Humans ; Myocardial Ischemia ; complications ; Tumor Necrosis Factor-alpha ; physiology ; Ventricular Fibrillation ; physiopathology

Cytokines are the main regulatory molecules of not only immune system but also sleep system. Research on the role of cytokines on sleep has greatly been expanding since the first report of sleep-promoting effects of interleukin-1, the first cytokine molecule. Interleukin-1 and tumor necrosis factor are most widely studied among various cytokines. Studies over about twenty years demonstrate that most cytokines promote sleep but several cytokines inhibit sleep. Slow wave sleep is the main part that cytokines have effects on. Besides normal sleep physiology, cytokines have more major roles on pathophysiology of various sleep disorders. Obstructive sleep apnea is the representative sleep disorder that shows how deeply cytokines are involved in their pathophysiologic mechanisms of sleep disorders. Though there are many controversial issues on this topic, more mysterious part of normal sleep physiology and sleep disorders will be revealed in near future through thorough studies on sleep and cytokine.
Cytokines ; Immune System ; Interleukin-1 ; Physiology ; Sleep Apnea, Obstructive ; Sleep Wake Disorders ; Tumor Necrosis Factor-alpha

The modeling of signal transduction pathways is a task of systems biology. However, such a task is very difficult because of the structure complexity, the strong nonlinearity of signaling pathways and the noised and incomplete measurements. The Levenberg-Marquardt algorithm (LM algorithm) is applied to estimate the unknown parameters of the signaling pathways. With this method, the identifiability of unknown parameters is appraised, and the sensitivity equations of original model are evaluated. Then we append the sensitivity equations to the original model in order to form the augmented model, and we apply the Levenberg-Marquardt algorithm to the augmented model in order to estimate parameters. TNFalpha mediated NF-kappaB signaling pathway is taken as an example to illustrate the effectiveness of this method, and the simulation results are given.
Algorithms ; Computer Simulation ; Humans ; Models, Theoretical ; NF-kappa B ; physiology ; Signal Transduction ; Systems Biology ; methods ; Tumor Necrosis Factor-alpha ; physiology

Periodontitis is an inflammatory disease involving the destruction of both soft and hard tissue in the periodontal region. Although dysbiosis of the local microbial community initiates local inflammation, over-activation of the host immune response directly activates osteoclastic activity and alveolar bone loss. Many studies have reported on the cytokine network involved in periodontitis and its crucial and pleiotropic effect on the recruitment of specific immunocytes, control of pathobionts and induction or suppression of osteoclastic activity. Nonetheless, particularities in the stimulation of pathogens in the oral cavity that lead to the specific and complex periodontal cytokine network are far from clarified. Thus, in this review, we begin with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response. In addition, we also summarize the latest cytokine-related therapeutic measures for periodontal disease.
Alveolar Bone Loss ; etiology ; Cytokines ; metabolism ; physiology ; Humans ; Inflammation ; Periodontal Diseases ; Periodontitis ; immunology ; microbiology ; Tumor Necrosis Factor-alpha ; physiology

Progranulin (PGRN) is a growth factor implicated in various pathophysiological processes, including wound healing, inflammation, tumorigenesis, and neurodegeneration. It was previously reported that PGRN binds to tumor necrosis factor receptors (TNFR) and has therapeutic effects in inflammatory arthritis (Tang et. al, in Science 332:478-484, 2011); however, Chen et al. reported their inability to demonstrate the PGRN-TNFR interactions under their own conditions (Chen et. al, in J Neurosci 33:9202-9213, 2013). A letter-to-editor was then published by the original group in response to the Chen et al. paper that discussed the reasons for the latter's inability to recapitulate the interactions. In addition, the group published follow-up studies that further reinforced and dissected the interactions of PGRN-TNFR. Recently, the dispute about the legitimacy of PGRN-TNFR interactions appears to be finally settled with independent confirmations of these interactions in various conditions by numerous laboratories. This review presents a chronological update on the story of PGRN-TNFR interactions, highlighting the independent confirmations of these interactions in various diseases and conditions.
Animals ; Humans ; Intercellular Signaling Peptides and Proteins ; metabolism ; Progranulins ; Receptors, Tumor Necrosis Factor ; metabolism ; Signal Transduction ; physiology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo review the relationship between the immune system and the mechanism of pain. Data sources Related researches published in the period of 1987-2005 were systematically reviewed. Study selection Articles about the immune system and pain were selected. Data extraction Data were mainly extracted from 74 articles which are listed in the reference section of this review.

