Institution
University of Gothenburg
Education•Gothenburg, Sweden•
About: University of Gothenburg is a education organization based out in Gothenburg, Sweden. It is known for research contribution in the topics: Population & Poison control. The organization has 23855 authors who have published 65241 publications receiving 2606327 citations. The organization is also known as: Göteborg University & Gothenburg University.
Topics: Population, Poison control, Health care, Implant, Dementia
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TL;DR: The DLVO theory has been used as a qualitative model, but also in a quantitative way to calculate adhesion free energy changes involved in microbial adhesion as mentioned in this paper, which has been shown to be effective in predicting bacterial adhesion to various interfaces using the classical Derjaguin-Landau-Verwey-Overbeek (DLVO) theory.
920 citations
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TL;DR: It is demonstrated that hIL-17 can specifically and selectively recruit neutrophils into the airways via the release of C-X-C chemokines from bronchial epithelial cells and suggest a novel mechanism linking the activation of T-lymphocytes to recruitment of neutrophil into theAirways.
Abstract: IL-17 is a recently discovered cytokine that can be released from activated human CD4+ T lymphocytes. This study assessed the proinflammatory effects of human (h) IL-17 in the airways. In vitro, hIL-17 increased the release of IL-8 in human bronchial epithelial and venous endothelial cells, in a time- and concentration-dependent fashion. This effect of hIL-17 was inhibited by cotreatment with an anti-hIL-17 Ab and was potentiated by hTNF-alpha. In addition, hIL-17 increased the expression of hIL-8 mRNA in bronchial epithelial cells. Conditioned medium from hIL-17-treated bronchial epithelial cells increased human neutrophil migration in vitro. This effect was blocked by an anti-hIL-8 Ab. In vivo, intratracheal instillation of hIL-17 selectively recruited neutrophils into rat airways. This recruitment of neutrophils into the airways was inhibited by an anti-hIL-17 Ab and accompanied by increased levels of rat macrophage inflammatory protein-2 (rMIP-2) in bronchoalveolar lavage (BAL) fluid. The BAL neutrophilia was also blocked by an anti-rMIP-2 Ab. The effect of hIL-17 on the release of hIL-8 and rMIP-2 was also inhibited by glucocorticoids, in vitro and in vivo, respectively. These data demonstrate that hIL-17 can specifically and selectively recruit neutrophils into the airways via the release of C-X-C chemokines from bronchial epithelial cells and suggest a novel mechanism linking the activation of T-lymphocytes to recruitment of neutrophils into the airways.
919 citations
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TL;DR: The findings suggest that bacteria from the oral cavity, and perhaps even the gut, may correlate with disease markers of atherosclerosis, and several bacterial taxa in the Oral cavity and the gut correlated with plasma cholesterol levels.
Abstract: Periodontal disease has been associated with atherosclerosis, suggesting that bacteria from the oral cavity may contribute to the development of atherosclerosis and cardiovascular disease. Furthermore, the gut microbiota may affect obesity, which is associated with atherosclerosis. Using qPCR, we show that bacterial DNA was present in the atherosclerotic plaque and that the amount of DNA correlated with the amount of leukocytes in the atherosclerotic plaque. To investigate the microbial composition of atherosclerotic plaques and test the hypothesis that the oral or gut microbiota may contribute to atherosclerosis in humans, we used 454 pyrosequencing of 16S rRNA genes to survey the bacterial diversity of atherosclerotic plaque, oral, and gut samples of 15 patients with atherosclerosis, and oral and gut samples of healthy controls. We identified Chryseomonas in all atherosclerotic plaque samples, and Veillonella and Streptococcus in the majority. Interestingly, the combined abundances of Veillonella and Streptococcus in atherosclerotic plaques correlated with their abundance in the oral cavity. Moreover, several additional bacterial phylotypes were common to the atherosclerotic plaque and oral or gut samples within the same individual. Interestingly, several bacterial taxa in the oral cavity and the gut correlated with plasma cholesterol levels. Taken together, our findings suggest that bacteria from the oral cavity, and perhaps even the gut, may correlate with disease markers of atherosclerosis.
