scholarly journals Cytokine control in human endometrium

Reproduction ◽  
2001 ◽  
pp. 3-19 ◽  
Author(s):  
RW Kelly ◽  
AE King ◽  
HO Critchley
Keyword(s):  
Direct Action ◽  
Progesterone Receptors ◽  
Interleukin 10 ◽  
Prostaglandin Synthesis ◽  
Leukaemia Inhibitory Factor ◽  
Interleukin 12 ◽  
Prostaglandin E ◽  
Inflammatory Drugs ◽  
Cytokine Synthesis ◽  
Anti Inflammatory

Cytokines within endometrium participate in both menstruation and implantation but also contribute to the defence mechanisms of the mucosal epithelium. Endometrium is under the control of steroid hormones, particularly progesterone and, thus, control of cytokines by this steroid is important. Although appreciable numbers of progesterone receptors are not found in endometrial leucocytes, progesterone can modulate cytokines by acting on uterine cells expressing the receptor. The NFkappaB pathway is important in the control of cytokine synthesis and can modulate production of chemokines, matrix metalloproteinases and the inducible prostaglandin synthesis enzyme COX-2. NFkappaB activity can be inhibited by progesterone by either stimulating synthesis of IkappaB, the molecule that restrains NFkappaB in the cytosol, or after binding to the nuclear receptor, competing with NFkappaB for recognition sites on the relevant gene. In this way, progesterone can limit pro-inflammatory pathways. The major palliatives for endometrial dysfunctions such as menorrhagia and dysmenorrhoea have been the non-steroidal anti-inflammatory drugs that inhibit prostaglandin synthesis. Prostaglandins have major effects on cytokine production but the direct action of prostaglandin E on leucocytes is not a pro-inflammatory response but is to stimulate interleukin 10 and inhibit interleukin 12 synthesis. The likely effect of the non-steroidal anti-inflammatory drugs is on the cells surrounding the small blood vessels, where a synergistic action between prostaglandin and chemokine will induce leucocyte entry and activation leading to lysis of connective tissue and menstruation. At the time of implantation, tight control of cytokine synthesis is required. Although leukaemia inhibitory factor is essential to implantation, the mouse knockout models show that the prostaglandin system is also essential but that there are mutually supportive pathways that compensate for the knockout of many cytokines.

scholarly journals Tobacco Exposure by Various Modes May Alter Proinflammatory (IL-12) and Anti-Inflammatory (IL-10) Levels and Affects the Survival of Prostate Carcinoma Patients: An Explorative Study in North Indian Population

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Shailendra Dwivedi ◽  
Apul Goel ◽  
Sanjay Khattri ◽  
Anil Mandhani ◽  
Praveen Sharma ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Prostate Carcinoma ◽  
Interleukin 10 ◽  
Interleukin 12 ◽  
Tobacco Exposure ◽  
Statistical Tool ◽  
Cytokine Levels ◽  
Test Graph ◽  
Anti Inflammatory ◽  
Alcohol Users

Objective. Inflammation is an important hallmark of all cancers and net inflammatory response is determined by a delicate balance between pro- and anti-inflammatory cytokines, which may be affected by tobacco exposure, so the present study was designed to explore the effect of various modes of tobacco exposure on interleukin-12 (IL-12) and interleukin-10 (IL-10) inflammatory cytokine levels and survival in prostate carcinoma (PCa) patients.Methods. 285 cancer patients and equal controls with 94 BPH (benign prostatic hyperplasia) were recruited; baseline levels of serum IL-12 and IL-10 were measured and analyzed in various tobacco exposed groups by appropriate statistical tool. Five-year survivals of patients were analyzed by Log-rank (Mantel-Cox) test (graph pad version 5).Results. The expression of serum proinflammatory (IL-12) and anti-inflammatory (IL-10) cytokines was correlated with tobacco exposed group as smokers, chewers, and alcohol users have shown significantly higher levels (P<0.001) with significantly lower median survivals (27.1 months, standard error = 2.86, and 95% CI: 21.4–32.62); than nonusers. Stages III and IV of tobacco addicted patients have also shown significantly increased levels of IL-12 and IL-10.Conclusions. IL-12 and IL-10 seem to be affected by various modes of tobacco exposure and inflammation also affects median survival of cancer patients.

