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Article ; Online: Mesenchymal stem cells utilize CXCR4-SDF-1 signaling for acute, but not chronic, trafficking to gastric mucosal inflammation.

Stoicov, Calin / Li, Hanchen / Liu, Jian Hua / Houghton, JeanMarie

2013 Volume 58, Issue 9, Page(s) 2466–2477

Abstract: Background: Helicobacter infection is the main risk factor in developing gastric cancer. Mesenchymal stem cells (MSCs) are non-hematopoietic stromal cells, which are able to differentiate into different cell lineages. MSC contribute to cancer ... ...

Abstract	Background: Helicobacter infection is the main risk factor in developing gastric cancer. Mesenchymal stem cells (MSCs) are non-hematopoietic stromal cells, which are able to differentiate into different cell lineages. MSC contribute to cancer development by forming the tumor directly, contributing to the microenvironment, or by promoting angiogenesis and metastasis. CXCR4/SDF-1 axis is used by MSC in trafficking, homing, and engraftment at chronic inflammation sites, and plays an important role in tumorigenesis. Aim: To determine if CXCR4 receptor has a role in MSC contribution to the development of Helicobacter-mediated gastric cancer. Methods: SDF-1 and CXCR4 expression in mouse gastric mucosa in the setting of acute and chronic inflammation was measured using RT-PCR. Mouse culture-adapted MSC express CXCR4. Wild-type C57BL/6 mice infected with Helicobacter felis for 6 months or controls were given IV injections of CXCR4 knock-down MSC. Animals were followed for another 4 months. Homing of MSC in the stomach was quantified using RT-PCR. MSC differentiation into gastric epithelia lineages was analyzed using immunohistochemistry and fluorescent in situ hybridization. Results: CXCR4 and SDF-1 are both upregulated in the settings of Helicobacter-induced chronic gastric inflammation. CXCR4 is fully required for homing of MSC to the stomach in acute gastric inflammation, but only partially in Helicobacter-induced gastric cancer. MSC lead to gastric intraepithelial neoplasia as early as 10 months of Helicobacter infection. Conclusions: Our results show that MSC have a tumorigenic effect by promoting an accelerated form of gastric cancer in mice. The engraftment of MSC in chronic inflammation is only partially CXCR4-dependent.
MeSH term(s)	Animals ; Cell Differentiation ; Epithelial Cells/cytology ; Ethanol ; Gastritis/complications ; Gastritis/metabolism ; Gastritis/microbiology ; Helicobacter Infections/complications ; Helicobacter Infections/metabolism ; Helicobacter felis ; Male ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, CXCR4/metabolism ; Signal Transduction/physiology ; Stomach/pathology ; Stomach Neoplasms/etiology ; Stomach Neoplasms/metabolism ; Stomach Neoplasms/pathology
Chemical Substances	CXCR4 protein, mouse ; Receptors, CXCR4 ; Ethanol (3K9958V90M)
Language	English
Publishing date	2013-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	304250-9
ISSN	1573-2568 ; 0163-2116
ISSN (online)	1573-2568
ISSN	0163-2116
DOI	10.1007/s10620-013-2782-y
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Article ; Online: Evaluation of small bowel bleeding.

Singh, Anupam / Baptista, Veronica / Stoicov, Calin / Cave, David R

Current opinion in gastroenterology

2013 Volume 29, Issue 2, Page(s) 119–124

Abstract: Purpose of review: The review focuses on the latest techniques that are evolving in the management of small bowel bleeding.: Recent findings: Video capsule endoscopy has the highest yield of diagnosis when it is performed within 48 h of the bleeding ... ...

