scholarly journals Immune Responses after Heavy Alcohol Consumption: Cytokine Concentrations in Hangover-Sensitive and Hangover-Resistant Drinkers

Healthcare ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 395
Author(s):  
Aurora JAE van de van de Loo ◽  
S. Jorinde Raasveld ◽  
Anna Hogewoning ◽  
Raymond de Zeeuw ◽  
Else R Bosma ◽  
...  
Keyword(s):  
Alcohol Intake ◽  
Immune Reactivity ◽  
Cytokine Concentration ◽  
Social Drinkers ◽  
Tnf Α ◽  
Heavy Alcohol Consumption ◽  
Saliva Collection ◽  
Alcohol Hangover ◽  
High Level ◽  
Necrosis Factor

This study investigated immunological changes during an alcohol hangover, and the possible difference between hangover-resistant and hangover-sensitive drinkers in terms of immune reactivity. Using a semi-naturalistic design, N = 36 healthy social drinkers (18 to 30 years old) provided saliva samples on a control day (after drinking no alcohol) and on a post-alcohol day. Hangover severity was rated directly after saliva collection. Cytokine concentrations, interleukin (IL)-1β, IL-6, IL-8, IL-10 and tumor necrosis factor (TNF)-α, and hangover severity were compared between both test days and between hangover-sensitive and -resistant drinkers. Data from N = 35 drinkers (17 hangover-sensitive and 18 hangover-resistant) were included in the statistical analyses. Relative to the control day, there were significant increases in saliva IL-6 and IL-10 concentrations on the post-alcohol day. No significant differences in cytokine concentrations were found between hangover-sensitive and hangover-resistant drinkers, nor did any change in cytokine concentration correlate significantly with hangover severity. In line with previous controlled studies assessing cytokines in blood, the current naturalistic study using saliva samples also demonstrated that the immune system responds to high-level alcohol intake. However, further research is warranted, as, in contrast to previous findings in blood samples, changes in saliva cytokine concentrations did not differ significantly between hangover-sensitive and hangover-resistant drinkers, nor did they correlate significantly with hangover severity.

Serum Levels of IL-17, IL-6, TNF-α and Disease Activity in Patients with Rheumatoid Arthritis

2016 ◽  
Vol 42 (04) ◽  
pp. 323-328 ◽  
Author(s):  
M. Beyazal ◽  
G. Devrimsel ◽  
M. Cüre ◽  
A. Türkyılmaz ◽  
E. Çapkın ◽  
...  
Keyword(s):  
Disease Activity ◽  
Severe Disease ◽  
Serum Levels ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
High Level ◽  
Necrosis Factor

Abstract Objective: The aim of this study was to evaluate serum levels of interleukin (IL)-17, IL-6, and tumor necrosis factor alpha (TNF-α) in RA patients and to assess the correlation of these cytokines with clinical and laboratory parameters. Materials and Methods: 48 patients with RA and 35 healthy volunteers were enrolled in the study. Disease activity was determined by disease activity score (DAS28) in patients with RA. Patients with RA were categorized as mild (DAS28≤3.2), moderate (3.2<DAS28≤5.1), and severe (5.1<DAS28) according to DAS28. The serum levels of IL-17, IL-6 and TNF-α cytokines were measured by enzyme-linked immuno sorbent assay. Results: The mean serum IL-17 and TNF-α levels did not differ between RA patients and controls (P>0.05). Serum IL-6 levels were significantly elevated in RA patients compared with controls (P<0.001). The increasing trend in mean serum IL-6 levels across group with mild, moderate, and severe disease activity was significant (P<0.001, respectively). In RA patients, serum IL-6 concentrations were significantly correlated with ESR, CRP, DAS28, and VAS (r=0.371, P=0.009; r=0.519, P<0.001; r=0.536, P<0.001; r=0.539, P<0.001, respectively). Also, Serum IL-17 concentrations demonstrated significant correlations with ESR, CRP, but not DAS28 (r=0.349, P=0.015; r=0.299, P=0.039; r=0.274, P=0.060, respectively). Serum TNF-α showed no significant correlation with disease activity indices. Conclusions: This study showed that patients with RA had significantly increased cytokine level for IL-6, but not IL-17 and TNF-α and high level of serum IL-6 cytokine was associated with disease activity. However, further follow-up studies involving large samples are required to clarify precise role of these cytokines in disease development and progress.

scholarly journals Immunomodulatory effect of melatonin supplementation in experimental diabetes

Pharmacia ◽  
2020 ◽  
Vol 67 (4) ◽  
pp. 223-228
Author(s):  
Yana I. Ivankiv ◽  
Oleksandra M. Oleshchuk
Keyword(s):  
Inflammatory Responses ◽  
Suppressive Effect ◽  
Male Rats ◽  
Immune Reactivity ◽  
Standard Diet ◽  
Tnf Α ◽  
Experimental Type ◽  
Necrosis Factor

Aim: To investigate the effect of melatonin on the immunomodulatory response in experimental type 1 and 2 diabetes mellitus. Methods: Experiments were performed on male rats (180–200 g), purchased from the Experimental Animal Holding,. Animals were maintained in standard diet conditions. Two pathological states were simulated on male rats: experimental type 1 and type 2 diabetes. Melatonin was introduced from 14 to 23 days of experiment intraperitoneally. Levels of immunoglobulin classes A, M and G (Ig A, M, G), circulating immune complexes (CIC), interleukin 1β (EE), interleukin 6 (IL-6), and tumor necrosis factor (TNF-a) were measured. Results: We demonstrated that melatonin in case of immune hyperactivity, can, provide a suppressive effect and is able to enhance immune reactivity under conditions of its limitation, indicating the immunostimulating activity. Furthermore, we found that administration of melatonin decreased inflammatory responses by mediating the levels of immunomodulatory factors, including TNF-α, IL-1β and IL-6. Conclusion: Melatonin is a positive regulator of immune system, may be a potential therapeutic agent, it has no reported side effects.

