Elisabeth Hultgren-Hörnquist
Örebro University
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Publication
Featured researches published by Elisabeth Hultgren-Hörnquist.
Alimentary Pharmacology & Therapeutics | 2015
Ignacio Rangel; Susana Fuentes; Heikamp-de Jong; Elisabeth Hultgren-Hörnquist; W.M. de Vos; Robert-Jan M. Brummer
A subset of irritable bowel syndrome (IBS) patients, denoted post‐infectious IBS (PI‐IBS), develop symptoms after an enteric infection. Bacterial dysbiosis and mucosal inflammation have been proposed to be involved in the pathophysiology of this entity.
Scandinavian Journal of Gastroenterology | 2014
Ignacio Rangel; Ashok Kumar Kumawat; Elisabeth Hultgren-Hörnquist; Robert J. Brummer
Abstract Background. Irritable bowel syndrome (IBS) is characterized by chronic abdominal symptoms such as pain, discomfort, and altered bowel habits. A subset of IBS patients, denoted as post-infectious IBS (PI-IBS) patients, develop symptoms after an enteric infection. Distinct abnormalities in the gut mucosa, including mucosal inflammation, have been proposed to contribute to or be the cause of PI-IBS. This study investigated lymphocyte subsets in PI-IBS patients compared to healthy controls. Materials and methods. Ten PI-IBS patients and nine healthy controls participated. All PI-IBS patients met the Rome III diagnostic criteria for IBS and reported sustained symptoms at least 1 year after an episode of acute gastroenteritis. Intraepithelial lymphocytes and lamina propria lymphocytes (LPLs), isolated from mucosal tissue samples, were stained and analyzed for a comprehensive set of cell markers using flow cytometry. Results. The number of LPLs in PI-IBS was significantly increased compared to those in healthy controls (p < 0.05). PI-IBS patients showed significantly increased proportions of CD45RO+ CD4+ activated/memory T cells (p < 0.05) and double-positive CD4+ CD8+ cells (p < 0.05), respectively, in the lamina propria. The number of CD19+ LPLs was decreased in PI-IBS patients compared to healthy controls (p < 0.001). Conclusion. This study presents new evidence that PI-IBS is associated with a sustained aberrant mucosal immune response and support future studies of anti-inflammatory or immune-modulating treatments in these patients.
PLOS ONE | 2012
K. Elgbratt; Andreas Jansson; Elisabeth Hultgren-Hörnquist
Mice deficient for the G protein subunit Gαi2 spontaneously develop colitis, a chronic inflammatory disease associated with dysregulated T cell responses. We and others have previously demonstrated a thymic involution in these mice and an aberrant thymocyte dynamics. The Gαi2−/− mice have a dramatically reduced fraction of double positive thymocytes and an increased fraction of single positive (SP) thymocytes. In this study, we quantify a number of critical parameters in order to narrow down the underlying mechanisms that cause the dynamical changes of the thymocyte development in the Gαi2−/− mice. Our data suggest that the increased fraction of SP thymocytes results only from a decreased number of DP thymocytes, since the number of SP thymocytes in the Gαi2−/− mice is comparable to the control littermates. By measuring the frequency of T cell receptor excision circles (TRECs) in the thymocytes, we demonstrate that the number of cell divisions the Gαi2−/− SP thymocytes undergo is comparable to SP thymocytes from control littermates. In addition, our data show that the mature SP CD4+ and CD8+ thymocytes divide to the same extent before they egress from the thymus. By estimating the number of peripheral TREC+ T lymphocytes and their death rate, we could calculate the daily egression of thymocytes. Gαi2−/− mice with no/mild and moderate colitis were found to have a slower export rate in comparison to the control littermates. The quantitative measurements in this study suggest a number of dynamical changes in the thymocyte development during the progression of colitis.
World Journal of Gastroenterology | 2015
Niki Daferera; Ashok Kumar Kumawat; Elisabeth Hultgren-Hörnquist; Simone Ignatova; Magnus Ström; Andreas Münch
In this case report, we examined the levels of cytokines expressed before and during fecal stream diversion and after intestinal continuity was restored in a patient with collagenous colitis. We report the case of a 46-year-old woman with chronic, active collagenous colitis who either failed to achieve clinical remission or experienced adverse effects with the following drugs: loperamide, cholestyramine, budesonide, methotrexate and adalimumab. Due to the intractable nature of the disease and because the patient was having up to 15 watery bowel movements per day, she underwent a temporary ileostomy. Colonic biopsies were analyzed for mucosal cytokine protein levels before and during fecal stream diversion and after intestinal continuity was restored. Mucosal protein levels of interleukin (IL)-1β, IL-2, IL-6, IL-12, IL-17 A, IL-23, TNF, IFN-γ, IL-4, IL-5, IL-10 and IL-13 were all higher during active disease and decreased to non-detectable or considerably lower levels during fecal stream diversion. One month after the restoration of bowel continuity, when the patient experienced a relapse of symptoms, IL-2, IL-23 and IL-21 levels were again increased. Our results indicate that fecal stream diversion in this patient suppressed the levels of all cytokines analyzed in colonic biopsies. With the recurrence of clinical symptoms and histological changes after bowel reconstruction, the levels of primarily proinflammatory cytokines increased. Our findings support the hypothesis that a luminal factor triggers the inflammation observed in collagenous colitis.
FEMS Microbiology Ecology | 2016
Ignacio Rangel; John Peter Ganda Mall; Roger Willén; Elisabeth Hultgren-Hörnquist
Archive | 2016
Sezin Günaltay; Dirk Repsilber; Gisela Helenius; Nils Nyhlin; Johan Bohr; Elisabeth Hultgren-Hörnquist
Immunology | 2014
Sezin Günaltay; Mohammed Ghiboub; Olov Hultgren; Elisabeth Hultgren-Hörnquist
Immunology | 2013
Ashok Kumar Kumawat; Curt Tysk; Johan Bohr; Olof Hultgren; Elisabeth Hultgren-Hörnquist
Immunology | 2013
Sezin Günaltay; Nils Nyhlin; Ashok Kumar Kumawat; Curt Tysk; Johan Bohr; Olov Hultgren; Elisabeth Hultgren-Hörnquist
Immunology | 2013
Sezin Günaltay; Nils Nyhlin; Ashok Kumar Kumawat; Johan Bohr; Curt Tysk; Olof Hultgren; Elisabeth Hultgren-Hörnquist