Abstract	Purpose of review: The review focuses on the latest techniques that are evolving in the management of small bowel bleeding. Recent findings: Video capsule endoscopy has the highest yield of diagnosis when it is performed within 48 h of the bleeding event (78 versus 48%). The pooled detection rate of double balloon endoscopy was noted to be 68.1% for obscure gastrointestinal bleeding according to a systematic review of 66 studies in the last 10 years. Also a recent review, which focused on analysis of 68 studies found that the procedural characteristics were comparable for double balloon, single balloon and spiral enteroscopy though the procedure time was fastest for the spiral enteroscopy group. Medical therapy for vascular lesions is in its infancy but shows promise. Summary: Advanced diagnostic and therapeutic endoscopic techniques are changing the paradigm of care for patients with small bowel bleeding.
MeSH term(s)	Capsule Endoscopy/methods ; Double-Balloon Enteroscopy/methods ; Endoscopy, Gastrointestinal/methods ; Endoscopy, Gastrointestinal/trends ; Gastrointestinal Hemorrhage/etiology ; Gastrointestinal Hemorrhage/surgery ; Humans ; Intestinal Diseases/diagnosis ; Intestinal Diseases/surgery ; Intestine, Small/pathology
Language	English
Publishing date	2013-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632571-3
ISSN	1531-7056 ; 0267-1379
ISSN (online)	1531-7056
ISSN	0267-1379
DOI	10.1097/MOG.0b013e32835bdc1a
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Article ; Online: Green tea inhibits Helicobacter growth in vivo and in vitro.

Stoicov, Calin / Saffari, Reza / Houghton, JeanMarie

International journal of antimicrobial agents

2009 Volume 33, Issue 5, Page(s) 473–478

Abstract: Helicobacter infection, one of the most common bacterial infections in man worldwide, is a type 1 carcinogen and the most important risk factor for gastric cancer. Helicobacter pylori bacterial factors, components of the host genetics and immune response, ...

Abstract	Helicobacter infection, one of the most common bacterial infections in man worldwide, is a type 1 carcinogen and the most important risk factor for gastric cancer. Helicobacter pylori bacterial factors, components of the host genetics and immune response, dietary cofactors and decreased acid secretion resulting in bacterial overgrowth are all considered important factors for induction of gastric cancer. Components found in green tea have been shown to inhibit bacterial growth, including the growth of Helicobacter spp. In this study, we assessed the bactericidal and/or bacteriostatic effect of green tea against Helicobacter felis and H. pylori in vitro and evaluated the effects of green tea on the development of Helicobacter-induced gastritis in an animal model. Our data clearly demonstrate profound growth effects of green tea against Helicobacter and, importantly, demonstrate that green tea consumption can prevent gastric mucosal inflammation if ingested prior to exposure to Helicobacter infection. Research in the area of natural food compounds and their effects on various disease states has gained increased acceptance in the past several years. Components within natural remedies such as green tea could be further used for prevention and treatment of Helicobacter-induced gastritis in humans.
MeSH term(s)	Animals ; Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/therapeutic use ; Gastric Mucosa/pathology ; Gastritis/prevention & control ; Helicobacter Infections/prevention & control ; Helicobacter felis/drug effects ; Helicobacter pylori/drug effects ; Humans ; Male ; Mice ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Tea/chemistry
Chemical Substances	Anti-Bacterial Agents ; Plant Extracts ; Tea
Language	English
Publishing date	2009-01-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1093977-5
ISSN	1872-7913 ; 0924-8579
ISSN (online)	1872-7913
ISSN	0924-8579
DOI	10.1016/j.ijantimicag.2008.10.032
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Zs.A 3368: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 500: Show issues

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Article ; Online: How the study of Helicobacter infection can contribute to the understanding of carcinoma development.

Stoicov, C / Li, H / Cerny, J / Houghton, J M

Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases

2009 Volume 15, Issue 9, Page(s) 813–822

Abstract: The inflammatory environment dramatically impacts the formation of cancer at many levels, acting on the stem cell to foster the initiation of cancer all the way through its contribution to metastatic disease. Using Helicobacter-induced gastric cancer as ... ...