Circulating monocytes are not the source of elevations in plasma IL-6 and TNF-α levels after prolonged running

2001 ◽  
Vol 280 (4) ◽  
pp. C769-C774 ◽  
Author(s):  
R. L. Starkie ◽  
J. Rolland ◽  
D. J. Angus ◽  
M. J. Anderson ◽  
M. A. Febbraio
Keyword(s):  
Tumor Necrosis ◽  
Cytokine Production ◽  
Stress Hormones ◽  
Intracellular Cytokine ◽  
Cytokine Concentration ◽  
Plasma Cytokine ◽  
Blood Samples ◽  
Tnf Α ◽  
Necrosis Factor ◽  
Number Of Cells

The present study was undertaken to examine the effect of prolonged running on monocyte intracellular cytokine production and plasma cytokine concentration. Blood samples were collected 1 h before, immediately after, 2 h after, and 24 h after a competitive marathon run. There was no change in the number of cells spontaneously producing tumor necrosis factor (TNF)-α; however, there was a decrease in the number of cells producing interleukin (IL)-1α and IL-6 ( P < 0.01) postexercise. In contrast, there was an increase in the number of monocytes that responded to lipopolysaccharide stimulation by producing IL-1α, TNF-α, and IL-6 ( P < 0.01) immediately and 2 h postexercise; however, these cells contained less cytokine ( P < 0.05). Plasma IL-6, TNF-α, epinephrine, norepinephrine, and cortisol concentrations were markedly increased ( P < 0.01) postexercise. These data demonstrate that circulating monocytes are not the source of elevated levels of plasma IL-6 and TNF-α after prolonged running. In addition, it is likely that stress hormones result in a decrease in the amount of cytokine produced by LPS-stimulated cells postexercise.

Hyperlipidemia Could Activate Platelet and Induce the Production of Plasma Inflammatory Factors in Rabbits, Which Lead to Atherosclerosis

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5369-5369
Author(s):  
Shuangfeng Xie ◽  
Songmei Yin ◽  
Danian Nie ◽  
Yiqing Li ◽  
Xiuju Wang ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Platelet Activation ◽  
Inflammatory Mediator ◽  
Inflammatory Factors ◽  
Tnf Α ◽  
Significant Difference ◽  
Set Up ◽  
High Level ◽  
Necrosis Factor ◽  
Time Point

Abstract Background: It had been proved by epidemiology and clinical trials that hypercholesterolemia (HC) and atherosclerosis (AS) had close relations. Lipid could take part in many pathological processes of the AS. Platelets played an important role in this process as an inflammatory mediator. We Chose Platelet aggregation maximum (PAG(M)) and plasma P-selectin as the index of platelet activation, try to explore the transfer of platelet activation and lymphocyte inflammatory reaction in atherosclerosis. Design: We set up the rabbit hyperlipidemia atherosclerosis model through 12 weeks’ hyper lipid feeding. PAG(M), concentrations of plasma P-selectin, Interleukin (IL)- 6, IL-1β, tumor necrosis factor (TNF)-α and mRNA expression of these factors in the lymphocyte were measured at 0 week, 6th week and 12th week time point. Results: At the 6th week time point of the hyper lipid feeding, the rabbit had elevated PAG(M) (68.12%±4.73% vs. 62.67%±3.13%; P=0.002, n=20). The PAG(M) was maintained in the high level at 12th week time point (68.83%±3.35% vs. 62.67%±3.13%; P=0.001, n=20). At the 6th week time point of the hyper lipid feeding, the rabbit had elevated plasma P-selectin, IL-6, IL-1β and TNF-α (6th week vs. 0 week, n=20, P-selectin P=0.005, IL-6 P=0.000, IL-1β P=0.001, TNF-α P=0.001). The expressions of IL-6/mRNA, IL-1β/mRNA and TNF-α/mRNA in lymphocytes were elevated too (6th week vs. 0 week, n=20, IL-6/mRNA P=0.000, IL-1β/mRNA P=0.002, TNF-α/mRNA P=0.000). At the 12th week time point, all of the parameters were maintained in the high level, while there had no significant difference between 12th week time point and 6th week time point. Conclusion: Hyperlipidemia could activate platelet. Increased PAG(M) and plasma P-selectin represented the platelet activation. Hyperlipidemia could induce the production of plasma IL-6, IL-1β and TNF-α. The increased plasma IL-6, IL-1β and TNF-α were partly from the lymphocyte secretion because The IL-1β/mRNA, IL-6/mRNA and TNF-α/mRNA expression of lymphocyte elevated. So in rabbit hyperlipidemia atherosclerosis model, platelet activation and inflammatory factors increasing was the main mechanism, while the lymphocyte took part in the inflammatory process.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor
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