RESULTSPain was classically viewed as being mediated solely by neurons. However, growing evidence has showed the possible relationships between the immune system and the central nervous system. In this article, we reviewed the role of the immune system in the development of pain, together with the importance of the glia in this process. These findings suggest a novel approach to pain control in the future.

CONCLUSIONSThe immune system plays a potential but important role in the development of pain.

Animals ; Brain ; immunology ; Humans ; Immune System ; physiology ; Interleukin-1 ; physiology ; Neuroglia ; physiology ; Pain ; etiology ; immunology ; TRPV Cation Channels ; physiology ; Tumor Necrosis Factor-alpha ; physiology ; Wounds and Injuries ; immunology

Adipose tissue is not simply a depot of energy, but is an active endocrine organ. The adipokines play an important role in the pathogenesis of metabolic syndrome. The proinflammatory adipokines secreted from expanded visceral adipose tissue directly induce insulin resistance and vascular injuries. A better understanding of the endocrine function of adipose tissue may lead to more rational therapy for metabolic syndrome.
Adiponectin ; physiology ; Adipose Tissue ; physiopathology ; Drug Design ; Leptin ; physiology ; Metabolic Syndrome ; drug therapy ; physiopathology ; Resistin ; physiology ; Tumor Necrosis Factor-alpha ; physiology

OBJECTIVE: To explore the effect of nitric oxide (NO) on the gene expression of hepatic TNF-α and IL-1β by crush injury of rat's soft tissues. METHODS: Rats were randomly divided into sham group, crush group, crush+aminoguanidine (AG) group, and crush+L-arginine (L-Arg) group. Activities of ALT and AST as well as NO level in serum were measured. Gene expressions of TNF-α and IL-1β were detected with RT-PCR. RESULTS: Obvious increase in TNF-α and IL-1β mRNA expression was detected in the crush group compared with the sham group (P<0.05). After pretreated L-Arg, expressions of TNF-α and IL-1β mRNA were markedly increased (P<0.05). After pretreated AG, those indices obviously decreased (P<0.05). Activities of ALT and AST enhanced and NO level increased in the crush group compared with the sham group (P<0.05). Pretreatment with L-Arg or AG led to substantial increased or reduced activities of ALT and AST as well as NO levels, respectively. CONCLUSION Endogenous NO mediated TNF-α, IL-1β mRNA up expression in liver induced by increased production of NO after crush injury of rat's soft tissues.
Animals ; Gene Expression ; Interleukin-1beta/metabolism* ; Liver ; Nitric Oxide/physiology* ; RNA, Messenger ; Rats ; Tumor Necrosis Factor-alpha/metabolism* ; Wounds and Injuries

Epidermal Growth Factor ; physiology ; Fetal Diseases ; therapy ; Hernia, Diaphragmatic ; complications ; therapy ; Hernias, Diaphragmatic, Congenital ; Humans ; Lung ; abnormalities ; pathology ; Prenatal Diagnosis ; Pulmonary Surfactants ; pharmacology ; Tumor Necrosis Factor-alpha ; physiology

Animals ; Diet ; Enterocolitis, Necrotizing ; etiology ; metabolism ; Humans ; Infant, Newborn ; NF-kappa B ; physiology ; Platelet Activating Factor ; chemistry ; metabolism ; Risk Factors ; Tumor Necrosis Factor-alpha ; physiology