| 11. |
- Josefson, Anna, et al.
(author)
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Nickel allergy and hand eczema : a 20-year follow up
- 2006
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In: Contact Dermatitis. - Oxford : Wiley. - 0105-1873 .- 1600-0536. ; 55:5, s. 286-290
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Journal article (peer-reviewed)abstract
- The aim of this study was to investigate the occurrence of hand eczema after 20 years in women patch tested to nickel during childhood. In 1982-1983, 960 schoolgirls were patch tested for nickel allergy; its prevalence was found to be 9%. 20 years later, the same individuals received a questionnaire regarding hand eczema and factors of importance for the development of hand eczema. 735 of 908 women (80.9%) answered the questionnaire. In total, 17.6% of respondents reported hand eczema after the age of 15 years, and the 1-year prevalence was 12.8%. There was no statistically significant difference in the occurrence of hand eczema between the groups who had previously tested positive and negative for nickel allergy. 38.3% of the respondents considered themselves to be nickel sensitive at the time they answered the questionnaire; in this group, the reported prevalence of hand eczema after age 15 was 22.5%. 31.4% of those with a history of atopic dermatitis reported hand eczema after age 15, compared with 10.6% of those without (P < 0.001). In conclusion, contact allergy to nickel in childhood did not seem to increase the prevalence of hand eczema later in life.
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| 12. |
- Josefson, Anna, et al.
(author)
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Nickel allergy as risk factor for hand eczema : a population-based study
- 2009
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In: British Journal of Dermatology. - : Oxford University Press (OUP). - 0007-0963 .- 1365-2133. ; 160:4, s. 828-834
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Journal article (peer-reviewed)abstract
- BACKGROUND: In population-based studies using self-reported nickel allergy, a hand eczema prevalence of 30-43% has been reported in individuals with nickel allergy. In a previous Swedish study, 958 schoolgirls were patch tested for nickel. In a questionnaire follow up 20 years later no association was found between nickel allergy and hand eczema. OBJECTIVES: To investigate further the relation between nickel allergy and hand eczema. METHODS: Three hundred and sixty-nine women, still living in the same geographical area, now aged 30-40 years, were patch tested and clinically investigated regarding hand eczema. RESULTS: Patch testing showed 30.1% nickel-positive individuals. The adjusted prevalence proportion ratio (PPR) for hand eczema after age 15 years in relation to nickel patch test results was 1.03 (95% confidence interval, CI 0.71-1.50). A history of childhood eczema was reported by 35.9%, and the PPR for hand eczema in relation to childhood eczema was 3.68 (95% CI 2.45-5.54). When analysing the relation separately in women with and without a history of childhood eczema a statistical interaction was found. The hand eczema risk was doubled in nickel-positive women without a history of childhood eczema, with a PPR of 2.23 (95% CI 1.10-4.49) for hand eczema after age 15 years. CONCLUSIONS: A doubled risk for hand eczema was found in nickel-positive women without a history of childhood eczema. When analysing all participants, there was no statistically significant difference between nickel-positive and nickel-negative women regarding occurrence of hand eczema. The most important risk factor for hand eczema was childhood eczema. The risk for hand eczema in nickel-positive women may previously have been overestimated.
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| 13. |
- Pasupuleti, Mukesh, et al.
(author)
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Antimicrobial activity of a C-terminal peptide from human extracellular superoxide dismutase
- 2009
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In: BMC research notes. - : Springer Science and Business Media LLC. - 1756-0500. ; 2, s. 136-
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Journal article (peer-reviewed)abstract
- BACKGROUND: Antimicrobial peptides (AMP) are important effectors of the innate immune system. Although there is increasing evidence that AMPs influence bacteria in a multitude of ways, bacterial wall rupture plays the pivotal role in the bactericidal action of AMPs. Structurally, AMPs share many similarities with endogenous heparin-binding peptides with respect to secondary structure, cationicity, and amphipathicity. FINDINGS: In this study, we show that RQA21 (RQAREHSERKKRRRESECKAA), a cationic and hydrophilic heparin-binding peptide corresponding to the C-terminal region of extracellular superoxide dismutase (SOD), exerts antimicrobial activity against Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, Bacillus subtilis and Candida albicans. The peptide was also found to induce membrane leakage of negatively charged liposomes. However, its antibacterial effects were abrogated in physiological salt conditions as well as in plasma. CONCLUSION: The results provide further evidence that heparin-binding peptide regions are multifunctional, but also illustrate that cationicity alone is not sufficient for AMP function at physiological conditions. However, our observation, apart from providing a link between heparin-binding peptides and AMPs, raises the hypothesis that proteolytically generated C-terminal SOD-derived peptides could interact with, and possibly counteract bacteria. Further studies are therefore merited to study a possible role of SOD in host defence.