scholarly journals Controlling Gut Inflammation by Restoring Anti-Inflammatory Pathways in Inflammatory Bowel Disease

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 397 ◽  
Author(s):  
Paolo Giuffrida ◽  
Sara Cococcia ◽  
Mariangela Delliponti ◽  
Marco Vincenzo Lenti ◽  
Antonio Di Sabatino
Keyword(s):  
Inflammatory Bowel Disease ◽  
Side Effects ◽  
Bowel Disease ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interleukin 10 ◽  
Interleukin 12 ◽  
Inflammatory Pathways ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Inflammatory bowel disease (IBD) is caused by a dysregulated immune response against normal components of the intestinal microflora combined with defective functioning of anti-inflammatory pathways. Currently, all therapies approved for IBD manipulate the immune system by inhibiting pro-inflammatory mechanisms, such as tumor necrosis factor-α, gut-homing α4β7 integrin, interleukin-12/interleukin-23, and Janus kinases. However, some IBD patients are non-responders to these drugs, which are also associated with serious side effects. Thus, it has been hypothesized that therapies aimed at restoring anti-inflammatory signals, by exploiting the tolerogenic potential of cytokines (interleukin-10, transforming growth factor-β, granulocyte macrophage colony-stimulating factor), immune cells (regulatory T cells, tolerogenic dendritic cells), or mesenchymal stem cells, might offer promising results in terms of clinical efficacy with fewer side effects. In this review, we provide new insights into putative novel treatments aimed at restoring anti-inflammatory signaling pathways in IBD.

scholarly journals Effects of Aspirin and Other Nonsteroidal Anti-Inflammatory Drugs on Biofilms and Planktonic Cells of Candida albicans

2004 ◽  
Vol 48 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Mohammed A. S. Alem ◽  
L. Julia Douglas
Keyword(s):  
Candida Albicans ◽  
Biofilm Formation ◽  
Significant Inhibition ◽  
Cyclooxygenase Inhibitors ◽  
Fungal Colonization ◽  
Prostaglandin E ◽  
Disk Model ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Biofilm Development

ABSTRACT Prostaglandins are now known to be produced by Candida albicans and may play an important role in fungal colonization. Their synthesis in mammalian cells is decreased by inhibitors of the cyclooxygenase isoenzymes required for prostaglandin formation. In the present study, a catheter disk model system was used to investigate the effects of nonsteroidal anti-inflammatory drugs (all cyclooxygenase inhibitors) on biofilm formation by three strains of C. albicans. Seven of nine drugs tested at a concentration of 1 mM inhibited biofilm formation. Aspirin, etodolac, and diclofenac produced the greatest effects, with aspirin causing up to 95% inhibition. Celecoxib, nimesulide, ibuprofen, and meloxicam also inhibited biofilm formation, but to a lesser extent. Aspirin was active against growing and fully mature (48-h) biofilms; its effect was dose related, and it produced significant inhibition (20 to 80%) at pharmacological concentrations. Simultaneous addition of prostaglandin E2 abolished the inhibitory effect of 25 or 50 μM aspirin. At 1 mM, aspirin reduced the viability of biofilm organisms to 1.9% of that of controls. Surviving cells had a wrinkled appearance, as judged by scanning electron microscopy, and consisted of both yeasts and hyphae. Treatment with other cyclooxygenase inhibitors, such as etodolac, resulted in biofilms that consisted almost entirely of yeast cells. In conventional assays for germ tube formation, these drugs produced significant inhibition, whereas aspirin had little effect. Our findings suggest that cyclooxygenase-dependent synthesis of fungal prostaglandin(s) is important for both biofilm development and morphogenesis in C. albicans and may act as a regulator in these physiological processes. Our results also demonstrate that aspirin possesses potent antibiofilm activity in vitro and could be useful in combined therapy with conventional antifungal agents in the management of some biofilm-associated Candida infections.

Migrating action potential complex of cholera: a possible prostaglandin-induced response.