919 citations
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University of Oxford1, King's College London2, University of Manchester3, Radboud University Nijmegen4, Wellcome Trust Sanger Institute5, University of London6, University of Sheffield7, Trinity College, Dublin8, Wellcome Trust9, Medical University of Graz10, University of Erlangen-Nuremberg11, Queen Mary University of London12, Western Infirmary13, Karolinska Institutet14, St George's, University of London15, University of Dundee16, University of Göttingen17, University of Gothenburg18, Sapienza University of Rome19, University of Cambridge20, University of Münster21, University College London22, Moorfields Eye Hospital23, University of Bristol24
TL;DR: These findings implicate pathways that integrate epidermal barrier dysfunction with innate and adaptive immune dysregulation in psoriasis pathogenesis and report compelling evidence for an interaction between the HLA-C and ERAP1 loci.
Abstract: To identify new susceptibility loci for psoriasis, we undertook a genome-wide association study of 594,224 SNPs in 2,622 individuals with psoriasis and 5,667 controls. We identified associations at eight previously unreported genomic loci. Seven loci harbored genes with recognized immune functions (IL28RA, REL, IFIH1, ERAP1, TRAF3IP2, NFKBIA and TYK2). These associations were replicated in 9,079 European samples (six loci with a combined P < 5 × 10⁻⁸ and two loci with a combined P < 5 × 10⁻⁷). We also report compelling evidence for an interaction between the HLA-C and ERAP1 loci (combined P = 6.95 × 10⁻⁶). ERAP1 plays an important role in MHC class I peptide processing. ERAP1 variants only influenced psoriasis susceptibility in individuals carrying the HLA-C risk allele. Our findings implicate pathways that integrate epidermal barrier dysfunction with innate and adaptive immune dysregulation in psoriasis pathogenesis.
919 citations
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TL;DR: The results indicate that resistin is a new and important member of the cytokine family with potent regulatory functions and makes it a novel and interesting therapeutic target in chronic inflammatory diseases such as rheumatoid arthritis.
Abstract: The adipokine resistin is suggested to be an important link between obesity and insulin resistance. In the present study, we assessed the impact of resistin as inflammatogenic cytokine in the setting of arthritis. In vitro experiments on human PBMC were performed to assess cytokine response and transcription pathways of resistin-induced inflammation. Proinflammatory properties of resistin were evaluated in animal model by intra-articular injection of resistin followed by histological evaluation of the joint. Levels of resistin were assessed by ELISA in 74 paired blood and synovial fluid samples of patients with rheumatoid arthritis. Results were compared with the control group comprised blood samples from 34 healthy individuals and 21 synovial fluids from patients with noninflammatory joint diseases. We now show that resistin displays potent proinflammatory properties by 1) strongly up-regulating IL-6 and TNF-α, 2) responding to TNF-α challenge, 3) enhancing its own activity by a positive feedback, and finally 4) inducing arthritis when injected into healthy mouse joints. Proinflammatory properties of resistin were abrogated by NF-κB inhibitor indicating the importance of NF-κB signaling pathway for resistin-induced inflammation. Resistin is also shown to specifically accumulate in the inflamed joints of patients with rheumatoid arthritis and its levels correlate with other markers of inflammation. Our results indicate that resistin is a new and important member of the cytokine family with potent regulatory functions. Importantly, the identified properties of resistin make it a novel and interesting therapeutic target in chronic inflammatory diseases such as rheumatoid arthritis.
916 citations
Authors
Showing all 24120 results
Name | H-index | Papers | Citations |
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Peter J. Barnes | 194 | 1530 | 166618 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Richard H. Friend | 169 | 1182 | 140032 |
Napoleone Ferrara | 167 | 494 | 140647 |
Timothy A. Springer | 167 | 669 | 122421 |
Anders Björklund | 165 | 769 | 84268 |
Hua Zhang | 163 | 1503 | 116769 |
Kaj Blennow | 160 | 1845 | 116237 |
Leif Groop | 158 | 919 | 136056 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Johan G. Eriksson | 156 | 1257 | 123325 |
Naveed Sattar | 155 | 1326 | 116368 |
Paul Elliott | 153 | 773 | 103839 |
Claude Bouchard | 153 | 1076 | 115307 |
Hakon Hakonarson | 152 | 968 | 101604 |