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  1. Home
  2. Browse by Author

Browsing by Author "Smith, Phillip D."

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    Brain angiogenesis inhibitor 1 is expressed by gastric phagocytes during infection with Helicobacter pylori and mediates the recognition and engulfment of human apoptotic gastric epithelial cells
    (2014) Das, Soumita; Sarkar, Arup; Ryan, Kieran A.; Fox, Sarah; Berger, Alice H.; Juncadella, Ignacio J.; Bimczok, Diane; Smythies, Lesley E.; Harris D., Paul R.; Ravichandran, Kodi S.; Crowe, Sheila E.; Smith, Phillip D.; Ernst, Peter B.
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    Different Strains of H. pylori Induce Tolerogenic Dendritic Cells in Children
    (2015) Serrano Honeyman, Carolina Andrea; Brawner, Kyle; Vera Cabezas, Macarena Alejandra; Hernández Vargas, Caroll Daffner; Villagran Torres, Andrea Alejandra; Smythies, Lesley E.; Smith, Phillip D.; Harris Diez Paul Richard
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    Eradication of Helicobacter pylori in Children Restores the Structure of the Gastric Bacterial Community to That of Noninfected Children
    (2019) Serrano Honeyman, Carolina; Pierre, Reinaldo; Van Der Pol, William J.; Morrow, Casey D.; Smith, Phillip D.; Harris D., Paul R.; Serrano Honeyman, Carolina; Pierre, Reinaldo; Van Der Pol, William J.; Morrow, Casey D.; Smith, Phillip D.; Harris D., Paul R.
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    Helicobacter pylori infection in children is associated with a mucosal T regulatory cell response and less severe gastritis than that of adults
    (2007) Wright, Shelton W.; Smythies, Lesley; Riera Cassorla, Francisca Paz; Espinoza Torres, Javiera Marcela; Novak, Lea; Schmitz, Julia; Lorenz, Robin G.; Serrano Honeyman, Carolina Andrea; Harris Diez, Paul Richard; Smith, Phillip D.
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    Helicobacter pylori infection induces a T regulatory response mediated by TGF-B and IL-10 in children, in contrast to the TH1 response characterized by IFN-G observed in adults
    (2006) Smythies, Lesley; Harris Diez, Paul Richard; Clements, Ronald H.; Mosteller-Barnum, Lisa M.; Perez-Perez, Guillermo; Smith, Phillip D.
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    Human intestinal stromal cells promote homeostasis in normal mucosa but inflammation in Crohn's disease in a retinoic acid-deficient manner
    (2024) Smythies, Lesley E.; Belyaeva, Olga V.; Alexander, Katie L.; Bimczok, Diane; Nick, Heidi J.; Serrano, Carolina A.; Huff, Kayci R.; Nearing, Marie; Musgrove, Lois; Poovey, Emily H.; Garth, Jaleesa; Russ, Kirk; Baig, Kondal R. K. K.; Crossman, David K.; Peter, Shajan; Cannon, Jamie A.; Elson, Charles O.; Kedishvili, Natalia Y.; Smith, Phillip D.
    Intestinal stromal cells (SCs), which synthesize the extracellular matrix that gives the mucosa its structure, are newly appreciated to play a role in mucosal inflammation. Here, we show that human intestinal vimentin+CD90+smooth muscle actin- SCs synthesize retinoic acid (RA) at levels equivalent to intestinal epithelial cells, a function in the human intestine previously attributed exclusively to epithelial cells. Crohn's disease SCs (Crohn's SCs), however, synthesized markedly less RA than SCs from healthy intestine (normal SCs). We also show that microbe-stimulated Crohn's SCs, which are more inflammatory than stimulated normal SCs, induced less RA-regulated differentiation of mucosal dendritic cells (DCs) (circulating pre-DCs and monocyte-derived DCs), leading to the generation of more potent inflammatory interferon-gamma hi/interleukin-17hi T cells than normal SCs. Explaining these results, Crohn's SCs expressed more DHRS3, a retinaldehyde reductase that inhibits retinol conversion to retinal and, thus, synthesized less RA than normal SCs. These findings uncover a microbe-SC-DC crosstalk in which luminal microbes induce Crohn's disease SCs to initiate and perpetuate inflammation through impaired synthesis of RA.
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    Interactions between H. pylori and the gastric microbiome: impact on gastric homeostasis and disease
    (ELSEVIER, 2021) Serrano Honeyman, Carolina Andrea; Harris Diez, Paul Richard; Smith, Phillip D.; Bimczok, Diane
    Like many seemingly inhospitable environments on our planet, the highly acidic human stomach harbors a diverse bacterial microflora. The best-known member of the human gastric flora, Helicobacter pylori, causes a number of gastric diseases, including peptic ulcer disease and gastric adenocarcinoma. In the absence of H. pylori infection, the gastric microbiota displays some features similar to the oral cavity with Firmicutes the most common phylum, followed by Proteobacteria and Bacteroidetes. When present, H. pylori dominates the gastric microbiome and reduces diversity and composition of other taxa. The composition of the gastric microbiome also is altered in the setting of proton pump inhibitor therapy and gastric neoplasia. This review summarizes foundational and recent studies that have investigated the composition of the human gastric microbiome in a variety of patient groups, with a focus on potential mechanisms involved in regulation of gastric microbial community structure.

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