scholarly journals The histamine H3 receptor agonistNα-methylhistamine produced byHelicobacter pylori does not alter somatostatin release from cultured rabbit fundic D-cells

Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 176-181 ◽  
Author(s):  
I L P Beales ◽  
J Calam
Keyword(s):  
Prolonged Exposure ◽  
Cell Function ◽  
Inhibitory Effects ◽  
Cell Content ◽  
Tnf Α ◽  
D Cell ◽  
D Cells ◽  
H Pylori ◽  
Factor Α ◽  
Dose Dependent

Background—The mechanisms underlying the suppression of somatostatin dependent reflexes in Helicobacter pylori infection are not fully determined. The H pyloriproduct Nα-methylhistamine and inflammatory mediators such as tumour necrosis factor-α (TNF-α) may be responsible for the alterations in somatostatin release.Aims—To examine the effect of Nα-methylhistamine on somatostatin release from cultured somatostatin-secreting D-cells.Methods—Rabbit fundic D-cells were obtained by collagenase-EDTA digestion and enriched by centrifugal elutriation and cultured for 40 hours. The effects ofNα-methylhistamine on somatostatin release soon after stimulation (two hours) and after more prolonged exposure (24 hours) were assessed.Results—Nα-Methylhistamine (1 nM–1 μM) had no effect on basal or carbachol or adrenaline stimulated release over two hours. Similarly with prolonged exposure no effect on somatostatin cell content or release was identified. In contrast, TNF-α (24 hours) led to a dose dependent fall in both somatostatin content and release.Conclusions—Nα-Methylhistamine had no direct inhibitory effects on D-cells, but TNF-α both significantly reduced the cellular content and inhibited release. Inflammatory cytokines, rather thanNα-methylhistamine, are therefore likely to be responsible for directly inhibiting D-cell function in H pylori infection.

scholarly journals Role of TNF-α-Inducing Protein Secreted by Helicobacter pylori as a Tumor Promoter in Gastric Cancer and Emerging Preventive Strategies

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 181
Author(s):  
Masami Suganuma ◽  
Tatsuro Watanabe ◽  
Eisaburo Sueoka ◽  
In Kyoung Lim ◽  
Hirota Fujiki
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cell Surface Receptor ◽  
Tumor Promoter ◽  
Cancer Development ◽  
Human Gastric Cancer ◽  
Tnf Α ◽  
Surface Receptor ◽  
H Pylori ◽  
Factor Α

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.

Dopaminergic suppression of pancreatic somatostatin secretion

1982 ◽  
Vol 101 (1) ◽  
pp. 56-61 ◽  
Author(s):  
Mitsuyasu Itoh ◽  
Brian L. Furman ◽  
John E. Gerich
Keyword(s):  
Pancreatic Islet ◽  
Cell Function ◽  
Potential Interaction ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist ◽  
Adrenergic Mechanism ◽  
D Cell ◽  
D Cells ◽  
Dopaminergic Antagonists

Abstract. To characterize dopaminergic influences on pancreatic islet D cell function and its potential interaction with islet A and B cell function, the effect of dopamine (0.5–100 μm) on immunoreactive somatostatin (IRS), insulin (IRI), and glucagon (IRG) release from rat islets incubated in vitro was studied. Dopamine significantly suppressed the release of IRS (P< 0.001) and IRI (P < 0.001) and augmented IRG release (P < 0.001). Maximum suppression of IRS and IRI release was evident at 20 μm dopamine with half-maximal suppression occurring at 0.5–1 μm. Maximal stimulation of IRG release was observed at 100 μm dopamine with a halfmaximal response occurring at 5–10 μm. Suppression of IRS secretion by dopamine (20 μm) was completely reversed by the dopaminergic antagonists haloperidol (5 μm) and pimozide (5 μm), but was only partially reversed by the alpha adrenergic antagonist phentolamine (2 μm), and was further suppressed by the beta adrenergic antagonist propranolol (2 μm). Suppression of IRI release by dopamine was completely reversed by propranolol, but was unaffected by haloperidol, pimozide, and phentolamine. There results indicate that dopamine directly affects pancreatic islet D cell function, and that islet B and D cells appear to be more sensitive to dopamine than are A cells. Dopamine suppresses IRS secretion predominantly through activation of dopaminergic receptors, whereas it suppresses IRI release through an alpha adrenergic mechanism and stimulates IRG release through a beta adrenergic mechanism.