1977 ◽  
Vol 232 (5) ◽  
pp. E529 ◽  
Author(s):  
J R Mathias ◽  
G M Carlson ◽  
G Bertiger ◽  
J L Martin ◽  
S Cohen
Keyword(s):  
Action Potential ◽  
Propagation Velocity ◽  
Secretory Component ◽  
Prostaglandin Synthesis ◽  
Induced Response ◽  
Prostaglandin F2alpha ◽  
New Zealand White Rabbits ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Potential Complex

Distal ileal loops of New Zealand white rabbits exposed to cholera toxin demonstrated the presence of a highly organized myoelectric pattern defined as the migrating action potential complex (MAPC). We investigated the mechanism by which cholera enterotoxin stimulates MAPC activity. Certain anti-inflammatory drugs have altered the secretory component of cholera diarrhea. We investigated effects of these anti-inflammatory drugs on the MAPC. Indomethacin, 5.0 mg/kg iv, abolished all MAPC activity. Indomethacin, 1.5 mg/kg iv, or acetylsalicylic acid, 150 mg/kg given intragastrically, altered propagation velocity and at times its direction of propagation, but did not abolish the MAPC. An infusion of prostaglandin F2alpha, 2 microng/kg per min intraluminally, induced MAPC activity similar to that of the cholera complex. Indomethacin, 5.0 mg/kg iv, produced no significant changes in number of complexes or propagation velocity. These observations suggested that inhibition of the cholera complex by indomethacin may result from the alteration of prostaglandin synthesis and that prostaglandins may initiate the motility component of cholera diarrhea.

Influence of Polymorphisms of Pro-Inflammatory (IL-12, TNFa and LTa) and Anti-Inflammatory Factors (IL-10 and CTLA4) in Autoimmune Hemolytic Anemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3751-3751
Author(s):  
Maria S. Figueiredo ◽  
Leandro S. D’Abronzo ◽  
Melca M. Oliveira ◽  
Juliana L. Dreyfuss ◽  
Jose Orlando Bordin
Keyword(s):  
Hemolytic Anemia ◽  
Patient Group ◽  
Autoimmune Hemolytic Anemia ◽  
Interleukin 10 ◽  
Inflammatory Factors ◽  
Interleukin 12 ◽  
Control Group ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Abstract The Autoimmune Hemolytic Anemia (AIHA) is caused by the destruction of antibody-coated red blood cells, but mechanisms that initiate the production of autoantibodies remains unclear. It had been suggest that decreased production of Th1-type cytokines and production of autoantibodies in AIHA can be secondary to the imbalance between anti- and pro-inflammatory factors. Moreover, the presence of single nucleotide polymorphisms (SNPs) showed association with different production of immunoregulatory factors which may modulate the disease expression in AIHA. OBJECTIVES: To determine the importance of SNPs of pro- and anti-inflammatory factors in the development of AIHA. PATIENTS: We studied 17 patients with AIHA who has been followed in the Hematology and Blood Transfusion Unit at the Federal University of Sao Paulo (UNIFESP/EPM), Brazil. The control group was composed by 40 healthy volunteer blood donors. METHODS: After DNA extraction from peripheral blood samples, the frequency of the SNPs was determinate by PCR-RFLP in patients and healthy individuals. The following SNPs were analyzed: Interleukin 12: IL-12 1188 (A/C), Tumor Necrosis Factor alpha: TNFa-308 (G/A), and Lymphotoxin alpha: Lta +252 (A/G); Interleukin 10: IL-10-592 (C/A), and Cytotoxic T-lymphocyte associated protein 4: CTLA4 exon 1 49 (A/G). RESULTS: The patient group was composed predominantly by female individuals (14 or 82%) and the median of age was 56 years old (18 to 76 years). The frequency observed for each allele studied in the patient group was: allele A of IL-12 = 0.82; allele G of FNTa = 0.85; allele A of Lta = 0.68; allele C of IL-10 = 0.82; allele G of CTLA4 = 0.59. No differences in allele frequency were found between patient and control groups. CONCLUSIONS: Our results suggest that these polymorphisms appear not to contribute for the development of the AIHA.

scholarly journals Antitumour and Anti-Inflammatory Effects of Palladium(II) Complexes on Ehrlich Tumour