Abstract	The inflammatory environment dramatically impacts the formation of cancer at many levels, acting on the stem cell to foster the initiation of cancer all the way through its contribution to metastatic disease. Using Helicobacter-induced gastric cancer as an example, it can be seen that, early on, chronic inflammation exhausts tissue stem cells, forcing the remaining stem cells to work overtime and calling in replacement cells from marrow sources. Marrow-derived stromal cells orchestrate growth and remodelling through secreted factors and cell-cell communication. Once cancer is present, the inflammatory environment is responsible for the continued growth signals to the cancer stem cells and to the stromal cells which become a vital part of the cancer niche as well as the pre-metastatic niche which will effectively lure cancer cells into peripheral organs for distant growth. This understanding of the inflammatory environment and its many effects on cancer throughout its natural history provides intervention targets directed at the unique aspects of cancer behaviour.
MeSH term(s)	Carcinoma/immunology ; Carcinoma/microbiology ; Helicobacter/pathogenicity ; Helicobacter Infections/complications ; Helicobacter Infections/immunology ; Helicobacter Infections/pathology ; Humans ; Inflammation/immunology ; Inflammation/pathology
Language	English
Publishing date	2009-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1328418-6
ISSN	1469-0691 ; 1470-9465 ; 1198-743X
ISSN (online)	1469-0691
ISSN	1470-9465 ; 1198-743X
DOI	10.1111/j.1469-0691.2009.02965.x
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Zs.A 4541: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 284: Show issues

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Article: Bone marrow cells as the origin of stomach cancer.

Stoicov, Calin / Li, Hanchen / Carlson, Jane / Houghton, Jeanmarie

Future oncology (London, England)

2005 Volume 1, Issue 6, Page(s) 851–862

Abstract: Cells derived from bone marrow are pluripotent, with the ability to differentiate into multiple cell types. Environmental cues dictate differentiation decisions. It should not be surprising then, that abnormal cell environments lead to abnormal ... ...

Abstract	Cells derived from bone marrow are pluripotent, with the ability to differentiate into multiple cell types. Environmental cues dictate differentiation decisions. It should not be surprising then, that abnormal cell environments lead to abnormal differentiation of these cells, and in some cases, malignant transformation. Identifying a role for bone marrow-derived cells in the initiation and progression of cancer allows a dramatic change in the way in which cancer is viewed. Identifying the cell responsible for initiating a tumor offers the exciting possibility of specifically targeting unique aspects of these cells and altering signaling properties for more effective therapeutic approaches.
MeSH term(s)	Animals ; Bone Marrow Cells/pathology ; Cell Differentiation ; Cell Transformation, Neoplastic ; Humans ; Stomach Neoplasms/pathology
Language	English
Publishing date	2005-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2274956-1
ISSN	1479-6694
ISSN	1479-6694
DOI	10.2217/14796694.1.6.851
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Zs.A 6478: Show issues

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Article: Stem cells and cancer: evidence for bone marrow stem cells in epithelial cancers.

Li, Han-Chen / Stoicov, Calin / Rogers, Arlin B / Houghton, JeanMarie

World journal of gastroenterology

2005 Volume 12, Issue 3, Page(s) 363–371

Abstract: Cancer commonly arises at the sites of chronic inflammation and infection. Although this association has long been recognized, the reason has remained unclear. Within the gastrointestinal tract, there are many examples of inflammatory conditions ... ...

