Antigens, Bacterial

Publication Title: 
Toxins

Tumor endothelium marker-8 (TEM8) and capillary morphogenesis protein-2 (CMG2) are the two well-characterized anthrax toxin receptors, each containing a von Willebrand factor A (vWA) domain responsible for anthrax protective antigen (PA) binding. Recently, a cell-based analysis was used to implicate another vWA domain-containing protein, integrin ?1 as a third anthrax toxin receptor. To explore whether proteins other than TEM8 and CMG2 function as anthrax toxin receptors in vivo, we challenged mice lacking TEM8 and/or CMG2.

Author(s): 
Liu, Shihui
Zhang, Yi
Hoover, Benjamin
Leppla, Stephen H.
Publication Title: 
Infection and Immunity

Incubation of mammalian tumor cells with either soluble of insoluble fractions (10 to 100 micrograms/ml) of Fusobacterium nucleatum sensitizes them to the destructive activity of antibody-dependent cellular cytotoxicity (ADCC) effector cells in the presence of anti-F. nucleatum antisera. All three types of ADCC effector cells are capable of destroying F. nucleatum-sensitized target cells with varying degrees of effectiveness (lymphocytes much greater than monocytes greater than neutrophils). Hyperimmune rabbit anti-F. nucleatum antisera were active at a dilution as high as 1/100,000.

Author(s): 
Lopatin, D. E.
Blackburn, E.
Publication Title: 
Anticancer Research

BACKGROUND: Ginger root (Zingiber officinale) has been used traditionally for the treatment of gastrointestinal ailments such as motion sickness, dyspepsia and hyperemesis gravidarum, and is also reported to have chemopreventative activity in animal models. The gingerols are a group of structurally related polyphenolic compounds isolated from ginger and known to be the active constituents.

Author(s): 
Mahady, Gail B.
Pendland, Susan L.
Yun, Gina S.
Lu, Zhi-Zhen
Stoia, Adina
Publication Title: 
American Journal of Physiology. Gastrointestinal and Liver Physiology

P-glycoprotein, the product of the multidrug resistance protein 1 (MDR1) gene, is a xenobiotic transporter that may contribute to the physiology of the intestinal barrier. Twenty-five percent of mdr1a-deficient (mdr1a(-/-)) mice spontaneously develop colitis at variable ages when maintained under specific pathogen-free conditions. We hypothesized that this disease would result from epithelial dysfunction and that conventional housing would increase incidence and severity of the colitis phenotype. Wild-type congenic FVB (+/+) mice were maintained under the same conditions as controls.

Author(s): 
Resta-Lenert, Silvia
Smitham, Jane
Barrett, Kim E.
Publication Title: 
Clinical Microbiology Reviews

Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide. Once H. pylori colonizes the gastric environment, it persists for the lifetime of the host, suggesting that the host immune response is ineffective in clearing this bacterium.

Author(s): 
Wroblewski, Lydia E.
Peek, Richard M.
Wilson, Keith T.
Publication Title: 
PloS One

Helicobacter pylori infects half the world's population, and carriage is lifelong without antibiotic therapy. Current regimens prescribed to prevent infection-associated diseases such as gastroduodenal ulcers and gastric cancer can be thwarted by antibiotic resistance. We reported that administration of 1% D,L-α-difluoromethylornithine (DFMO) to mice infected with H. pylori reduces gastritis and colonization, which we attributed to enhanced host immune response due to inhibition of macrophage ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis.

Author(s): 
Barry, Daniel P.
Asim, Mohammad
Leiman, David A.
de Sablet, Thibaut
Singh, Kshipra
Casero, Robert A.
Chaturvedi, Rupesh
Wilson, Keith T.
Publication Title: 
Gastroenterology

BACKGROUND & AIMS: Helicobacter pylori-induced gastric carcinogenesis has been linked to the microbial oncoprotein cytotoxin-associated gene A (CagA). Spermine oxidase (SMO) metabolizes the polyamine spermine into spermidine and generates H(2)O(2), which causes apoptosis and DNA damage. We determined if pathogenic effects of CagA are attributable to SMO.

Author(s): 
Chaturvedi, Rupesh
Asim, Mohammad
Romero-Gallo, Judith
Barry, Daniel P.
Hoge, Svea
de Sablet, Thibaut
Delgado, Alberto G.
Wroblewski, Lydia E.
Piazuelo, M. Blanca
Yan, Fang
Israel, Dawn A.
Casero, Robert A.
Correa, Pelayo
Gobert, Alain P.
Polk, D. Brent
Peek, Richard M.
Wilson, Keith T.
Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

A strong cellular cross-talk exists between the pathogen Helicobacter pylori and high-output NO production. However, how NO and H. pylori interact to signal in gastric epithelial cells and modulate the innate immune response is unknown. We show that chemical or cellular sources of NO induce the anti-inflammatory effector heme oxygenase-1 (HO-1) in gastric epithelial cells through a pathway that requires NF-κB. However, H. pylori decreases NO-induced NF-κB activation, thereby inhibiting HO-1 expression. This inhibitory effect of H.

Author(s): 
Gobert, Alain P.
Asim, Mohammad
Piazuelo, M. Blanca
Verriere, Thomas
Scull, Brooks P.
de Sablet, Thibaut
Glumac, Ashley
Lewis, Nuruddeen D.
Correa, Pelayo
Peek, Richard M.
Chaturvedi, Rupesh
Wilson, Keith T.
Publication Title: 
Gut Microbes

We have recently reported that Helicobacter pylori strains expressing the virulence factor cytotoxin-associated gene A (CagA) stimulate increased levels of spermine oxidase (SMO) in gastric epithelial cells, while cagA⁻ strains did not. SMO catabolizes the polyamine spermine and produces H₂O₂ that results in both apoptosis and DNA damage. Exogenous overexpression of CagA confirmed these findings, and knockdown or inhibition of SMO blocked CagA-mediated apoptosis and DNA damage.

Author(s): 
Chaturvedi, Rupesh
de Sablet, Thibaut
Peek, Richard M.
Wilson, Keith T.
Publication Title: 
Cellular Microbiology

The cytotoxin-associated gene A protein (CagA) plays a pivotal role in the aetiology of Helicobacter pylori-associated gastric diseases. CagA is injected into the cytoplasm of host cells by a type IV secretion system, and is phosphorylated on tyrosine residues by the host enzyme c-Src. We previously reported that the enzyme haem oxygenase-1 (HO-1) inhibits IL-8 secretion by H. pylori-infected cells. However, the cellular mechanism by which HO-1 regulates the innate immune function of infected cells remains unknown.

Author(s): 
Gobert, Alain P.
Verriere, Thomas
de Sablet, Thibaut
Peek, Richard M.
Chaturvedi, Rupesh
Wilson, Keith T.

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