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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    Helicobacter pylori infection and UBT-13C values are associated with changes in body mass index in children and adults
    (2022) Bruera, Maria J.; Amezquita, Maria V.; Riquelme, Arnoldo J.; Serrano, Carolina A.; Harris, Paul R.
    Background: The urea breath test (UBT-13C) is a non-invasive technique that allows the diagnosis and confirmation of eradication of Helicobacter pylori infection. Aim: To evaluate H. pylori positivity and values of UBT-C-13 among infected Chilean children and adults, and to analyze its variation in relation to sex, nutritional status, and age of the patients. Material and Methods: Retrospective study of 1141 patients aged 6 to 94 years, with an indication for a UBT-C-13 either for diagnosis or for confirmation of eradication of H. pylori infection. C-13 enrichment was measured using an infrared spectrometer calculating the delta C-13 values before and after the ingestion of C-13 marked urea. The clinical data of the patients were obtained at the time of the examination. Results: We included 241 children and 900 adults. Infected children obtained lower UBT-C-13 delta values than infected adults (16.1 +/- 8.7 and 37 +/- 52.9, respectively). The rates of infection were higher in males who were recruited for diagnosis. Significant differences were obtained between positivity for H. pylori in overweight and obese children but not adults. UBT-C-13 titers were significantly associated with the body mass index (BMI) only in adults. Conclusions: H. pylori infection rates are similar between sexes and are higher in children probably because of selection bias. In children, H. pylori positivity is associated with higher BMI and excess malnutrition although with similar UBT-C-13 values. In adults, H. pylori infection is not related with BMI, but a higher BMI impacts UBT-C-13 titers.
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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.