scholarly journals GAS6 Inhibits Granulocyte Adhesion to Endothelial Cells

Blood ◽  
1998 ◽  
Vol 91 (7) ◽  
pp. 2334-2340
Author(s):  
Gian Carlo Avanzi ◽  
Margherita Gallicchio ◽  
Flavia Bottarel ◽  
Loretta Gammaitoni ◽  
Giuliana Cavalloni ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Platelet Activating Factor ◽  
Polymorphonuclear Cells ◽  
Vascular Endothelial ◽  
Tnf Α ◽  
High Concentrations ◽  
Adhesive Interactions ◽  
Factor Α ◽  
Dose Dependent

GAS6 is a ligand for the tyrosine kinase receptors Rse, Axl, and Mer, but its function is poorly understood. Previous studies reported that both GAS6 and Axl are expressed by vascular endothelial cells (EC), which play a key role in leukocyte extravasation into tissues during inflammation through adhesive interactions with these cells. The aim of this work was to evaluate the GAS6 effect on the adhesive function of EC. Treatment of EC with GAS6 significantly inhibited adhesion of polymorphonuclear cells (PMN) induced by phorbol 12-myristate 13-acetate (PMA), platelet-activating factor (PAF), thrombin, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), but not that induced by FMLP and IL-8. GAS6 did not affect adhesion to resting EC. Titration experiments showed that high concentrations of GAS6 were needed to inhibit PMN adhesion and that inhibition was dose-dependent at the concentration range of 0.1 to 1 μg/mL. One possibility was that high concentrations were needed to overwhelm the effect of endogenous GAS6 produced by EC. In line with this possibility, treatment of resting EC with soluble Axl significantly potentiated PMN adhesion. Analysis of localization of GAS6 by confocal microscopy and cytofluorimetric analysis showed that it is concentrated along the plasma membrane in resting EC and treatment with PAF induces depletion and/or redistribution of the molecule. These data suggest that GAS6 functions as a physiologic antiinflammatory agent produced by resting EC and depleted when proinflammatory stimuli turn on the proadhesive machinery of EC.

scholarly journals Standardization of Solvent Extracts from Onopordum acanthium Fruits by GC-MS, HPLC-UV/DAD, HPLC-TQMS and 1H-NMR and Evaluation of their Inhibitory Effects on the Expression of IL-8 and E-selectin in Immortalized Endothelial Cells (HUVECtert)

2014 ◽  
Vol 9 (7) ◽  
pp. 1934578X1400900
Author(s):  
Armond Daci ◽  
Markus Gold-Binder ◽  
Davide Garzon ◽  
Alessio Patea ◽  
Giangiacomo Beretta
Keyword(s):  
1H Nmr ◽  
1H Nmr Spectroscopy ◽  
Inhibitory Effects ◽  
Traditional Medicines ◽  
Inflammatory Agent ◽  
Onopordum Acanthium ◽  
Tnf Α ◽  
Study Support ◽  
Anti Inflammatory ◽  
Dose Dependent

In this work we have characterized and standardized the solvent extracts of the fruits of Onopordum acanthium, a plant widely distributed from Europe to Asia and used in different traditional medicines. Fruits were extracted with methanol (ME) and n-hexane (HE) and the extract compositions determined by GC-MS, HPLC-UV/DAD, HPLC-TQMS and 1H NMR spectroscopy. Anti-inflammatory activity (IL-8 and E-selectin, qPCR and ELISA) was investigated in HUVECtert cells stimulated with TNF-α and LPS. Arctiin and isochlorogenic acid were found in ME (87±2%, w/w, and 10.2±0.2%, w/w; 38.0±3.2 mg/gFRUITS and 3.5 ± 0.4 mg/gFRUITS) and (ii) paraffins in the HE (195.6 ± 5.6 mg/g). A dose dependent (from 15 to 40 μgME/mL corresponding to 20–75 μM arctiin) inhibition of E-selectin and of the induction of IL-8 was induced by LPS. The results of this study support the use of O. acanthium fruits in traditional medicine as an anti-inflammatory agent and for cancer prevention and treatment.

Epigallocatechin Gallate Modulates Cytokine Production by Bone Marrow-Derived Dendritic Cells Stimulated with Lipopolysaccharide or Muramyldipeptide, or Infected with Legionella pneumophila

2005 ◽  
Vol 230 (9) ◽  
pp. 645-651 ◽  
Author(s):  
James Rogers ◽  
Izabella Perkins ◽  
Alberto van Olphen ◽  
Nicholas Burdash ◽  
Thomas W. Klein ◽  
...  
Keyword(s):  
Legionella Pneumophila ◽  
Tumor Necrosis ◽  
Epigallocatechin Gallate ◽  
Dependent Manner ◽  
Enhanced Production ◽  
Tnf Α ◽  
Factor Α ◽  
Dose Dependent ◽  
Antimicrobial Immunity ◽  
Necrosis Factor

