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| 2. |
- Fahlgren, Anna, et al.
(författare)
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β-Defensin-3 and -4 in intestinal epithelial cells display increased mRNA expression in ulcerative colitis
- 2004
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Ingår i: Clinical and Experimental Immunology. - Oxford : Blackwell Publishing. - 0009-9104 .- 1365-2249. ; 137:2, s. 379-385
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Tidskriftsartikel (refereegranskat)abstract
- mRNA expression of two recently described human beta-defensins (hBD-3 and hBD-4) in epithelial cells of normal small and large intestine and the impact of chronic intestinal inflammation on their expression levels was investigated. Intestinal specimens from patients with ulcerative colitis (UC), Crohn's disease (CD) and controls with no history of inflammatory bowel disease were studied. hBD-3 and hBD-4 mRNAs were determined in freshly isolated epithelial cells by real-time quantitative reverse transcription-polymerase chain reaction (QRT-PCR) and by in situ hybridization. The effect of proinflammatory cytokines on hBD-3 and hBD-4 mRNA expression in colon carcinoma cells was also investigated. Purified epithelial cells of normal small and large intestine expressed both hBD-3 and hBD-4 mRNA, with higher expression levels of hBD-3 mRNA. In situ hybridization revealed higher levels of mRNA expression in the crypt- compared to the villus/luminal-compartment. Interferon (IFN)-gamma, but not tumour necrosis factor (TNF)-alpha or IL-1beta, augmented hBD-3 mRNA expression. None of these agents stimulated hBD-4 expression. Colonic epithelial cells from patients with UC displayed a significant increase in hBD-3 and hBD-4 mRNA compared to epithelial cells of controls. In contrast, small intestinal epithelial cells from CD patients did not show increased expression levels compared to the corresponding control cells. Moreover, Crohn's colitis did not show increased expression of hBD-4 mRNA, while the data are inconclusive for hBD-3 mRNA. We conclude that the chronic inflammatory reaction induced in the colon of UC patients enhances hBD-3 and hBD-4 mRNA expression in the epithelium, whereas in CD this is less evident.
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| 3. |
- Hammarström, Sten, et al.
(författare)
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Peter Perlmann 1919-2005
- 2006
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Ingår i: Scandinavian journal of immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 63:6, s. 487-489
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Hedberg, Maria E., et al.
(författare)
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Prevotella jejuni sp. nov., isolated from the small intestine of a child with celiac disease.
- 2013
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Ingår i: International journal of systematic and evolutionary microbiology. - : Microbiology Society. - 1466-5034 .- 1466-5026. ; 63:11, s. 4218-4223
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Tidskriftsartikel (refereegranskat)abstract
- Five obligately anaerobic, Gram-negative, saccharolytic and proteolytic, non-spore-forming bacilli (CD3:27, CD3:28T, CD3:33, CD3:32 and CD3:34) are described. All five strains were isolated from the small intestine of a female child with celiac disease. The cells of the five strains were observed to be short rods or coccoid cells with longer filamentous forms seen sporadically. The organisms produced acetic acid and succinic acid as major metabolic end products. Phylogenetic analysis, based on comparative 16S rRNA gene sequence analysis revealed close relationships between CD3:27, CD3:28T and CD3:33 on one hand, between CD3:32 and P. histicola CCUG 55407T and between CD3:34 and P. melaninogenica CCUG 4944BT on the other. The strains CD3:27, CD3:28T and CD3:33 were clearly different from any other species within the genus Prevotella and most closely related to but distinct from P. melaninogenica. Based on 16S rRNA gene, RNA polymerase β-subunit gene and 60-kDa chaperonin protein subunit gene sequencing, phenotypic, chemical and biochemical properties strains CD3:27, CD3:28T and CD3:33 have been determined to represent a novel species within the genus Prevotella, named Prevotella jejuni sp. nov. Strain CD3:28T (CCUG 60371T = DSM 26989T) is the type strain of the proposed new species. All five strains were able to form homologous aggregates, in which tube-like structures were connecting individual bacteria cells. The five strains were able to bind to human intestinal carcinoma cell lines at 37 °C.
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| 5. |
- Niklasson, Mia, et al.
(författare)
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Membrane-Depolarizing Channel Blockers Induce Selective Glioma Cell Death by Impairing Nutrient Transport and Unfolded Protein/Amino Acid Responses
- 2017
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Ingår i: Cancer Research. - : AMER ASSOC CANCER RESEARCH. - 0008-5472 .- 1538-7445. ; 77:7, s. 1741-1752
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Tidskriftsartikel (refereegranskat)abstract
- Glioma-initiating cells (GIC) are considered the underlying cause of recurrences of aggressive glioblastomas, replenishing the tumor population and undermining the efficacy of conventional chemotherapy. Here we report the discovery that inhibiting T-type voltage-gated Ca2+ and KCa channels can effectively induce selective cell death of GIC and increase host survival in an orthotopic mouse model of human glioma. At present, the precise cellular pathways affected by the drugs affecting these channels are unknown. However, using cell-based assays and integrated proteomics, phosphoproteomics, and transcriptomics analyses, we identified the downstreamsignaling events these drugs affect. Changes in plasma membrane depolarization and elevated intracellular Na+, which compromised Na+-dependent nutrient transport, were documented. Deficits in nutrient deficit acted in turn to trigger the unfolded protein response and the amino acid response, leading ultimately to nutrient starvation and GIC cell death. Our results suggest new therapeutic targets to attack aggressive gliomas.
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