Macrophages infiltrating the tissue in chronic pancreatitis express the chemokine receptor CCR5

Goecke, Helmuth; Forssmann, Ulf; Uguccioni, Mariagrazia; Frieß, Helmut; Conejo-Garcia, José R.; Zimmermann, Arthur; Baggiolini, Marco; Büchler, Markus W.

doi:10.1067/msy.2000.108613

Cited by 63 publications

(46 citation statements)

References 38 publications

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“…Inflammatory pancreatitis is believed to be a risk factor for pancreatic cancer (4). 6 Cytokines, chemokines and their receptors have varied biological functions including inflammatory response, immune-cell trafficking, angiogenesis, and metastasis. Most pancreatic tumors are characterized by intense desmoplasia (5), and there is evidence that proinflammatory cytokines, chemokines, and their receptors are expressed in pancreatic cells and infiltrating immune cells within inflamed pancreatic tissues (6).…”

Section: Introductionmentioning

confidence: 99%

“…6 Cytokines, chemokines and their receptors have varied biological functions including inflammatory response, immune-cell trafficking, angiogenesis, and metastasis. Most pancreatic tumors are characterized by intense desmoplasia (5), and there is evidence that proinflammatory cytokines, chemokines, and their receptors are expressed in pancreatic cells and infiltrating immune cells within inflamed pancreatic tissues (6). A number of studies have implicated these molecules as playing a role in pancreatitis progression and tumor development (3,(6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inflammation, Genetic Polymorphisms in Proinflammatory Genes TNF-A, RANTES, and CCR5, and Risk of Pancreatic Adenocarcinoma

Duell

Casella

Burk

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

101

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Adenocarcinoma of the exocrine pancreas is the fourth leading cause of cancer-related death in men and women in the U.S. Cytokines and other proinflammatory mediators have been implicated in inflammatory pancreatic diseases including pancreatitis and cancer. We analyzed cytokine gene polymorphisms as risk factors for pancreatic cancer using questionnaire data obtained by in-person interviews and germ line DNA collected in a population-based case-control study of pancreatic cancer (532 cases and 1,701 controls) conducted in the San Francisco Bay Area. We used mass spectrometry and gel-based methods to genotype 308 cases and 964 population-based controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression analysis and included adjustment for age, sex, and smoking. We assessed potential interactions between these polymorphisms, proinflammatory conditions (e.g., pancreatitis, ulcer, and obesity), and smoking as risk factors for pancreatic cancer. There was no overall association between pancreatic cancer risk and tumor necrosis factor-A (TNF-A À308G/A), regulated upon activation, normally T cellexpressed, and presumably secreted (RANTES À403G/A), and CC chemokine receptor 5 (CCR5-D32) polymorphisms. There was a nearly 7-fold increased relative risk estimate for pancreatic cancer in individuals with a history of pancreatitis (adjusted OR, 6.9; 95% CI, 3.4-14.1). Among patients with pancreatic cancer, pancreatitis was significantly associated with TNF-A À308 GA + AA (OR, 3.1; 95% CI, 1.3-7.4) and with RANTES À403 GA + AA (OR, 2.3; 95% CI, 1.0-5.4). There was evidence for a possible interaction between current active smoking and CCR5-32del. Our results lend support for the hypothesis that proinflammatory gene polymorphisms, in combination with proinflammatory conditions, may influence the development of pancreatic cancer.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inflammation, Genetic Polymorphisms in Proinflammatory Genes TNF-A, RANTES, and CCR5, and Risk of Pancreatic Adenocarcinoma

Duell

Casella

Burk

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

101

View full text Add to dashboard Cite

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“…Similar to acute pancreatitis, CXCR2 inhibition had a protective effect in experimental chronic pancreatitis (86). Significant increase in CCR5 and its chemokine ligands CCL5 and CCL3 mRNA in the pancreas was evident in patients with chronic pancreatitis (29). Moreover, the majority of the CCR5-positive cells by immunostaining were CD68-positive, suggesting a role for CCR5 in monocyte/macrophage recruitment in chronic pancreatitis.…”

Section: Mediators For Immune Cell Recruitmentmentioning

confidence: 77%

“…Alternatively activated macrophages are abundant in chronic pancreatitis especially in the vicinity of the fibrosis and activated PSCs (29,98). Differences in inflammatory infiltrates with increase in lymphocytes and macrophages as well as dendritic cells around the ducts were reported in non-alcohol-versus alcohol-related chronic pancreatitis pathologies (20).…”

Section: Chronic Pancreatitismentioning

confidence: 99%

Immune modulation in acute and chronic pancreatitis

Habtezion¹

The Pancreapedia: Exocrine Pancreas Knowledge Base

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“…The cell signaling mechanism mediating this effect will be discussed in the subsequent section of this review. Other less common mutations associated with pancreatic cancer include p53, BRaf, Mek and Cox2, and deletion of SMAD4 and p16INK4A (44).…”

Section: Smoking and Genetic Mutationsmentioning

confidence: 99%

Smoking induced pancreatitis and pancreatic cancer

Edderkaoui¹

The Pancreapedia: Exocrine Pancreas Knowledge Base

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Abstract:Acute pancreatitis, chronic pancreatitis, and pancreatic cancer are three major pancreatic diseases without any effective treatment. In this character, the latest knowledge regarding the association between these diseases and tobacco smoking is reviewed. Clinical evidence of the association is presented, followed by an overview of scientific evidence, and the potential pathways that mediate smoking-induced pancreatitis and pancreatic cancer.

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Macrophages infiltrating the tissue in chronic pancreatitis express the chemokine receptor CCR5

Cited by 63 publications

References 38 publications

Inflammation, Genetic Polymorphisms in Proinflammatory Genes TNF-A, RANTES, and CCR5, and Risk of Pancreatic Adenocarcinoma

Inflammation, Genetic Polymorphisms in Proinflammatory Genes TNF-A, RANTES, and CCR5, and Risk of Pancreatic Adenocarcinoma

Immune modulation in acute and chronic pancreatitis

Smoking induced pancreatitis and pancreatic cancer

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