The primary polyphenol in green tea extract is the catechin epigallocatechin gallate (EGCG). Various studies have shown significant suppressive effects of catechin on mammalian cells, either tumor or normal cells, including lymphoid cells. Previous studies from this laboratory reported that EGCG has marked suppressive activity on murine macrophages infected with the intracellular bacterium Legionella pneumophila (Lp), an effect mediated by enhanced production of both tumor necrosis factor-α (TNF-α) and γ-interferon (IFN-γ). In the present study, primary murine bone marrow (BM)-derived dendritic cells (DCs), a phagocytic monocytic cell essential for innate immunity to intracellular microorganisms, such as Lp, were stimulated in vitro with the microbial stimulant lipopolysaccharide (LPS) from gram-negative bacteria, the cell wall component from gram-positive bacteria muramyldipeptide (MDP) or infected with Lp. Production of the T helper cell (Th1)-activating cytokine, interleukin-12 (IL-12) and the proinflammatory cytokine, tumor necrosis factor-α (TNF-α), produced mainly by phagocytic cells and important for antimicrobial immunity, was determined in cell culture supernatants by enzyme-linked immunosorbent assay (ELISA). Treatment of the cells with EGCG inhibited, in a dose-dependent manner, production of IL-12. In contrast, enhanced production of TNF-α occurred in a dose-dependent manner in the DC cultures stimulated with either soluble bacterial product or infected with Lp. Thus, the results of this study show that the EGCG catechin has a marked effect in modulating production of these immunoregulatory cytokines in stimulated DCs, which are important for antimicrobial immunity, especially innate immunity. Further studies are necessary to characterize the physiologic function of the effect of EGCG on TNF-α and IL-12 during Lp infection, and the mechanisms involved.

035. THE ROLE OF THE SERTOLI CELL IN REGULATING SPERMATOGENESIS, IMMUNE RESPONSES AND INFLAMMATORY DISEASE: MULTIPLE FUNCTIONS, COMMON MECHANISMS?

2009 ◽  
Vol 21 (9) ◽  
pp. 8
Author(s):  
M. P. Hedger ◽  
J. A. Muir ◽  
W. R. Winnall
Keyword(s):  
Sertoli Cell ◽  
Inflammatory Cytokines ◽  
Cell Function ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Tight Junction Formation ◽  
Interleukin 1Α ◽  
Factor Α ◽  
Necrosis Factor

There is increasing evidence that the Sertoli cell, in addition to modulating responses to direct antigenic challenges (eg. intratesticular allografts), is central to the response of the testis to inflammation and infection. Systemic inflammation exerts an inhibitory effect on spermatogenesis, which has been attributed to the effects of fever, vascular disturbances, or loss of androgenic support. However, recent studies point to more direct effects of inflammation on spermatogenesis. The discovery that Sertoli cells express Toll-like receptors (TLR), and react to TLR ligands by producing inflammatory cytokines and other mediators, provides a mechanism to account for this direct inhibition. Moreover, the pattern of cytokines produced by the Sertoli cell during inflammation is highly characteristic. For example, when stimulated with TLR ligands the Sertoli cell produces the pro-inflammatory cytokines, interleukin-1α (IL1α) and IL6, and the regulatory cytokine, activin A, but does not produce IL1β and tumour necrosis factor-α, which are major pro-inflammatory products of activated macrophages. The disruptive effects of inflammation on spermatogenesis may be attributed to the elevated production of these cytokines, all of which have stimulatory or inhibitory effects on germ cell mitosis, meiosis and apoptosis and Sertoli cell tight junction formation, In addition, activation of TLR/IL1 mediated inflammatory pathways in the Sertoli cell inhibits its ability to respond to its principal trophic hormone, follicle-stimulating hormone. Studies on the regulation of these interactions will further establish the role of the Sertoli cell in inflammation and infection. However, such studies also have important implications for normal Sertoli cell function, as TLRs can respond to endogenous ligands as well. Consequently, the Sertoli cell may be viewed as a sentinel cell, supporting and protecting spermatogenesis when conditions are optimal, but rapidly shutting down spermatogenesis in the presence of infection or illness. Intriguingly, these apparently disparate roles appear to involve common inflammation-related mechanisms.

scholarly journals Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains

Gut ◽  
1997 ◽  
Vol 41 (4) ◽  
pp. 442-451 ◽  
Author(s):  
Y Yamaoka ◽  
M Kita ◽  
T Kodama ◽  
N Sawai ◽  
K Kashima ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Expression Patterns ◽  
Mucosal Inflammation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Biopsy Specimens ◽  
Tnf Α ◽  
Polymerase Chain ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Background—Helicobacter pyloristrains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8.Aims—To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA).Patients and methods—In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1β, IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor α (TNF-α) in antral biopsy specimens were measured by ELISA.Results—Mucosal levels of IL-1β, IL-6, IL-8, and TNF-α were significantly higher in H pyloripositive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1β and IL-8 were significantly higher in specimens infected with cagApositive strains than in those infected with cagAnegative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1β (p<0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-α (p<0.0001).Conclusion—These findings suggest that the ability to induce cytokines differs among the strains;cagA+ strains induce various kinds of cytokines and may cause severe inflammation, whereascagA− strains induce IL-8 and IL-1β only weakly and may cause only mild inflammation. However, as most patients infected with the cagA+ strains have gastritis, these strains may not be equivalent to ulcerogenic strains.