Abstract	Cancer commonly arises at the sites of chronic inflammation and infection. Although this association has long been recognized, the reason has remained unclear. Within the gastrointestinal tract, there are many examples of inflammatory conditions associated with cancer, and these include reflux disease and Barrettos adenocarcinoma of the esophagus, Helicobacter infection and gastric cancer, inflammatory bowel disease and colorectal cancer and viral hepatitis leading to hepatocellular carcinoma. There are several mechanisms by which chronic inflammation has been postulated to lead to cancer which includes enhanced proliferation in an endless attempt to heal damage, the presence of a persistent inflammatory environment creating a pro-carcinogenic environment and more recently a role for engraftment of circulating marrow-derived stem cells which may contribute to the stromal components of the tumor as well as the tumor mass itself. Here we review the recent advances in our understanding of the contributions of circulating bone marrow-derived stem cells to the formation of tumors in animal models as well as in human beings.
MeSH term(s)	Animals ; Bone Marrow Cells/physiology ; Humans ; Inflammation ; Models, Theoretical ; Neoplasms, Glandular and Epithelial/pathology ; Neoplasms, Glandular and Epithelial/physiopathology ; Stem Cells/physiology
Language	English
Publishing date	2005-07-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v12.i3.363
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Article: Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells.

Li, Hanchen / Cai, Xun / Fan, Xueli / Moquin, Brian / Stoicov, Calin / Houghton, Jeanmarie

American journal of physiology. Gastrointestinal and liver physiology

2007 Volume 294, Issue 1, Page(s) G263–75

Abstract: When cells within the gastric mucosa progress from metaplasia to dysplasia to cancer, they acquire a Fas Ag apoptosis-resistant phenotype. It is unusual to completely abolish the pathway, suggesting other forms of Fas Ag signaling may be important or ... ...

Abstract	When cells within the gastric mucosa progress from metaplasia to dysplasia to cancer, they acquire a Fas Ag apoptosis-resistant phenotype. It is unusual to completely abolish the pathway, suggesting other forms of Fas Ag signaling may be important or even necessary for gastric cancer to progress. Little is known about alternate signaling of the Fas Ag pathway in gastric mucosal cells. Using a cell culture model of rat gastric mucosal cells, we show that gastric mucosal cells utilize a type II signaling pathway for apoptosis. Under conditions of low receptor stimulation or under conditions where apoptosis is blocked downstream of the death-inducing signal complex, Fas Ag signaling proceeds toward proliferative signaling. Under conditions favoring proliferative signaling, cFLIP is recruited to the Fas-associated death domain-like interleukin-1beta-converting enzyme at the death-inducing signal complex and activates ERK1/2. ERK1/2 in turn activates NF-kappaB. ERK1/2 stimulates proliferation, whereas NF-kappaB activation results in upregulation of the antiapoptotic protein survivin, further promoting proliferation over apoptosis. These results suggest that factors that inhibit apoptosis confer a growth advantage to the cells beyond the survival advantage of avoiding apoptosis and in effect convert the Fas Ag signaling pathway from a tumor suppressor to a tumor promoter.
MeSH term(s)	Animals ; Apoptosis ; CASP8 and FADD-Like Apoptosis Regulating Protein/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/immunology ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Death Domain Receptor Signaling Adaptor Proteins/metabolism ; Epithelial Cells/enzymology ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Fas Ligand Protein/metabolism ; Gastric Mucosa/enzymology ; Gastric Mucosa/immunology ; Gastric Mucosa/metabolism ; Gastric Mucosa/pathology ; Humans ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; NF-kappa B/metabolism ; Phosphorylation ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Time Factors ; Transfection ; fas Receptor/genetics ; fas Receptor/metabolism
Chemical Substances	CASP8 and FADD-Like Apoptosis Regulating Protein ; Death Domain Receptor Signaling Adaptor Proteins ; FASLG protein, human ; Fas Ligand Protein ; Faslg protein, rat ; NF-kappa B ; Recombinant Fusion Proteins ; fas Receptor ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; MAP Kinase Kinase Kinases (EC 2.7.11.25)
Language	English
Publishing date	2007-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00267.2007
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Article: Helicobacter felis eradication restores normal architecture and inhibits gastric cancer progression in C57BL/6 mice.

Cai, Xun / Carlson, Jane / Stoicov, Calin / Li, Hanchen / Wang, Timothy C / Houghton, JeanMarie

Gastroenterology

2005 Volume 128, Issue 7, Page(s) 1937–1952

Abstract: Background & aims: The impact of Helicobacter eradication therapy on the progression or regression of gastric lesions is poorly defined. This study examined the effects of eradication therapy on inflammation, atrophy, metaplasia, dysplasia, and cancer ... ...

