C-reactive protein (CRP) is secreted by hepatocytes as a pentameric molecule made up of identical monomers, circulates in the plasma as pentamers, and localizes in atherosclerotic lesions. In some cases, localized CRP was detected by using monoclonal antibodies that did not react with native pentameric CRP but were specific for isolated monomeric CRP. It has been reported that, once CRP is bound to certain ligands, the pentameric structure of CRP is altered so that it can dissociate into monomers. Accordingly, the monomeric CRP found in atherosclerotic lesions may be a stationary, ligand-bound, by-product of a ligand-binding function of CRP. CRP binds to modified forms of low-density lipoprotein (LDL). The binding of CRP to oxidized LDL requires acidic pH conditions; the binding at physiological pH is controversial. The binding of CRP to enzymatically-modified LDL occurs at physiological pH; however, the binding is enhanced at acidic pH. Using enzymatically-modified LDL, CRP has been shown to prevent the formation of enzymatically-modified LDL-loaded macrophage foam cells. CRP is neither pro-atherogenic nor atheroprotective in ApoE-/-and ApoB100/100Ldlr-/-murine models of atherosclerosis, except in one study where CRP was found to be slightly atheroprotective in ApoB100/100Ldlr-/-mice. The reasons for the ineffectiveness of human CRP in murine models of atherosclerosis are not defined. It is possible that an inflammatory environment, such as those characterized by acidic pH, is needed for efficient interaction between CRP and atherogenic LDL during the development of atherosclerosis and to observe the possible atheroprotective function of CRP in animal models.

C-reactive protein (CRP) is an acute phase protein produced by hepatocytes whose serum concentration increases in inflammatory conditions including cardiovascular complications. Statins that are used in the treatment of cardiovascular diseases to reduce cholesterol also lower serum CRP levels. In human hepatoma Hep3B cells, CRP is induced in response to cytokines IL-6 and IL-1β. The objective of the study was to determine the mechanism of regulation of CRP gene expression in Hep3B cells in response to cytokines and to determine the effect of statins on CRP expression. Key findings of our research were: 1. IL-1β-activated NF-κB p50/p65 acted synergistically with IL-6-activated C/EBPβ in inducing CRP transactivation through the proximal CRP promoter. 2. A NF-κB site was localized in the proximal CRP promoter centered at position -69 overlapping the known OCT-1/HNF-1/HNF-3 sites. 3. The synergy between IL-6 and IL-1β in inducing CRP gene expression was partially mediated through the NF-κB site. 4. In the absence of C/EBPβ, a complex containing C/EBPζ and RBP-Jκ was formed at the C/EBP-p50-site. 5. Overexpressed C/EBPζ repressed both (IL-6+IL-1β)-induced and C/EBPβ-induced CRP expression. 6. OCT-1 repressed (IL-6+IL-1β)-induced CRP transactivation through the proximal CRP promoter. 7. Statins reduce cytokine-induced CRP gene expression at the transcriptional level. These findings led us to conclude that: 1. CRP transcription is determined by the relative levels of various transcription factors such as C/EBPβ, C/EBPζ, NF-κB and OCT-1 and their interaction with the proximal CRP promoter. 2. Inhibition of CRP transcription by statins is not due to an anti-inflammatory effect but due to the direct effect on CRP gene expression.

Background: Surgical stress during resection surgery for colon cancer has previously been shown to be associated with adverse postoperative outcomes. Statin and beta-blocker treatment have been shown to lower postoperative complications and mortality, and been hypothesized to reduce the surgical stress response, although this correlation has not been studied clinically. Aim: To investigate whether perioperative beta-blocker and/or statin treatment reduce the postoperative C-reactive protein (CRP) response. Material and methods: All patients who underwent right sided hemicolectomy or sigmoid resection for cancer at Örebro University Hospital during 2012-2017 were included in this study. Initially, any treatment with statins, beta-blockers or both were compared to those with no treatment. After initial analyses, four treatment groups were compared regarding postoperative CRP response, namely no treatment, statin, beta-blocker, and combination treatment. Comparisons regarding complications were also performed for the four groups. Results: A total of 260 patients were included in this study. The no treatment group had a lower peak postoperative CRP than the treatment group, when comparing any treatment versus no treatment. There were no significant differences in postoperative CRP within the four treatment groups. There was no significant difference in complication rate between any of the treatment groups when compared to no treatment. Conclusion: Treatment with statin or beta-blocker therapy does not reduce the postoperative CRP response. A combination of both treatments demonstrated a trend towards a reduction regarding postoperative CRP response compared with the two treatments individually assessed. Larger studies are needed to verify the results of this study.