2013 ◽  
Vol 68 (7-8) ◽  
pp. 293-301
Author(s):  
Marcela B. Quilles ◽  
Camila B. A. Carli ◽  
Sandra R. Ananias ◽  
Lucas S. Ferreira ◽  
Livia C. A. Ribeiro ◽  
...  
Keyword(s):  
Mutagenic Activity ◽  
Interleukin 10 ◽  
Interleukin 12 ◽  
Tnf Α ◽  
Ehrlich Ascites Tumour ◽  
Eat Cells ◽  
Anti Inflammatory ◽  
Diphenyl Tetrazolium Bromide ◽  
Factor Α

Palladium(II) complexes are an important class of cyclopalladated compounds that play a pivotal role in various pharmaceutical applications. Here, we investigated the antitumour, anti-inflammatory, and mutagenic effects of two complexes: [Pd(dmba)(Cl)tu] (1) and [Pd(dmba)(N3)tu] (2) (dmba = N,N-dimethylbenzylamine and tu = thiourea), on Ehrlich ascites tumour (EAT) cells and peritoneal exudate cells (PECs) from mice bearing solid Ehrlich tumour. The cytotoxic effects of the complexes on EAT cells and PECs were assessed using the 3-(4,5-dimethylthiazol-3-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. The effects of the complexes on the immune system were assessed based on the production of nitric oxide (NO) (Griess assay) and tumour necrosis factor-α (TNF-α), interleukin-12 (IL-12), and interleukin-10 (IL-10) (ELISA). Finally the mutagenic activity was assessed by the Ames test using the Salmonella typhimurium strain TA 98. Cisplatin was used as a standard. The IC50 ranges for the growth inhibition of EAT cells and PECs were found to be (72.8 ± 3.23) μM and (137.65 ± 0.22) μM for 1 and (39.7 ± 0.30) μM and (146.51 ± 2.67) μM for 2, respectively. The production of NO, IL-12, and TNF-α, but not IL-10, was induced by both complexes and cisplatin. The complexes showed no mutagenicity in vitro, unlike cisplatin, which was mutagenic in the strain. These results indicate that the complexes are not mutagenic and have potential immunological and antitumour activities. These properties make them promising alternatives to cisplatin

Naproxen (naprosyn) and ketoprofen (orudis)

1974 ◽  
Vol 12 (7) ◽  
pp. 25-27
Keyword(s):  
Prostaglandin Synthesis ◽  
New Drugs ◽  
Inflammatory Activity ◽  
Inhibit Prostaglandin Synthesis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Low Incidence ◽  
Gastric Irritation

Naproxen (Naprosyn - Syntex) and ketoprofen (Orudis - M & B) are new drugs for treating various forms of arthropathy. For both drugs the manufacturers claim good anti-inflammatory activity with a low incidence of unwanted effects, particularly gastric irritation, in comparison with other non-steroidal anti-inflammatory drugs. If these claims can be substantiated these preparations would be valuable. Like aspirin and other non-steroidal anti-inflammatory drugs they both inhibit prostaglandin synthesis. Both are chemically related to other such drugs, for example ibuprofen (Brufen - Boots).

scholarly journals Pathogenesis of Nonsteroidal Anti-Inflammatory Drug Gastropathy: Clues to Preventative Therapy

1999 ◽  
Vol 13 (2) ◽  
pp. 123-127 ◽  
Author(s):  
Salim MA Bastaki ◽  
John L Wallace
Keyword(s):  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Barrier Properties ◽  
Prostaglandin Synthesis ◽  
Preventative Therapy ◽  
Mucosal Integrity ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Reduced Toxicity ◽  
Chronic Use

Gastric ulceration and bleeding are major impediments to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs). The development of effective therapies for prevention of these adverse effects requires better understanding of their pathogenesis. Several features of NSAIDs contribute to the development of damage in the stomach, including the topical irritant effects of these drugs on the epithelium, impairment of the barrier properties of the mucosa, suppression of gastric prostaglandin synthesis, reduction of gastric mucosal blood flow and interference with the repair of superficial injury. The presence of acid in the lumen of the stomach also contributes to the pathogenesis of NSAID-induced ulcers and bleeding in a number of ways. Acid impairs the restitution process, interferes with hemostasis and can inactivate several growth factors that are important in mucosal integrity and repair. Profound suppression of gastric acid secretion has been shown to be effective in preventing NSAID-induced ulceration. There is a strong possibility that new NSAIDs entering the market will have greatly reduced toxicity in the gastrointestinal tract.

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