Features of disorders of the system of cytokines and lipid peroxidation in acute ulcerative gastroduodenal hemorrhages

Aim. Investigation of the local and systemic levels of some pro- and anti-inflammatory cytokines as well as the system of lipid peroxidation - antioxidant defense of the organism in acute ulcerative gastroduodenal hemorrhages, taking into account the severity of the blood loss. Methods. We performed the investigation of cytokines in the blood (tumor necrosis factor α, interferon γ, interleukin-1, -2, -4, -6, -8, -10) and parameters of lipoperoxidation (in plasma - diene conjugates, malonic dialdehyde, catalase; in erythrocytes - reduced glutathione, glutathione peroxidase, total antioxidant activity), interleukin-6 in gastric content and urine, diene conjugates and malonic dialdehyde in biopsy samples from the ulcer edges from patients with acute ulcerative gastroduodenal bleeding. The blood serum of 156 patients with mild (54), moderate (51) and severe (51) bleeding was studied. Interleukin-6 in gastric contents was determined in 37 patients, diene conjugates and malonic dialdehyde in biopsy samples taken from periulcerous zone - in 20 patients. Results. Patients had a statistically significant increase of serum levels of tumor necrosis factor α, interferon γ, interleukins-1, -2, -4, -6, -8, and decrease of interleukin-10 concentration in comparison with the control group. The level of interleukin-6 in gastric juice was 37.5% lower, and in urine - 8.2 times higher than the control value. In plasma and biopsy samples, the content of diene conjugates and malonic dialdehyde was statistically significantly higher, in erythrocytes the level of reduced glutathione was lower than the control value. The depth of imbalance in the system of cytokines and lipid peroxidation - antioxidant defense increased with increasing of blood loss severity. Conclusion. The relationship between cytokine production and lipid peroxidation indices is established, which confirms the role of local and systemic disorders of cytokine and antioxidant status in the occurrence of ulcer bleeding.

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Complement Factor I Is Upregulated in Rat Hepatocytes by Interleukin-6 But Not by Interferon-γ , Interleukin-1β or Tumor Necrosis Factor-α

Biological Chemistry ◽

10.1515/bc.2001.137 ◽

2001 ◽

Vol 382 (7) ◽

Cited By ~ 4

Author(s):

Gerald Schlaf ◽

Thorsten Demberg ◽

Milena Koleva ◽

Kurt Jungermann ◽

Otto Götze

Keyword(s):

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Rat Hepatocytes ◽

Interferon Γ ◽

Complement Factor ◽

Factor I ◽

Factor Α ◽

Necrosis Factor

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Maternal serum interleukin-6, interleukin-8, tumor necrosis factor-α and interferon-γ in preterm labor

Acta Obstetricia Et Gynecologica Scandinavica ◽

10.1080/j.1600-0412.2003.00156.x ◽

2003 ◽

Vol 82 (6) ◽

pp. 543-549

Author(s):

Ahmed M. Bahar ◽

Hashim W. Ghalib ◽

Riyad A. Moosa ◽

Zaki M. S. Zaki ◽

Chet Thomas ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Preterm Labor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Interferon Γ ◽

Maternal Serum ◽

Interleukin 8 ◽

Factor Α ◽

Necrosis Factor

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Systemic Sclerosis Fibroblasts Show Specific Alterations of Interferon-γ and Tumor Necrosis Factor-α-induced Modulation of Interleukin 6 and Chemokine Ligand 2

The Journal of Rheumatology ◽

10.3899/jrheum.111132 ◽

2012 ◽

Vol 39 (5) ◽

pp. 979-985 ◽

Cited By ~ 8

Author(s):

ALESSANDRO ANTONELLI ◽

POUPAK FALLAHI ◽

SILVIA MARTINA FERRARI ◽

DILIA GIUGGIOLI ◽

MICHELE COLACI ◽

...

Keyword(s):

Systemic Sclerosis ◽

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Interferon Γ ◽

Tnf Α ◽

Ifn Γ ◽

Factor Α ◽

Necrosis Factor

Objective.We evaluated the effect of interferon-γ (IFN-γ) and/or tumor necrosis factor-α (TNF-α) on the secretion of prototype proinflammatory cytokine interleukin 6 (IL-6), compared to T-helper 1 [Th1; chemokine (C-X-C motif) ligand 10 (CXCL10)] or Th2 [chemokine (C-C motif) ligand 2 (CCL2)] chemokines, in primary cultured fibroblasts from patients with systemic sclerosis (SSc) at an early stage of the disease.Methods.Fibroblast cultures from 5 SSc patients (disease duration < 2 yrs) and 5 healthy controls were evaluated for the production of IL-6, CXCL10, and CCL2 at the basal level and after stimulation with IFN-γ and/or TNF-α.Results.SSc fibroblasts basally produced higher levels of IL-6 than controls, while no difference was observed about CCL2 and CXCL10. TNF-α was able to dose-dependently induce IL-6 and CCL2 secretion in SSc, but not in control fibroblasts. By stimulation with increasing doses of IFN-γ, SSc fibroblasts were induced to secrete CCL2 and CXCL10, while no effect was observed on IL-6. The combination of IFN-γ and TNF-α induced a strong secretion of IL-6 and CCL2 in SSc fibroblasts but not in controls. In contrast, the synergistic effect of IFN-γ and TNF-α on CXCL10 secretion was similar in SSc fibroblasts and in controls.Conclusion.SSc fibroblasts participate in the self-perpetuation of inflammation by releasing IL-6, CXCL10, and CCL2 under the influence of IFN-γ and/or TNF-α. SSc fibroblasts are more active than controls in the secretion of IL-6 at baseline, and in the production of IL-6 and CCL2 under the combined IFN-γ/TNF-α stimulation.

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