ObjectiveVitamin D deficiency is a public health problem that occurs more frequently than expected. The aim of this study is to evaluate the vitamin D levels of children attending the paediatrics unit of the Bertamiráns primary care centre (A Coruña NW Spain). This is an observational study carried out during 1 year on a random sample of the pediatric population aged between 5 and 15 years. The levels of vitamin D (25(OH)D) were determined by immunoassay (ADVIA Centaur Vitamin D®). The results were classified as sufficient (> 20 ng/ml), insufficient (10–20 ng/ml) and deficient (< 10 ng/ml).Results153 analyses of vitamin D were carried out (58.2% in girls and 41.8% in boys), distributed in two age groups: 5–10 (62) and 10–15 (91). 66% of the total of the sample presented some degree of vitamin D deficit (60.1% insufficient (92) and 5.9% (11) deficient). In Galicia, there is a high prevalence of vitamin D deficiency/insufficiency in the healthy population, which increases if the patients present some kind of chronic pathology, thus leading to a public health problem. It is advisable to increase the consumption of fortified foods and/or to reconsider the administration of vitamin supplements.Electronic supplementary materialThe online version of this article (10.1186/s13104-018-3903-7) contains supplementary material, which is available to authorized users.
Background:C-reactive protein (CRP) is an acute-phase protein that is used as an established biomarker to follow disease severity and progression in a plethora of inflammatory diseases. However, its pathophysiologic mechanisms of action are still poorly defined and remain elusive. CRP, in its pentameric form, exhibits weak anti-inflammatory activity. On the contrary, the monomeric isoform (mCRP) exhibits potent pro-inflammatory properties in endothelial cells, leukocytes, and platelets. So far, no data exists regarding mCRP effects in human or mouse chondrocytesObjectives:This work aimed to verify the pathophysiological relevance of mCRP in the etiology and/or progression of osteoarthritis (OA)Methods:We investigated the effects of mCRP in cultured human primary chondrocytes and in the chondrogenic ATDC5 mouse cell line. We determined mRNA and protein levels of relevant factors involved in inflammatory responses and the modulation of nitric oxide synthase type II (NOS2), an early inflammatory molecular target.Results:We demonstrate, for the first time, that monomeric C reactive protein increases NOS2, COX2, MMP13, VCAM1, IL-6, IL-8, and LCN2 expression in human and murine chondrocytes. We also demonstrated that NF-kB is a key factor in the intracellular signaling of mCRP-driven induction of pro-inflammatory and catabolic mediators in chondrocytes.Conclusion:mCRP exerts a sustained catabolic effect on human and murine chondrocytes, increasing the expression of inflammatory mediators and proteolytic enzymes, which can promote extracellular matrix (ECM) breakdown in healthy and OA cartilage. In addition, our results implicate the NF-kB signaling pathway in catabolic effects mediated by mCRP.References:[1]Sproston NR, Ashworth JJ. Role of C-reactive protein at sites of inflammation and infection. Front Immunol. 2018;9(APR). doi:10.3389/fimmu.2018.00754[2]Francisco V, Pérez T, Pino J, et al. Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks. J Orthop Res. 2018;36(2):594-604. doi:10.1002/jor.23788[3]Kozijn AE, Tartjiono MT, Ravipati S, et al. Human C-reactive protein aggravates osteoarthritis development in mice on a high-fat diet. Osteoarthr Cartil. 2019;27(1):118-128. doi:10.1016/j.joca.2018.09.007[4]Rajab IM, Majerczyk D, Olson ME, et al. C-reactive protein in gallbladder diseases: diagnostic and therapeutic insights. Biophys Reports. 2020;6(2-3):49-67. doi:10.1007/s41048-020-00108-9[5]Wu Y, Potempa LA, El Kebir D, Filep JG. C-reactive protein and inflammation: conformational changes affect function. Biol Chem. 2015;396(11):1181-1197. doi:10.1515/hsz-2015-0149[6]Thiele JR, Zeller J, Bannasch H, Stark GB, Peter K, Eisenhardt SU. Targeting C-Reactive Protein in Inflammatory Disease by Preventing Conformational Changes. Mediators Inflamm. 2015;2015(372432):9. doi:10.1155/2015/372432[7]Khreiss T, József L, Hossain S, Chan JSD, Potempa LA, Filep JG. Loss of pentameric symmetry of C-reactive protein is associated with delayed apoptosis of human neutrophils. J Biol Chem. 2002;277(43):40775-40781. doi:10.1074/jbc.M205378200[8]Jia ZK, Li HY, Liang YL, Potempa LA, Ji SR, Wu Y. Monomeric C-reactive protein binds and neutralizes receptor activator of NF-κB ligand-induced osteoclast differentiation. Front Immunol. 2018;9(FEB). doi:10.3389/fimmu.2018.00234[9]Francisco V, Ruiz-Fernández C, Pino J, et al. Adipokines: Linking metabolic syndrome, the immune system, and arthritic diseases. Biochem Pharmacol. 2019;165:196-206. doi:10.1016/j.bcp.2019.03.030[10]Ullah N, Ma FR, Han J, et al. Monomeric C-reactive protein regulates fibronectin mediated monocyte adhesion. Mol Immunol. 2020;117:122-130. doi:10.1016/j.molimm.2019.10.013[11]Boras E, Slevin M, Alexander MY, et al. Monomeric C-reactive protein and Notch-3 co-operatively increase angiogenesis through PI3K signalling pathway. Cytokine. 2014;69(2):165-179. doi:10.1016/j.cyto.2014.05.027Disclosure of Interests:None declared
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.