Browsing by Author "Serrano, Carolina A."

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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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    Inverse correlation between allergy markers and Helicobacter pylori infection in children is associated with elevated levels of TGF-beta
    (LIPPINCOTT WILLIAMS & WILKINS, 2011) Serrano, Carolina A.; Talesnik, Eduardo; Pena, Alfredo; Rollan, Antonio; Duarte, Ignacio; Torres, Javiera; Majerson, Daniela; Einisman, Helly; Viviani, Paola; Harris, Paul R.
    Objectives We evaluated allergy/hypersensitivity clinical markers and their correlation with Helicobactor pylori infection in children and adults to analyze how early acquisition of H. pylori could modulate allergic disorder expression.
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    Lack of Diagnostic Utility of Specific Immunoglobulin M in Helicobacter pylori Infection in Children
    (LIPPINCOTT WILLIAMS & WILKINS, 2008) Serrano, Carolina A.; Gonzalez, Carmen G.; Rollan, Antonio R.; Duarte, Ignacio; Torres, Javiera; Pena, Alfredo J.; Harris, Paul R.
    Background: Helicobacter pylori infection results in ill a systemic immune response characterized by the initial rise of immunoglobulin (Ig) M followed by the elevation of IgG and IgA-specific antibody levels in serum. Age and regional considerations may modify the accuracy of serological tests.
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    Maternal H. pylori is associated with differential fecal microbiota in infants born by vaginal delivery
    (2020) Hernández, Caroll D.; Shin, Hakdong; Troncoso, Paula A.; Vera, Macarena H.; Villagran, Andrea A.; Rodríguez-Rivera, Selena M.; Ortiz, Marlene A.; Serrano, Carolina A.; Borzutzky Schachter, Arturo; Domínguez-Bello, María Gloria; Harris, Paul R.
    Helicobacter pylori colonization may affect the mucosal immune system through modification of microbiota composition and their interactions with the host. We hypothesized that maternal H. pylori status affects the maternal intestinal microbiota of both mother and newborn. In this study, we determine the structure of the fecal microbiota in mothers and neonates according to maternal H. pylori status and delivery mode. We included 22 mothers and H. pylori infection was determined by fecal antigen test. Eleven mothers (50%) were H. pylori-positive (7 delivering vaginally and 4 by C-section), and 11 were negative (6 delivering vaginally and 5 by C-section). Stool samples were obtained from mothers and infants and the fecal DNA was sequenced. The fecal microbiota from mothers and their babies differed by the maternal H. pylori status, only in vaginal birth, not in C-section delivery. All 22 infants tested negative for fecal H. pylori at 15 days of age, but those born vaginally –and not those by C-section- showed differences in the infant microbiota by maternal H. pylori status (PERMANOVA, p = 0.01), with higher abundance of Enterobacteriaceae and Veillonella, in those born to H. pylori-positive mothers. In conclusion, the structure of the infant fecal microbiota is affected by the maternal H. pylori status only in infants born vaginally, suggesting that the effect could be mediated by labor and birth exposures.