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Bakgrund: Gingivit kännetecknas av svullet/lättblödande och ibland ömt tandkött. Gingivit är en inflammatoriskt orsakad reaktion som uppkommer i samband med närvaro av bakterier. För att motverka utvecklingen av gingivit rekommenderas munhygienvård regelbundet. Gingivit kan utvecklas till parodontit med skador på upphängningsapparaten och benstödet, orsaken till detta är idag dock ej helt klarlagd. Kliniska variabler (blödning vid sondering) är vedertagna diagnostiska metoderna för diagnostisk av gingivit idag. I pilotstudier har laktoferrinkoncentrationer setts vara förhöjda i stimulerad helsaliv och gingivalexsudat hos patienter med kronisk parodontit jämfört med patienter utan parodontit. Mål: Undersöka hur koncentrationen laktoferrin i ostimulerad helsaliv förändrades hos individer som utvecklade gingivit i en experimentell gingivitstudie och om C-reaktivt protein är en tillförlitlig markör för gingival inflammationsgrad.Material och metod: En experimentell gingivitstudie genomfördes med 13 försöksdeltagare där munhygienvanor kontrollerades och förändrades under 3 perioder á 2 veckor. Helsalivprov och mätning av CRP genomfördes. Resultat: Gingivalindex och CRP höjdes signifikant under försöksperioden Dag 0 till Dag 13(p=0,002 och p=0,027). Laktoferrin sågs först signifikant förhöjd under mitten av avslutningsperioden (Dag 20) (p=0,015). Laktoferrinkoncentrationen återgick inte till baselinevärdet under studien. Signifikant korrelation sågs mellan gingivalindex och laktoferrin från Dag 0 fram till Dag 13 (r=0,224, p=0,042). Utvecklingen av CRP sågs inte korrelera med någon variabel under försöket. Konklusion: Resultaten indikerar att utvecklingen av experimentell gingivit påverkar laktoferrinkoncentrationen över tid och kan därför vara en potentiell biomarkör för gingivit. De låga skillnader hos CRP visar att den inte är en tillförlitlig markör vid gingivit. / Background: Gingivitis is characterized by swollen and bleeding tissue, an inflammatory reaction with presence of pathological bacteria. To counteract the development of gingivitis, regular oral hygiene care is recommended. Gingivitis can progress into periodontitis which damages the periodontal tissue and bone. Clinical variables (bleeding on probing, plaque occurrence) are diagnostic methods for gingivitis. Elevated concentrations of lactoferrin in stimulated whole saliva and gingival crevicular fluid has been seen in patients with chronic periodontitis compared to patients without periodontitis.Objectives: Investigate the salivary concentration of lactoferrin in subjects enrolled in the experimental gingivitis model, the response of capillary CRP was also investigated.Methods: Thirteen individuals participated in a 14-day experimental gingivitis model and 10-day gingival healing period, measurements of whole saliva lactoferrin and CRP was performed. Results: Gingival index and CRP was increased statistical significant during the induction of gingivitis (p=0.002 and p=0,027). Lactoferrin increased during the experimental phase and reached a peak at day 20, which was statistical significant compared to baseline (p=0.015). A statistical significant correlation between gingival index and lactoferrin was seen from day 0 to day 13 (r=0.224, p=0.042). CRP did not match any correlation to any other measured variable from day 0 to day 24.Conclusion: These results indicate that gingivitis may have a systemic effect, which in this study has been expressed as increased levels of salivary lactoferrin. Lactoferrin may be a potential biomarker for gingivitis. Due to low changes in concentrations and because CRP is systemically affected it makes an unreliable biomarker for gingivitis.