Abstract	Background & aims: The impact of Helicobacter eradication therapy on the progression or regression of gastric lesions is poorly defined. This study examined the effects of eradication therapy on inflammation, atrophy, metaplasia, dysplasia, and cancer progression. Methods: C57BL/6 mice were infected with Helicobacter felis and received bacterial eradication therapy after 2, 6, or 12 months of infection. The gastric mucosa was examined at early, mid, and late intervals after eradication and graded for histology, expression pattern of alpha-catenin and beta-catenin, and IQGAP1. Results: Eradication of Helicobacter infection after 2 or 6 months of infection led to a regression of inflammation, restoration of parietal cell mass, and reestablishment of normal architecture. Progression to adenocarcinoma was prevented. Bacterial eradication at 1 year was associated with the reappearance of parietal cells, partial regression of inflammation, and restoration of architecture. Hyperplasia scores significantly improved, and dysplasia did not progress. Infected mice developed antral adenocarcinoma and gastric outlet obstruction by 24 months. Only 30% of the mice receiving bacterial eradication therapy at 12 months developed antral carcinoma. Bacterial eradication at any time during the first year of infection prevented death due to gastric outlet obstruction. The expression pattern of alpha-catenin, beta-catenin, and IQGAP1 varied with cell type and paralleled histologic changes. Conclusions: Inflammation, metaplasia, and dysplasia are reversible with early eradication therapy; progression of dysplasia was arrested with eradication therapy given as late as 1 year and prevented gastric cancer-related deaths.
MeSH term(s)	Adenocarcinoma/microbiology ; Adenocarcinoma/prevention & control ; Animals ; Anti-Bacterial Agents/therapeutic use ; Atrophy ; Disease Models, Animal ; Gastric Mucosa/immunology ; Gastric Mucosa/pathology ; Helicobacter Infections/complications ; Helicobacter Infections/drug therapy ; Helicobacter felis/pathogenicity ; Male ; Mice ; Mice, Inbred C57BL ; Precancerous Conditions/microbiology ; Precancerous Conditions/pathology ; Stomach Neoplasms/microbiology ; Stomach Neoplasms/prevention & control ; Tetracycline/therapeutic use
Chemical Substances	Anti-Bacterial Agents ; Tetracycline (F8VB5M810T)
Language	English
Publishing date	2005-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2005.02.066
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Ui V Zs.44: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: T-bet knockout prevents Helicobacter felis-induced gastric cancer.

Stoicov, Calin / Fan, Xueli / Liu, Jian Hua / Bowen, Glennice / Whary, Mark / Kurt-Jones, Evelyn / Houghton, JeanMarie

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 183, Issue 1, Page(s) 642–649

Abstract: Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk. Elevated TNF-alpha, IL-1beta, and low IL-10 are associated with the highest risk. In ... ...

