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- Luthje, P, et al.
(författare)
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Estrogen supports urothelial defense mechanisms
- 2013
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Ingår i: Science translational medicine. - : American Association for the Advancement of Science (AAAS). - 1946-6242 .- 1946-6234. ; 5:190, s. 190ra80-
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Tidskriftsartikel (refereegranskat)abstract
- Estrogen supports urothelial defense against infection by increasing the expression of antimicrobial peptides and by protecting epithelial integrity.
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- Georgieva, V., et al.
(författare)
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Association between vitamin D, antimicrobial peptides and urinary tract infection in infants and young children
- 2019
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Ingår i: Acta Paediatrica, International Journal of Paediatrics. - : Wiley. - 0803-5253 .- 1651-2227. ; 108:3, s. 551-556
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Tidskriftsartikel (refereegranskat)abstract
- Aim: Vitamin D stimulates production of the endogenous antimicrobial peptides cathelicidin and β-defensin-2, which are expressed in the urinary tract. We investigated vitamin D status and levels of cathelicidin and β-defensin-2 and their association with urinary tract infection (UTI). Methods: The study included 120 children under three years of age: 76 children with UTIs and 44 otherwise healthy children with congenital hydronephrosis. Serum 25-hydroxycholecalciferol levels were measured by direct competitive electro-chemiluminescence immunoassay, and plasma cathelicidin and β-defensin-2 concentrations were analysed by enzyme-linked immunosorbent assay. Results: We found that vitamin D insufficiency and deficiency are prevalent in young children (21%). Serum vitamin D levels negatively correlated with age and were significantly lower in girls. Levels of vitamin D positively correlated with levels of cathelicidin but not with β-defensin-2. Low concentrations of vitamin D were associated with UTIs in girls, but we did not see any correlation with the recurrence of infection at one-year follow-up. Conclusion: Vitamin D deficiency is common and may prove to be a risk factor for UTIs especially in girls. We hypothesise that adequate supplementation with vitamin D may become a way to prevent first-time UTIs.
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- Gustavsson, Martin, et al.
(författare)
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Improved cell surface display of Salmonella enterica serovar Enteritidis antigens in Escherichia coli
- 2015
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Ingår i: Microbial Cell Factories. - : Springer Science and Business Media LLC. - 1475-2859. ; 14:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Salmonella enterica serovar Enteritidis (SE) is one of the most potent pathogenic Salmonella serotypes causing food-borne diseases in humans. We have previously reported the use of the β-autotransporter AIDA-I to express the Salmonella flagellar protein H:gm and the SE serotype-specific fimbrial protein SefA at the surface of E. coli as live bacterial vaccine vehicles. While SefA was successfully displayed at the cell surface, virtually no full-length H:gm was exposed to the medium due to extensive proteolytic cleavage of the N-terminal region. In the present study, we addressed this issue by expressing a truncated H:gm variant (H:gmd) covering only the serotype-specific central region. This protein was also expressed in fusion to SefA (H:gmdSefA) to understand if the excellent translocation properties of SefA could be used to enhance the secretion and immunogenicity. Results: H:gmd and H:gmdSefA were both successfully translocated to the E. coli outer membrane as full-length proteins using the AIDA-I system. Whole-cell flow cytometric analysis confirmed that both antigens were displayed and accessible from the extracellular environment. In contrast to H:gm, the H:gmd protein was not only expressed as full-length protein, but it also seemed to promote the display of the protein fusion H:gmdSefA. Moreover, the epitopes appeared to be recognized by HT-29 intestinal cells, as measured by induction of the pro-inflammatory interleukin 8. Conclusions: We believe this study to be an important step towards a live bacterial vaccine against Salmonella due to the central role of the flagellar antigen H:gm and SefA in Salmonella infections and the corresponding immune responses against Salmonella.
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- Jung, K, et al.
(författare)
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Low immunogenicity allows Staphylococcus epidermidis to cause PD peritonitis
- 2011
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Ingår i: Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. - : SAGE Publications. - 1718-4304 .- 0896-8608. ; 31:6, s. 672-678
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Tidskriftsartikel (refereegranskat)abstract
- Peritonitis is a common and serious complication of peritoneal dialysis (PD). Coagulase-negative staphylococci from the patient's own skin flora are the most commonly found micro-organisms. Objective In the present study we aim to elucidate the immune response in the early stage of infection and to clarify the importance of bacterial attachment to fibrinogen. Methods Clinical Staphylococcus epidermidis isolates collected from PD peritonitis or the residential skin flora of healthy individuals were used to infect monocytes, macrophages, and peripheral blood mononuclear cells (PBMC) in the presence or absence of fibrinogen. The S. epidermidis strain HB (fbe+), expressing the fibrinogen-binding protein Fbe, and its isogenic mutant STO56 (fbe– ) were used to study the impact of Fbe during cell infection. Immune induction was measured as interleukin-8 (IL-8) production determined by ELISA. Modulation of CD11b/CD18 expression in neutrophils incubated in conditioned medium from these experiments was analyzed in order to judge the cellular response. Results S. epidermidis causing peritonitis was less immunogenic compared to strains belonging to the residential skin flora, as measured by IL-8 induction in monocytes and CD11b/CD18 expression in neutrophils. At low bacterial concentrations, attachment to fibrinogen was a prerequisite for an IL-8 induction in monocytes and PBMC. The fibrinogen-binding protein Fbe did not, however, influence immune induction under this condition. Conclusions We suggest that S. epidermidis strains may be able to cause clinical infection by evoking an inadequate immunological response in the early stage of infection. Bacterial attachment to fibrinogen is a relevant event during this phase but independent of the fibrinogen-binding protein Fbe.
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- Luthje, P, et al.
(författare)
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Statins influence epithelial expression of the anti-microbial peptide LL-37/hCAP-18 independently of the mevalonate pathway
- 2019
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Ingår i: Clinical and experimental immunology. - : Oxford University Press (OUP). - 1365-2249 .- 0009-9104. ; 195:2, s. 265-276
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Tidskriftsartikel (refereegranskat)abstract
- Anti-microbial resistance increases among bacterial pathogens and new therapeutic avenues needs to be explored. Boosting innate immune mechanisms could be one attractive alternative in the defence against infectious diseases. The cholesterol-lowering drugs, statins, have been demonstrated to also affect the immune system. Here we investigate the effect of statins on the expression of the human cathelicidin anti-microbial peptide (CAMP) LL-37/hCAP-18 [encoded by the CAMP gene] and explore the underlying mechanisms in four epithelial cell lines of different origin. Simvastatin induced CAMP expression in bladder epithelial cells telomerase-immortalized uroepithelial cells (TERT-NHUCs), intestinal cells HT-29 and keratinocytes HEKa, but not in airway epithelial cells A549. Gene induction in HEKa cells was reversible by mevalonate, while this effect was independent of the cholesterol biosynthesis pathway in TERT-NHUCs. Instead, inhibition of histone deacetylases by simvastatin seems to be involved. For HT-29 cells, both mechanisms may contribute. In addition, simvastatin increased transcription of the vitamin D-activating enzyme CYP27B1 which, in turn, may activate LL-37/hCAP-18 production. Taken together, simvastatin is able to promote the expression of LL-37/hCAP-18, but cell line-specific differences in efficacy and the involved signalling pathways exist.
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- Zabel, M, et al.
(författare)
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Corrigendum
- 2019
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Ingår i: ESC heart failure. - : Wiley. - 2055-5822. ; 6:4, s. 899-899
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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