Studies of the Systemic Inflammation in Psoriasis

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Fältnamn	Indikatorer	Metadata
000		05736nam a2200409 4500
001		oai:DiVA.org:liu-151988
003		SwePub
008		181012s2018 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
020		a 9789176852569q print
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1519882 URI
024	7	a https://doi.org/10.3384/diss.diva-1519882 DOI
040		a (SwePub)liu
041		a engb eng
042		9 SwePub
072	7	a vet2 swepub-contenttype
072	7	a dok2 swepub-publicationtype
100	1	a Sigurdardottir, Gunnthorunn,d 1975-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten4 aut0 (Swepub:liu)gunsi16
245	1 0	a Studies of the Systemic Inflammation in Psoriasis
264	1	a Linköping :b Linköping University Electronic Press,c 2018
300		a 93 s.
338		a electronic2 rdacarrier
490	0	a Linköping University Medical Dissertations,x 0345-0082 ;v 1632
520		a Psoriasis is a common immune-mediated disease, where an increased prevalence of extra cutaneous diseases and mortality is observed. Common inflammatory mechanisms are implicated. The general aim of this thesis was to investigate markers of inflammation and cardiovascular disease in psoriasis, now considered a systemic disease, assumed to reflect the systemic inflammation.In Study I, Th1-, Th2- and Th17-associated chemokines were elevated in the blood of psoriasis patients in comparison to controls and, in Study II, six markers of cardiovascular risk were demonstrated to be systemically elevated. After adjustment for body mass index and waist: hip ratio in Study II, only one marker, the total plasminogen activator inhibitor-1, showed sustained elevated levels. The levels of the chemokines and the cardiovascular markers were unaffected after treatment with narrowband UVB therapy (NB-UVB), despite a significant improvement in skin lesions, indicating more local than systemic effects of NBUVB. This was further strengthened by the fact that the response to in-vitro stimulation in the peripheral blood mononuclear cells (PBMCs) of psoriasis patients before and after NB-UVB treatment was unaffected. In Study I, CCL20 was shown to correlate to the psoriasis area severity index (PASI), but this correlation was lost after phototherapy, suggesting sources of CCL20 other than the skin. Conversely, systemic treatment with TNF-α inhibition in Study II alleviated the elevated systemic levels of the cardiovascular risk markers. In Study III, the levels of 17 potential biomarkers, with the emphasis on endothelial and adipocyte dysfunction, soluble receptors and the innate mechanisms were studied. Endocan-1, CXCL16, and sVEGFR1, were found to be systemically decreased in psoriasis patients at baseline. Endocan-1 showed a negative correlation to the PASI. In contrast to the results in Studies I and II, NB-UVB therapy affected the systemic levels of investigated markers; Endocan-1 and CXCL16 were restored to normal levels, while sVEGF1, FABP3, FABP4 and sIL-1R1 showed a significant reduction following NB-UVB. In Study IV, the focus was on the contribution of innate immune mechanisms and the effects of the cytokines IL-17 and TNF-α on systemic inflammation. In keratinocytes, the gene and protein expression of inflammasome components was increased upon exposure to IL-17 and TNF-α. Systemically, the constitutive expression of the inflammasome components NLRP1, NLRP3 and AIM2 was detected in neutrophils, classical monocytes, CD4+ lymphocytes and B-cell subsets from psoriasis patients. Upon exposure to IL-17 and TNF-α, increased systemic caspase-1 levels were detected, confirming systemic inflammasome activity.In conclusion, these studies support the hypothesis that there is a systemic inflammation in psoriasis to which both innate and adaptive immune mechanisms contribute. The systemic inflammation may be explained, to some extent, but not completely, by body weight and fat distribution. The different effects of NB-UVB therapy on the systemic levels of the investigated markers may reflect their different roles in psoriasis, but the ameliorating effects of the TNF-α inhibitor on the elevated cardiovascular markers suggests that systemic treatment should be evaluated in psoriasis patients with signs of a systemic inflammatory burden.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Dermatologi och venereologi0 (SwePub)302042 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Dermatology and Venereal Diseases0 (SwePub)302042 hsv//eng
700	1	a Enerbäck, Charlotta,d 1965-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Region Östergötland, Hudkliniken i Östergötland4 ths0 (Swepub:liu)chaen00
700	1	a Bivik, Cecilia,d 1978-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten4 ths0 (Swepub:liu)cecbi55
700	1	a Synnerstad, Ingrid,d 1968-u Linköpings universitet,Medicinska fakulteten4 ths0 (Swepub:liu)ingsy94
700	1	a Bradley, Maria,c Docentu Karolinska Institutet, Stockholm, Sweden4 opn
710	2	a Linköpings universitetb Avdelningen för cellbiologi4 org
856	4	u https://doi.org/10.3384/diss.diva-151988y Fulltext
856	4	u https://liu.diva-portal.org/smash/get/diva2:1255460/FULLTEXT01.pdfx primaryx Raw objecty fulltext
856	4	u https://liu.diva-portal.org/smash/get/diva2:1255460/COVER01.pdfy cover
856	4	u https://liu.diva-portal.org/smash/get/diva2:1255460/PREVIEW01.pngx Previewy preview image
856	4	u http://liu.diva-portal.org/smash/get/diva2:1255460/FULLTEXT01
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-151988
856	4 8	u https://doi.org/10.3384/diss.diva-151988

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