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| 14. |
- Pasupuleti, Mukesh, et al.
(author)
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Antimicrobial activity of human prion protein is mediated by its N-terminal region
- 2009
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In: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 4:10, s. e7358-
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Journal article (peer-reviewed)abstract
- BACKGROUND: Cellular prion-related protein (PrP(c)) is a cell-surface protein that is ubiquitously expressed in the human body. The multifunctionality of PrP(c), and presence of an exposed cationic and heparin-binding N-terminus, a feature characterizing many antimicrobial peptides, made us hypothesize that PrP(c) could exert antimicrobial activity. METHODOLOGY AND PRINCIPAL FINDINGS: Intact recombinant PrP exerted antibacterial and antifungal effects at normal and low pH. Studies employing recombinant PrP and N- and C-terminally truncated variants, as well as overlapping peptide 20mers, demonstrated that the antimicrobial activity is mediated by the unstructured N-terminal part of the protein. Synthetic peptides of the N-terminus of PrP killed the Gram-negative bacteria Escherichia coli and Pseudomonas aeruginosa, and the Gram-positive Bacillus subtilis and Staphylococcus aureus, as well as the fungus Candida parapsilosis. Fluorescence studies of peptide-treated bacteria, paired with analysis of peptide effects on liposomes, showed that the peptides exerted membrane-breaking effects similar to those seen after treatment with the "classical" human antimicrobial peptide LL-37. In contrast to LL-37, however, no marked helix induction was detected for the PrP-derived peptides in presence of negatively charged (bacteria-mimicking) liposomes. PrP furthermore showed an inducible expression during wounding of human skin ex vivo and in vivo, as well as stimulation of keratinocytes with TGF-alpha in vitro. CONCLUSIONS: The demonstration of an antimicrobial activity of PrP, localisation of its activity to the N-terminal and heparin-binding region, combined with results showing an increased expression of PrP during wounding, indicate that PrPs could have a previously undisclosed role in host defense.
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| 15. |
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| 16. |
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| 17. |
- Wågsäter, Dick, 1976-
(author)
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CXCL16 and CD137 in atherosclerosis
- 2005
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Doctoral thesis (other academic/artistic)abstract
- Atherosclerosis is a progressive inflammatory disease that is characterized by the accumulation of lipids, infiltrated cells and fibrous elements in large arteries. This thesis focuses on the molecular mechanisms behind foam cell formation and inflammation, two central processes in the development of atherosclerosis. More specific, we studied the effects of proinflammatory cytokines on CXCL16 expression and its role as scavenger receptor on macrophages and smooth muscle cells in atherogenesis. CXCL16 is defined as a chemokine and a scavenger receptor, regulating adhesion and chemoattraction of CXCR6 expressing cells and uptake of oxLDL. We show that the expression of CXCL16 and its receptor CXCR6 are more pronounced in human atherosclerotic lesions compared with non-atherosclerotic vessels. Increased expression of CXCL16 was also seen in atherosclerotic aortas of apoE-/- mice compared with aortas of non-atherosclerotic, age-matched C57BL/6 mice. In vitro, IFN gamma induced CXCL16 expression in primary human monocytes and smooth muscle cells which resulted in an increased uptake of oxLDL. Treatment of mice with IFN gamma also induced CXCL16 expression in atherosclerotic lesions. Thus, we have demonstrated a role for IFN gamma in foam cell formation through upregulation of CXCL16. The expression of CXCR6 was defined to the same regions as for CXCL16 in the lesion, indicating the presence of cells able to respond to CXCL16. Consequently, CXCL16 could serve as a molecular link between lipid metabolism and immune activity in atherosclerotic lesion. CD137 belongs to the TNF family and mediates several important processes in inflammation. CD137 is involved in the activation of T cells, NK cells, B cells and monocytes and regulate cytokine production, proliferation and apoptosis in these cells. A limited number of studies have demonstrated CD137 expression on smooth muscle cells and endothelial cells. Our results show that CD137 mRNA is higher expressed in human atherosclerotic lesions compared with unaffected vessels. We found that endothelial cells express CD137 in atherosclerotic lesions and that cultured endothelial cells and smooth muscle cells express CD137 and CD137 ligand in vitro. CD137 was regulated differentially by proinflammatory cytokines (i.e. IFN gamma, TNF alpha, IL-1 beta) and bacterial lipopolysaccharide depending on cell type. Furthermore, we investigated the effects of CD137 signalling, demonstrating that binding of the CD137 ligand to its receptor increases proliferation and migration of smooth muscle cells. In summary, this thesis has focused on the expression, regulation and role of CXCL16 and CD137, two genes that have not been described earlier in the concept of atherosclerosis. The findings demonstrate some of the molecular mechanisms involved in vascular inflammation and may increase our knowledge about the development of atherosclerosis.
