Relation between major depressive disorder as regards severity in a sample of Egyptian population and serum level of tumor necrosis factor alpha

2016 ◽  
Vol 33 (S1) ◽  
pp. S412-S412
Author(s):  
S. Harby ◽  
T. Molokhia ◽  
H. Aboelwafa ◽  
D. Elneely

IntroductionDepression is a life threatening psychiatric disorder. STAR-D study stated that remission rates decrease, and relapse rates increase. It produces chronic diseases and worsens mean health when co-morbid with these diseases. The depressive symptoms in humans are analogous to the ‘sickness behavior’ syndrome seen in animals when injected by pro-inflammatory cytokines.ObjectiveThis study was done to clarify the relation between the severity of depression and serum level of tumor necrosis factor alpha (TNF), so improving the quality of pharmacological management.AimThis study was done to prove that inflammatory process is involved in the pathogenesis of depression by assessing the serum level tumor necrosis factor alpha (TNF alpha)MethodsOur study is comparing between 60 patients with major depressive disorder and 30 healthy controls regarding the serum level of tumor necrosis factor alpha. Patients were diagnosed by a semi-structured interview using Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Patients were subdivided into mild, moderate and severe depression according to Hamilton Rating Scale for Depression (17 items). Assessment of serum level of tumor necrosis factor alpha was done using enzyme- linked immunoassay technique.ResultsSerum level of TNF alpha was significantly higher among patients than among controls (Z = 4.710*P ≤ 0.001*) regardless the severity of depression.ConclusionsSerum TNF alpha can be used as a biomarker of depression but not for the disorder severity. However, further study is needed to detect if there is a relation between major depressive disorder and serum level of other inflammatory markers as C-reactive protein.Disclosure of interestThe authors have not supplied their declaration of competing interest.

2019 ◽  
Vol 85 (10) ◽  
pp. S333
Author(s):  
Conrad Stasieluk ◽  
Edwin Meresh ◽  
Debra Hoppensteadt ◽  
Jawed Fareed ◽  
James Sinacore ◽  
...  

1994 ◽  
Vol 14 (10) ◽  
pp. 6561-6569
Author(s):  
L Klampfer ◽  
T H Lee ◽  
W Hsu ◽  
J Vilcek ◽  
S Chen-Kiang

Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) activate transcription of the TSG-6 gene in normal human fibroblasts through a promoter region (-165 to -58) that encompasses an AP-1 and a NF-IL6 site. We show by deletion analysis and substitution mutagenesis that both sites are necessary for activation by TNF-alpha. Activation by IL-1 requires the NF-IL6 site and is enhanced by the AP-1 site. These results suggest that the NF-IL6 and AP-1 family transcription factors functionally cooperate to mediate TNF-alpha and IL-1 signals. Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the AP-1 site, and NF-IL6 activates the native TSG-6 promoter. Activation by NF-IL6 requires an intact NF-IL6 site and is modulated by the ratio of activator to inhibitor NF-IL6 isoforms that are translated from different in-frame AUGs. However, the inhibitor isoform can also bind to the AP-1 site and repress AP-1 site-mediated transcription. The finding that the inhibitor isoform antagonizes activation of the native TSG-6 promoter by IL-1 and TNF-alpha suggests that NF-IL6 has a physiologic role in these cytokine responses. Thus, the functionally distinct NF-IL6 isoforms cooperate with Fos and Jun to positively and negatively regulate the native TSG-6 promoter by TNF-alpha and IL-1.


1998 ◽  
Vol 21 (6) ◽  
pp. 638-640 ◽  
Author(s):  
Masaaki ISHIKAWA ◽  
Shu-ichi KANNO ◽  
Motoaki TAKAYANAGI ◽  
Yoshio TAKAYANAGI ◽  
Ken-ichi SASAKI

1992 ◽  
Vol 263 (5) ◽  
pp. E897-E902 ◽  
Author(s):  
M. Beylot ◽  
H. Vidal ◽  
G. Mithieux ◽  
M. Odeon ◽  
C. Martin

Tumor necrosis factor-alpha (TNF-alpha) stimulates hepatic lipogenesis. Therefore, it could play a role in the control of ketogenesis. To test this hypothesis, we measured simultaneously free fatty acids (FFA; [1–13C]palmitate) and ketone body (KB; [3,4–13C2]acetoacetate) kinetics, before and after intraperitoneal injection of saline or TNF-alpha, in postabsorptive rats or rats starved for 24 h. In both groups of rats, TNF-alpha injection did not modify insulinemia and induced a moderate increase of FFA concentrations and appearance rates (P < 0.05). Despite increased FFA availability, ketogenesis was impaired after TNF-alpha injection, as shown by lower KB concentrations and appearance rates; this effect was more important in postabsorptive than in starved rats. The percentage of FFA flux used for ketogenesis was decreased by TNF-alpha in the postabsorptive group (P < 0.05) and starved (P < 0.05) rats. In both groups, maximal liver acetyl-coenzyme A carboxylase activity and estimated phosphorylation state were not modified by TNF-alpha injection, but hepatic concentrations of citrate were increased (P < 0.05). This increased citrate level could be related to a mobilization of glucose stored as glycogen since liver glycogen was decreased by TNF-alpha injection (P < 0.05). In conclusion, TNF-alpha injection in rats decreased hepatic ketogenesis. This action could be related to an increased mobilization and utilization of carbohydrate stores.


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