<p>Examining the effect of a modernized collaborative care intervention for depression consisting of both behavioral and pharmacologic treatments on 12-month change in individual somatic depressive symptoms (hyperphagia, poor appetite, hypersomnia, and disturbed sleep) and 12-month change in</p> <p>cardiometabolic biomarkers (HOMA-IR, BMI, hsCRP, leptin, and ghrelin). Further examining whether 12-month change in individual somatic depressive symptoms mediates the eIMPACT intervention’s effect on 12-month change in cardiometabolic biomarkers.</p>

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By 2030 major depression is predicted to be the leading cause of disease burden in the world; as such, it is critical to understand factors that contribute to the development of depression. The social signal transduction theory of depression hypothesizes that adversity and social threat upregulate pro-inflammatory biomarkers leading to depression. The current study examined whether pro-inflammatory biomarkers (interleukin-6, interleukin-8, c-reactive protein, and tumor necrosis factor alpha) mediate the association between various types of childhood maltreatment (physical abuse, sexual abuse, emotional abuse, physical neglect, emotional neglect) and adult depression symptoms in a sample of 740 adults (372 female; Mage= 51.6 years, SD = 13.6) who provided retrospective report of childhood maltreatment as part of the Midlife in the United States (MIDUS) Refresher Biomarker study. Additionally, it explored whether these relations differ for males versus females. A series of linear regression analyses were run in SPSS; separate models were run for each form of childhood maltreatment and for interleukin-6, interleukin-8, c-reactive protein, and tumor necrosis factor-alpha. The results showed that childhood maltreatment is a robust predictor of adulthood depression; however, this association did not differ between biological sexes. In addition, only interleukin-6 was shown to partially mediate the association between childhood maltreatment and adulthood depression. These findings highlight the need to explore the use of interleukin-6 to screen for depression in youth. / M.S. / By 2030 major depression is predicted to be the leading cause of disease burden in the world; as such, it is critical to understand factors that contribute to the development of depression. It has been hypothesized that adversity and social threat activate pro-inflammatory biomarkers, which are proteins that can detect inflammation in the body, leading to depression. The current study examined whether several pro-inflammatory biomarkers explain the association between several types of childhood maltreatment (physical abuse, sexual abuse, emotional abuse, physical neglect, emotional neglect) and adult depression symptoms in a sample of 740 adults (372 female; Mage= 51.6 years, SD = 13.6) who provided report of past experiences of childhood maltreatment. Additionally, it explored whether these relations differ for males versus females. The results showed that childhood maltreatment is a robust predictor of adulthood depression for males and females. Of the inflammatory biomarkers examined, only interleukin-6 was shown to partially explain the association between childhood maltreatment and adulthood depression symptoms. These findings highlight the need to explore the use of interleukin-6 to screen for depression in youth.

Yes / The development of androgenetic alopecia is associated with a risk of developing cardiovascular diseases, but the association of alopecia areata with cardiovascular diseases in humans is largely unexplored. We measured the plasma level of two common cardiovascular disease markers, cardiac troponin I and Creactive protein, in alopecia areata and androgenetic alopecia-affected subjects. Also, we investigated the possible presence of pro-apoptotic factors in the plasma of hair loss subjects. The mean plasma cardiac troponin I level was highest in alopecia areata subjects, moderately higher in androgenetic alopecia subjects, and lowest in subjects without hair loss (p < 0.05). Alopecia areata subjects not receiving treatments had highest levels of cardiac troponin I (p < 0.05). Alopecia areata plasma samples with high cardiac troponin I levels also induced significantly higher rates of cardiomyocyte apoptosis in cell culture assays. The results suggest the potential for increased heart remodelling. Close monitoring of cardiovascular health in alopecia areata subjects, as well as subsets of androgenetic alopecia patients, may be appropriate. / Canadian Institutes of Health Research (CIHR; MOP-82927). EW is the recipient of a Banting Postdoctoral Fellowship (SAC-92845).