scholarly journals Interleukin-6, Tumor Necrosis Factor-α, and High-sensitivity C-reactive Protein in Diabetic Patients with Helicobacter pylori in Kosovo

2020 ◽  
Vol 8 (B) ◽  
pp. 172-175
Author(s):  
Greta Begolli-Stavileci ◽  
Gramos Begolli ◽  
Luljeta Begolli
Keyword(s):  
Helicobacter Pylori ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Helicobacter pylori is a Gram-negative spiral-shaped bacterium that infects from 30% to 50% of the world’s population and it is one of the most important in dyspeptic syndrome causes of gastritis and peptic ulcer. H. pylori is one of the most common chronic bacterial infections especially in the development countries because the socioeconomic contribute to chronic disease. The infection induces an acute polymorphonuclear infiltration in the gastric mucosa. Infection with H. pylori has been epidemiologically linked to some extra digestive conditions, including ischemic heart disease, diabetes mellitus (DM), and others. The patients with DM are at risk for H. pylori infection, since they have coupled susceptibility of to a wide range of infections as a result of chronic elevation of blood glucose level and impairment of immune functions. Chronic inflammation is a risk factor for coronary heart disease, because inflammation, vascular injury and thrombosis are considered to cause atherosclerosis. The risk of cardiovascular events is associated with increased levels of the acute phase proteins, C-reactive protein (CRP), and pro-inflammatory cytokines. Interleukin 6 (IL-6), a major pro-inflammatory cytokine is produced in a variety of tissues, including activated leukocytes, adipocytes, and endothelial cells. CRP is the principal downstream mediator of the acute phase response and is primarily derived through IL-6-dependent hepatic biosynthesis. Tumor necrosis factor-α (TNF-α), as an important inflammatory factor, has been shown to play a central role in the pathogenesis of diabetes. CRP and IL-6 were determinant of risk for the development of type 2 DM in apparently healthy middle-aged women. Since the prevalence of infected persons with H. pylori in Kosovo is high, the aim of this study was the evaluation of cytokines (IL1, TNF-α) and CRP in diabetic type 2 patients with positive H. pylori.

scholarly journals Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

2021 ◽  
Author(s):  
Ghorbanali Rahimian ◽  
Milad Shahini Shams Abadi ◽  
Reza Ahmadi ◽  
Mohammedhadi Shafigh ◽  
Fatemeh Azadegan-Dehkordi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Treg Cells ◽  
Infected Group ◽  
Ulcer Disease ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

Comparison of SP-A and LPS effects on the THP-1 monocytic cell line

2000 ◽  
Vol 279 (1) ◽  
pp. L110-L117 ◽  
Author(s):  
Mingchen Song ◽  
David S. Phelps
Keyword(s):  
Protein A ◽  
Surfactant Protein ◽  
Polymyxin B ◽  
Inhibitory Effects ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Monocytic Cells ◽  
Similar Treatment ◽  
Tnf Α ◽  
Factor Α

Surfactant protein A (SP-A) increases production of proinflammatory cytokines by monocytic cells, including THP-1 cells, as does lipopolysaccharide (LPS). Herein we report differences in responses to these agents. First, polymyxin B inhibits the LPS response but not the SP-A response. Second, SP-A-induced increases in tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-8 are reduced by >60% if SP-A is preincubated with Survanta (200 μg/ml) for 15 min before addition to THP-1 cells. However, the LPS effects on TNF-α and IL-8 are inhibited by <20% and the effect on IL-1β by <50%. Third, at Survanta levels of 1 mg/ml, SP-A-induced responses are reduced by >90%, and although the inhibitory effects on LPS action increase, they still do not reach those seen with SP-A. Finally, we tested whether SP-A could induce tolerance as LPS does. Pretreatment of THP-1 cells with LPS inhibits their response to subsequent LPS treatment 24 h later, including TNF-α, IL-1β, and IL-8. Similar treatment with SP-A reduces TNF-α, but IL-1β and IL-8 are further increased by the second treatment with SP-A rather than inhibited as with LPS. Thus, whereas both SP-A and LPS stimulate cytokine production, their mechanisms differ with respect to inhibition by surfactant lipids and in ability to induce tolerance.

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