Effect of cyclosporine a on serum tumor necrosis factor α in new-onset type I (insulin-dependent) diabetes mellitus

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.

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Serum tumor necrosis factor-α and interleukin-6 in overweight and obese patients with obstructive sleep apnea–hypopnea syndrome

Sleep Medicine ◽

10.1016/j.sleep.2015.02.1476 ◽

2015 ◽

Vol 16 ◽

pp. S225

Author(s):

X. Xu ◽

H. Yi ◽

S. Yin

Keyword(s):

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Obese Patients ◽

Obstructive Sleep ◽

Factor Α ◽

Hypopnea Syndrome ◽

Necrosis Factor ◽

Serum Tumor Necrosis

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Mo1860 - High Fecal and Serum Tumor Necrosis Factor-α Levels are Associated with Non-Response to Infliximab in Patients with Ulcerative Colitis

Gastroenterology ◽

10.1016/s0016-5085(18)32824-5 ◽

2018 ◽

Vol 154 (6) ◽

pp. S-829

Author(s):

Hadar Meringer-Milwidsky ◽

Nitsan Maharshak ◽

Yulia Ron ◽

Henit A. Yanai ◽

Sarit Cohen-Kedar ◽

...

Keyword(s):

Ulcerative Colitis ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Factor Α ◽

Necrosis Factor ◽

Serum Tumor Necrosis

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

Frontiers in Immunology ◽

10.3389/fimmu.2021.642715 ◽

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.

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