◽  
Lei Shi ◽  
Kathy A. Weedon ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Diabetic Patients ◽  
Type I ◽  
Resolution Of Inflammation ◽  
Markers Of Inflammation ◽  
Factor Α ◽  
Necrosis Factor

Background Digestion of collagen with clostridial collagenase (CC) produces peptides that can induce cellular responses consistent with wound healing in vivo. However, nonhealing human wounds are typically in a state of chronic inflammation. We evaluated the effects of CC on markers of inflammation in cell culture and wound fluid from diabetic patients. Methods Lipopolysaccharide-induced release of tumor necrosis factor-α and interleukin-6 from interferon-γ–activated THP-1 monocytes was measured in the presence or absence of CC or CC collagen digests. In the clinical study, 17 individuals with mildly inflamed diabetic foot ulcers were randomized to receive CC ointment (CCO) or hydrogel. Weekly assessments included wound appearance and measurements. Wound exudate was collected at baseline and at 2 and 4 weeks of treatment. A multiplex assay was used to measure levels of analytes, including those associated with inflammation and with inflammation resolution. Results Lower levels of tumor necrosis factor-α and interleukin-6 were found in media of cells cultured with CC or CC digests of collagen type I or III than for untreated lipopolysaccharide controls (P &lt; .05). Clinically, CCO and hydrogel resulted in improvement in wound appearance and a decrease in mean wound area. The CCO, but not the hydrogel, was found to increase the level of analytes associated with resolution of inflammation while decreasing those associated with inflammation. There was a general correlation between resolution of inflammation and healing. Conclusions These results support a hypothesis that debridement with CCO is associated with decreased inflammation and greater progress toward healing.

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