Abstract	Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk. Elevated TNF-alpha, IL-1beta, and low IL-10 are associated with the highest risk. In this study, we used C57BL/6 mice to identify T-bet as a central regulator of the cytokine environment during Helicobacter felis infection. We infected male and female C57BL/6 and C57BL/6-T-bet knockout (KO) litter mates with H. felis and examined the bacterial colonization, immune response, and mucosal damage at varying time points. T-bet KO mice maintained infection for 15 mo at similar levels to wild-type mice. Infection and immune response did not differ between male and female mice. Despite sustained infection, T-bet KO mice respond with a blunted Th1 response associated with preservation of parietal and chief cells and protection from the development of gastric cancer. Unexpectedly, T-bet KO mice develop a gastric environment that would not be expected based on the phenotype of T-bet KO CD4 cells alone. T-bet KO mice respond to H. felis infection with a markedly blunted IL-1beta and TNF-alpha and elevated IL-10 levels. Activity of this one master regulator modulates the expression of the key gastric mucosal cytokines associated with gastric cancer and may be a target for therapy to restore immune balance clinically in patients at risk for gastric cancer.
MeSH term(s)	Adenocarcinoma/immunology ; Adenocarcinoma/microbiology ; Adenocarcinoma/prevention & control ; Animals ; Female ; Gastric Mucosa/immunology ; Gastric Mucosa/microbiology ; Gastric Mucosa/pathology ; Genetic Predisposition to Disease ; Helicobacter Infections/immunology ; Helicobacter Infections/pathology ; Helicobacter Infections/prevention & control ; Helicobacter felis/immunology ; Interleukin-1beta/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Stomach Neoplasms/immunology ; Stomach Neoplasms/microbiology ; Stomach Neoplasms/prevention & control ; T-Box Domain Proteins/deficiency ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/physiology ; Tumor Necrosis Factor-alpha/physiology
Chemical Substances	Interleukin-1beta ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2009-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.0900511
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Article: Major histocompatibility complex class II inhibits fas antigen-mediated gastric mucosal cell apoptosis through actin-dependent inhibition of receptor aggregation.

Stoicov, Calin / Cai, Xun / Li, Hanchen / Klucevsek, Kristine / Carlson, Jane / Saffari, Reza / Houghton, Jeanmarie

Infection and immunity

2005 Volume 73, Issue 10, Page(s) 6311–6321

Abstract: Escape from normal apoptotic controls is thought to be essential for the development of cancer. During Helicobacter pylori infection, the leading cause of gastric cancer, activation of the Fas antigen (Fas Ag) apoptotic pathway is responsible for early ... ...

Abstract	Escape from normal apoptotic controls is thought to be essential for the development of cancer. During Helicobacter pylori infection, the leading cause of gastric cancer, activation of the Fas antigen (Fas Ag) apoptotic pathway is responsible for early atrophy and tissue loss. As disease progresses, metaplastic and dysplastic glands arise which express Fas Ag but are resistant to apoptosis and are believed to be the precursor cells for adenocarcinoma. In this report, we show that one mechanism of acquired Fas resistance is inhibition of receptor aggregation via a major histocompatibility complex class II (MHCII)-mediated, actin-dependent mechanism. For these studies we used the well-described C57BL/6 mouse model of Helicobacter pylori and Helicobacter felis infection. Under normal conditions, Fas Ag is expressed at low levels, and MHCII expression on gastric mucosal cells is negligible. With infection and inflammation, both receptors are upregulated, and 6.1% of gastric mucosal cells express MHCII in combination with Fas Ag. Using the rat gastric mucosal cell line RGM-1 transfected with murine Fas Ag and MHCIIalphabeta chains, we demonstrate that MHCII prevents Fas receptor aggregation and inhibits Fas-mediated signaling through its effects on the actin cytoskeleton. Depolymerization of actin with cytochalasin D allows receptors to aggregate and restores Fas sensitivity. These findings offer one mechanism by which gastric mucosal cells acquire Fas resistance.
MeSH term(s)	Actins/metabolism ; Animals ; Apoptosis ; Cells, Cultured ; Cytochalasin D/pharmacology ; Gastric Mucosa/immunology ; Gastric Mucosa/microbiology ; Gastric Mucosa/pathology ; Helicobacter Infections/immunology ; Helicobacter Infections/metabolism ; Helicobacter Infections/pathology ; Helicobacter felis ; Helicobacter pylori ; Histocompatibility Antigens Class II/genetics ; Histocompatibility Antigens Class II/metabolism ; Interferon-gamma/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Rats ; Receptor Aggregation/drug effects ; Signal Transduction ; fas Receptor/genetics ; fas Receptor/metabolism
Chemical Substances	Actins ; Histocompatibility Antigens Class II ; fas Receptor ; Cytochalasin D (22144-77-0) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2005-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.73.10.6311-6321.2005
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito