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Oral spray wintertime vitamin D3 supplementation has no impact on inflammation in Gaelic footballers.
Todd, JJ, McSorley, EM, Pourshahidi, LK, Madigan, SM, Crowe, W, Laird, EJ, Healy, M, McNeilly, A, Magee, PJ
Scandinavian journal of medicine & science in sports. 2017;(11):1300-1307
Abstract
Vitamin D inadequacy [total 25(OH)D <50 nmol/L] is widespread in athletes. The biologically active metabolite, 1,25-dihydroxyvitamin D, may be involved in regulating inflammation although in vitro findings have not been consistently replicated in human intervention trials. This study, conducted at a latitude of 55°N, aimed to assess inflammatory biomarkers in Gaelic footballers before and after a wintertime vitamin D3 intervention. Samples from a 12-week double-blind, randomized, placebo-controlled trial, in which 42 Gaelic footballers received 3000 IU (75 μg) vitamin D3 daily or placebo via oral spray solutions, were analysed for a range of inflammatory biomarkers. Cytokines (interleukin-8 and tumor necrosis factor-α), cathelicidin and high sensitivity C-reactive protein were quantified by multiplex assay, enzyme-linked immunosorbent assay and clinical biochemistry, respectively. White blood cell, lymphocyte, and neutrophil concentrations were determined by full blood profile. Data on total 25-hydroxyvitamin D, measured by LC-MS/MS, were available from the previous study. Vitamin D3 supplementation significantly increased mean total 25-hydroxyvitamin D concentrations from 47 to 84 nmol/L (P = 0.006); yet this had no effect on white blood cell count (P = 0.699), lymphocyte (P = 0.694), neutrophil (P = 0.594), interleukin-8 (P = 0.334), tumor necrosis factor-α (P = 0.587), cathelicidin (P = 0.745) or high sensitivity C-reactive protein concentration (P = 0.621) compared to placebo. 12-weeks vitamin D3 supplementation did not impact the immune profile of Gaelic footballers. This is likely because biomarkers were within their respective normal range or at a concentration similar to that of the general population at baseline. Future studies are encouraged to use inflammation as their primary outcome measure and recruit athletes at risk of compromised immunity.
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Scuba diving induces nitric oxide synthesis and the expression of inflammatory and regulatory genes of the immune response in neutrophils.
Sureda, A, Batle, JM, Capó, X, Martorell, M, Córdova, A, Tur, JA, Pons, A
Physiological genomics. 2014;(17):647-54
Abstract
OBJECTIVE Scuba diving, characterized by hyperoxia and hyperbaria, could increase reactive oxygen species production which acts as signaling molecules to induce adaptation against oxidative stress. The aim was to study the effects of scuba diving immersion on neutrophil inflammatory response, the induction of oxidative damage, and the NO synthesis. DESIGN Nine male divers performed a dive at 50 m depth for a total time of 35 min. Blood samples were obtained at rest before the dive, after the dive, and 3 h after the diving session. MEASUREMENTS Markers of oxidative and nitrosative damage, nitrite, and the gene expression of genes related with the synthesis of nitric oxide and lipid mediators, cytokine synthesis, and inflammation were determined in neutrophils. RESULTS The mRNA levels of genes related with the inflammatory and immune response of neutrophils, except TNF-α, myeloperoxidase, and toll-like receptor (TLR) 2, significantly increased after the recovery period respect to predive and postdive levels. NF-κB, IL-6, and TLR4 gene expression reported significant differences immediately after diving respect to the predive values. Protein nitrotyrosine levels significantly rose after diving and remained high during recovery, whereas no significant differences were reported in malondialdehyde. Neutrophil nitrite levels as indicative of inducible nitric oxide synthase (iNOS) activity progressively increased after diving and recovery. The iNOS protein levels maintained the basal values in all situations. CONCLUSION Scuba diving which combines hyperoxia, hyperbaria, and acute exercise induces nitrosative damage with increased nitrotyrosine levels and an inflammatory response in neutrophils.
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Effects of postoperative immune-enhancing enteral nutrition on the immune system, inflammatory responses, and clinical outcome.
Jiang, XH, Li, N, Zhu, WM, Wu, GH, Quan, ZW, Li, JS
Chinese medical journal. 2004;(6):835-9
Abstract
OBJECTIVE This study was conducted to evaluate the effects of postoperative immune enhancing enteral nutrition on the immune system, inflammatory responses, and clinical outcome of patients undergoing major abdominal surgery. METHODS This study was designed as a multicenter, prospective, randomized and controlled clinical trial. One hundred twenty-four patients undergoing major abdominal surgery were randomly assigned to receive either an immune enhancing enteral diet or an isocaloric and isonitrogenous control enteral diet for seven days. Enteral feeding was initiated 24 hours after surgery. Host immunity was evaluated by measuring levels of IgG, IgM, IgA, CD4, CD8, and CD4/CD8, and the inflammatory response was determined by assessing IL-1alpha, IL-2, IL-6, IL-10, and TNF-alpha levels. Infectious complications were also recorded. RESULTS One hundred twenty patients completed the study and four patients were excluded. On postoperative day 9, among patients receiving an immune enhancing diet, IgG, IgA, CD4 and CD4/CD8 levels were significantly higher and TNF-alpha and IL-6 concentrations were significantly lower compared to the control group. Moreover, among patients receiving an immune enhancing diet, when comparing preoperation to day 9 postoperation levels, increases in IgA, CD4, and CD4/CD8 levels were significantly higher than in control patients and increases in TNF-alpha concentrations were significantly lower. No statistically significant differences were found between the two groups with regard to infectious complications. CONCLUSIONS Postoperative administration of immune enhancing enteral nutrition in patients undergoing major abdominal surgery can positively modulate postoperative immunosuppressive and inflammatory responses.
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Antimonial therapy induces circulating proinflammatory cytokines in patients with cutaneous leishmaniasis.
Kocyigit, A, Gur, S, Gurel, MS, Bulut, V, Ulukanligil, M
Infection and immunity. 2002;(12):6589-91
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Abstract
The objective of this study was to evaluate the association between antimonial therapy and circulating levels of proinflammatory cytokines in patients with cutaneous leishmaniasis (CL). Patients were treated with conventional chemotherapy by using pentavalent antimonium salts (Glucantime) for 3 weeks. Circulating plasma levels of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, IL-8, and tumor necrosis factor alpha (TNF-alpha) were determined for CL patients and healthy subjects before and 3 weeks after the treatment was started. Plasma IL-1beta, IL-6, IL-8, and TNF-alpha levels were significantly higher for pretreatment CL patients than for healthy subjects. Proinflammatory cytokines significantly increased after 21 days postinfection compared to levels for the pretreatment patients. These increments were approximately 3-fold for IL-1beta and TNF-alpha levels, 10-fold for IL-6 levels, and 20-fold for IL-8 levels in patients with CL. Taken together these results indicate that circulating proinflammatory cytokine levels were increased in patients with CL as a consequence of host defense strategies, and antimonial therapy may induce these cytokines by affecting the macrophage or other components of the host defense system.
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Innate immunity associated with inflammatory responses and cytokine production against common dietary proteins in patients with autism spectrum disorder.
Jyonouchi, H, Sun, S, Itokazu, N
Neuropsychobiology. 2002;(2):76-84
Abstract
OBJECTIVES Children with autism spectrum disorder (ASD) frequently reveal various gastrointestinal (GI) symptoms that may resolve with an elimination diet along with apparent improvement of some of the behavioral symptoms. Evidence suggests that ASD may be accompanied by aberrant (inflammatory) innate immune responses. This may predispose ASD children to sensitization to common dietary proteins (DP), leading to GI inflammation and aggravation of some behavioral symptoms. METHODS We measured IFN-gamma, IL-5, and TNF-alpha production against representative DPs [gliadin, cow's milk protein (CMP), and soy] by peripheral blood mononuclear cells (PBMCs) from ASD and control children [those with DP intolerance (DPI), ASD siblings, and healthy unrelated children]. We evaluated the results in association with proinflammatory and counter-regulatory cytokine production with endotoxin (LPS), a microbial product of intestinal flora and a surrogate stimulant for innate immune responses. RESULTS ASD PBMCs produced elevated IFN-gamma and TNF-alpha, but not IL-5 with common DPs at high frequency as observed in DPI PBMCs. ASD PBMCs revealed increased proinflammatory cytokine responses with LPS at high frequency with positive correlation between proinflammatory cytokine production with LPS and IFN-gamma and TNF-alpha production against DPs. Such correlation was less evident in DPI PBMCs. CONCLUSION Immune reactivity to DPs may be associated with apparent DPI and GI inflammation in ASD children that may be partly associated with aberrant innate immune response against endotoxin, a product of the gut bacteria.