Partial Protection against<i>Helicobacter pylori</i>in the Absence of Mast Cells in Mice

Ding, Hua; Nedrud, John G.; Wershil, Barry K.; Redline, Raymond W.; Blanchard, Thomas G.; Czinn, Steven J.

doi:10.1128/iai.00532-09

Cited by 16 publications

(18 citation statements)

References 39 publications

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“…pylori stomach infection and histopathology. An in vivo H. pylori gastric infection model system has been previously described (13,14,17,18). In this system, colonization efficiency is routinely Ͼ90% as determined by the percent of infected animals from which H. pylori can be recovered, either as viable bacteria and by testing for bacterial urease, oxidase, and catalase activities to confirm their identity as H. pylori, or by real-time RT-PCR for bacterial gene sequences (e.g., urease C).…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, mice were infected by gastric intubation on two consecutive days with 0.5 ml of log phase cultures of H. pylori strain SS1 (14) at 1.0 ϫ 10 7 colony forming units/animal as described (18). Mice were killed by intraperitoneal pentobarbital injection at 4 wk postinfection, the time of maximal neutrophil infiltration of the gastric mucosa using our in vivo infection model system (14). Stomach strips were fixed in K-2 fixative (2.0% paraformaldehyde, 2.5% glutaraldehyde, 0.1 M sodium cacodylate buffer, 0.025% CaCl 2), and the fixative was replaced with 0.1 M sodium cacodylate buffer (4°C) containing sodium azide (pH 7.35 to 7.40) (14).…”

Section: Methodsmentioning

confidence: 99%

“…H. pylori strain 26695 (51) was maintained on Columbia blood agar containing 7% defibrinated horse blood (Cleveland Scientific, Bath, OH), 20 g/ml bacitracin, 20 g/ml trimethoprim, 16 g/ml cefsulodin, 6.0 g/ml vancomycin, and 2.5 g/ml fungizone (Sigma) under microaerophilic conditions as described (14). For treatment of AGS cells, bacteria were grown in static liquid cultures of Brucella broth (Difco, Detroit, MI) containing 10% heat inactivated FBS and antibiotics at 37°C with 10% CO 2.…”

Section: Methodsmentioning

confidence: 99%

“…Mice were killed by intraperitoneal pentobarbital injection at 4 wk postinfection, the time of maximal neutrophil infiltration of the gastric mucosa using our in vivo infection model system (14). Stomach strips were fixed in K-2 fixative (2.0% paraformaldehyde, 2.5% glutaraldehyde, 0.1 M sodium cacodylate buffer, 0.025% CaCl 2), and the fixative was replaced with 0.1 M sodium cacodylate buffer (4°C) containing sodium azide (pH 7.35 to 7.40) (14). Tissues were paraffin embedded and sectioned for analysis by Giemsa staining.…”

Section: Methodsmentioning

confidence: 99%

“…Tissue sections were Giemsa stained and the numbers of neutrophils were quantified in a blinded fashion as described (14). Each group contained 4 to 6 mice.…”

Section: A: Muc1mentioning

confidence: 99%

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Suppression of IL-8 production in gastric epithelial cells by MUC1 mucin and peroxisome proliferator-associated receptor-γ

Park

Guang

Blanchard

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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MUC1 is a membrane-tethered mucin expressed on the apical surface of epithelial cells. Our previous report (Guang W, Ding H, Czinn SJ, Kim KC, Blanchard TG, Lillehoj EP. J Biol Chem 285: 20547–20557, 2010) demonstrated that expression of MUC1 in AGS gastric epithelial cells limits Helicobacter pylori infection and reduces bacterial-driven IL-8 production. In this study, we identified the peroxisome proliferator-associated receptor-γ (PPARγ) upstream of MUC1 in the anti-inflammatory pathway suppressing H. pylori- and phorbol 12-myristate 13-acetate (PMA)-stimulated IL-8 production. Treatment of AGS cells with H. pylori or PMA increased IL-8 levels in cell culture supernatants compared with cells treated with the respective vehicle controls. Prior small interfering (si)RNA-induced MUC1 silencing further increased H. pylori - and PMA-stimulated IL-8 levels compared with a negative control siRNA. MUC1-expressing AGS cells pretreated with the PPARγ agonist troglitazone (TGN) had reduced H. pylori - and PMA-stimulated IL-8 levels compared with cells treated with H. pylori or PMA alone. However, following MUC1 siRNA knockdown, no differences in IL-8 levels were seen between TGN/ H. pylori and H. pylori -only cells or between TGN/PMA and PMA-only cells. Finally, TGN-treated AGS cells had increased Muc1 promoter activity, as measured using a Muc1-luciferase reporter gene, and greater MUC1 protein levels by Western blot analysis, compared with vehicle controls. These results support the hypothesis that PPARγ stimulates MUC1 expression by AGS cells, thereby attenuating H. pylori - and PMA-induced IL-8 production.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Tissue sections were Giemsa stained and the numbers of neutrophils were quantified in a blinded fashion as described (14). Each group contained 4 to 6 mice.…”

Section: A: Muc1mentioning

confidence: 99%

See 3 more Smart Citations

Suppression of IL-8 production in gastric epithelial cells by MUC1 mucin and peroxisome proliferator-associated receptor-γ

Park

Guang

Blanchard

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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The Mast Cell in Innate and Adaptive Immunity

Shelburne

Abraham

2011

Mast Cell Biology

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Mast cells (MCs) were once considered only as effector cells in pathogenic IgE- and IgG-mediated responses such as allergy. However, developments over the last 15 years have suggested that MCs have evolved in vertebrates as beneficial effector cells that are involved in the very first inflammatory responses generated during infection. This pro-inflammatory environment has been demonstrated to be important for initiating innate responses in many different models of infection and more recently, in the development of adaptive immunity as well. Interestingly this latter finding has led to the discovery that small MC-activating compounds can behave as adjuvants in vaccine formulations. Thus, our continued understanding of the MC in the context of infectious disease is likely to not only expand our scope of the MC in the normal processes of immunity, but provide new therapeutic targets to combat disease.

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Vaccination Against Helicobacter pylori Infection

Raghavan

Quiding‐Järbrink

2016

Helicobacter Pylori Research

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Partial Protection againstHelicobacter pyloriin the Absence of Mast Cells in Mice

Cited by 16 publications

References 39 publications

Suppression of IL-8 production in gastric epithelial cells by MUC1 mucin and peroxisome proliferator-associated receptor-γ

Suppression of IL-8 production in gastric epithelial cells by MUC1 mucin and peroxisome proliferator-associated receptor-γ

The Mast Cell in Innate and Adaptive Immunity

Vaccination Against Helicobacter pylori Infection

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