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C-C motif chemokine 7 precursor (Monocyte chemoattractant protein 3) (Monocyte chemotactic protein 3) (MCP-3) (NC28) (Small-inducible cytokine A7) [MCP3] [SCYA6] [SCYA7] ==Publications== {{medline-entry |title=Increased cardiovascular and atherosclerosis markers in blood of older patients with atopic dermatitis. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31622668 |abstract=Atopic dermatitis (AD) is associated with increased systemic inflammation and cardiovascular risk. Although previous studies have found increased inflammatory proteins in the blood of patients with AD, detailed comparison among patients with AD of different ages is unavailable. To characterize the blood proteomic signature of patients with AD as a function of age. We used the OLINK high-throughput proteomic assay to measure serum inflammatory and cardiovascular risk proteins in 71 patients with moderate to severe AD from 3 age groups (18-40 years old [n = 26], 41-60 years old [n = 24], and >60 years old [n = 21]) compared with 37 age-matched controls. Total and allergen-specific serum IgEs were also measured. When we compared patients with AD from 3 different age groups with their respective controls, we identified a total of 172 differentially expressed proteins. T 2 chemokines (CCL13, CCL17) were consistently elevated in patients with AD across all ages (P < .05), whereas T 1 (CXCL10) and T 17 (KYNU, CCL20) markers incrementally increased with age in both patients with AD and healthy subjects. Elderly patients with AD (>60 years old) exhibited striking upregulation of key proinflammatory proteins, including markers of atherosclerosis (CCL4, [[CCL7]], SORT1), cardiovascular risk (GDF15, [[MPO]], ST2), cell adhesion (CDH3), and apoptosis (FAS; all P < .05) compared with younger patients with AD and age-matched controls. We also found that total and allergen-specific serum IgEs decreased significantly with age in patients with AD (P < .05). Elderly patients with AD had increased levels of systemic inflammatory markers, including those associated with cardiovascular and atherosclerosis risk, which may explain their increased incidence of cardiovascular disease. This finding suggests that older patients with AD may benefit from cardiovascular disease screening and prevention. |mesh-terms=* Adolescent * Adult * Age Factors * Aged * Aging * Apoptosis * Atherosclerosis * Biomarkers * Cardiovascular Diseases * Cell Adhesion * Chemokines * Dermatitis, Atopic * Humans * Immunoglobulin E * Inflammation * Middle Aged * Severity of Illness Index * Th1 Cells * Th17 Cells * Young Adult |full-text-url=https://sci-hub.do/10.1016/j.anai.2019.10.013 }} {{medline-entry |title=Advanced atherosclerosis is associated with inflammation, vascular dysfunction and oxidative stress, but not hypertension. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28017665 |abstract=Although hypertension may involve underlying inflammation, it is unknown whether advanced atherosclerosis - a chronic inflammatory condition - can by itself promote hypertension. We thus tested if advanced atherosclerosis in chronically hypercholesterolemic mice is associated with systemic and end-organ inflammation, vascular dysfunction and oxidative stress, and whether blood pressure is higher than in control mice. Male ApoE and wild-type (C57Bl6J) mice were placed on a high fat or chow diet, respectively, from 5 to 61 weeks of age. Expression of several cytokines (including IL-6, [[TNF]]-α, IFN-γ and/or IL-1β) was elevated in plasma, brain, and aorta of ApoE mice. Aortic superoxide production was ∼3.5-fold greater, and endothelium-dependent relaxation was markedly reduced in aorta and mesenteric artery of ApoE versus wild-type mice. There was no difference in blood pressure of aged ApoE (104±3mmHg, n=13) and wild-type mice (113±1mmHg, n=18). To clarify any effects of aging alone, findings from 61 week-old wild-type mice were compared with those from young (8-12 weeks old) chow-fed wild-type mice. The data indicate that aging alone increased renal and aortic expression of numerous cytokines (including [[CCL2]], [[CCL7]] and IL-1β). Aging had no effect on blood pressure, systemic inflammation, oxidative stress or endothelial function. Despite systemic and end-organ inflammation, oxidative stress and endothelial dysfunction, advanced atherosclerosis does not necessarily result in elevated blood pressure. |mesh-terms=* Animals * Aorta * Apolipoproteins E * Atherosclerosis * Blood Pressure * Chemokine CCL2 * Chemokine CCL7 * Diet, High-Fat * Disease Models, Animal * Endothelium, Vascular * Hypertension * Inflammation * Interferon-gamma * Interleukin-1beta * Interleukin-6 * Male * Mesenteric Arteries * Mice * Mice, Inbred C57BL * Oxidative Stress * Superoxides * Tumor Necrosis Factor-alpha * Vascular Diseases |keywords=* Aging * Atherosclerosis * Endothelial dysfunction * Hypertension * Inflammation * Oxidative stress |full-text-url=https://sci-hub.do/10.1016/j.phrs.2016.12.032 }}
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