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| 18. |
- Westermark, Gunilla T., et al.
(author)
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Serum amyloid A and protein AA : molecular mechanisms of a transmissible amyloidosis
- 2009
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In: FEBS Letters. - : Wiley. - 0014-5793 .- 1873-3468. ; 583:16, s. 2685-2690
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Research review (peer-reviewed)abstract
- Systemic AA-amyloidosis is a complication of chronic inflammatory diseases and the fibril protein AA derives from the acute phase reactant serum AA. AA-amyloidosis can be induced in mice by an inflammatory challenge. The lag phase before amyloid develops can be dramatically shortened by administration of a small amount of amyloid fibrils. Systemic AA-amyloidosis is transmissible in mice and may be so in humans. Since transmission can cross species barriers it is possible that AA-amyloidosis can be induced by amyloid in food, e.g. foie gras. In mice, development of AA-amyloidosis can also be accelerated by other components with amyloid-like properties. A new possible risk factor may appear with synthetically made fibrils from short peptides, constructed for tissue repair.
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| 19. |
- Kucinskiene, Vesta, et al.
(author)
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Home sampling and pooling of vaginal samples are effective tools for genetic screening of Chlamydia trachomatis among high school female students in Lithuania
- 2008
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In: Scandinavian Journal of Infectious Diseases. - London : Taylor & Francis. - 0036-5548 .- 1651-1980. ; 40:2, s. 88-93
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Journal article (peer-reviewed)abstract
- The aims were 1) to estimate the prevalence of C. trachomatis infection among sexually active female students in Kaunas, Lithuania; 2) to investigate the usefulness of personal invitation, self-sampling, and pooling of samples for screening; and 3) to evaluate the costs of the approaches used. A cross-sectional study inviting 795 female students (18–31 y of age) from 7 high schools and 1 college in Kaunas was performed. The response rate was 67% (533/795). Self-obtained vaginal samples were analysed, individually and pooled (n=3), using Digene Hybrid Capture II CT/NG Test. The overall prevalence of C. trachomatis infection was 5.6%. Among the sexually active female students 20–24 y of age (n=424), the prevalence was 7.1%; however, the prevalence varied from 0% to 14.2% at the different schools. For estimation of the population prevalence based solely on identification of C. trachomatis positive pools, the pooling strategy reduced the costs by 85%. For estimation of population prevalence and for diagnosis of each individual sample, pooling reduced the costs by 70%. Targeted screening, using pooling to reduce the expenses, mainly of 3rd and 4th y Lithuanian female students could be recommended. By extended personal contact and internet-based communication, increased participation rates may be attained.
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| 20. |
- Karlsson, Isabella, 1980, et al.
(author)
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Photodegradation of Dibenzoylmethanes: Potential Cause of Photocontact Allergy to Sunscreens
- 2009
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In: Chemical Research in Toxicology. - : American Chemical Society (ACS). - 0893-228X .- 1520-5010. ; 22:11, s. 1881-1892
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Journal article (peer-reviewed)abstract
- One of the most frequently observed photoallergens today is the sunscreen agent 4-tert-butyl-4′-methoxy dibenzoylmethane (1a). The structurally similar compound, 4-isopropyldibenzoylmethane (1b), was a common cause of sunscreen allergy in the eighties and early nineties but was removed from the market in 1993 and replaced with dibenzoylmethane 1a. We have studied the photodegradation of the dibenzoylmethane 1a, to better understand how these substances cause an immune reaction. Several expected degradation products were formed and identified. Of these, arylglyoxals and benzils were of particular interest because they were unexplored as potential contact allergens. The allergenic potential of photodegraded 1a was evaluated by screening the formed arylglyoxals and benzils for their sensitizing capacity in the murine local lymph node assay. The arylglyoxals were found to be strong sensitizers. They were also found to be highly reactive toward the nucleophile arginine, which indicates that the immunogenic hapten-protein complex could be formed via an electrophilic-nucleophilic pathway. By varying the electron-withdrawing or -donating capacity of the substituent in the para position of the arylglyoxal, the electronic effects were shown to have no significant impact on either the sensitizing or the electrophilic power of arylglyoxals. Thus, a change in the substitution pattern of the parent dibenzoylmethane will not influence the sensitizing capacity of the products formed from them upon photodegradation. Furthermore, the combined studies of benzils, using the local lymph node assay and a cell proliferation assay, indicate that the benzils are cytotoxic rather than allergenic. Taken together, this study presents strong indication that photocontact allergy to dibenzoylmethanes is caused by the arylglyoxals that are formed upon photodegradation.
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