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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Review Article

Non-pharmacological Strategies Against Systemic Inflammation: Molecular Basis and Clinical Evidence

Author(s): Rita Del Pinto, Davide Pietropaoli, Annalisa Monaco, Giovambattista Desideri, Claudio Ferri and Davide Grassi*

Volume 26, Issue 22, 2020

Page: [2620 - 2629] Pages: 10

DOI: 10.2174/1381612826666200403122600

Price: $65

Abstract

Systemic inflammation is a common denominator to a variety of cardiovascular (CV) and non-CV diseases and relative risk factors, including hypertension and its control, metabolic diseases, rheumatic disorders, and those affecting the gastrointestinal tract. Besides medications, a non-pharmacological approach encompassing lifestyle changes and other complementary measures is mentioned in several updated guidelines on the management of these conditions. We performed an updated narrative review on the mechanisms behind the systemic impact of inflammation and the role of non-pharmacological, complementary measures centered on lowering systemic phlogosis for preserving or restoring a good global health. The central role of genetics in shaping the immune response is discussed in conjunction with that of the microbiome, highlighting the interdependence and mutual influences between the human genome and microbial integrity, diversity, and functions. Several plausible strategies to modulate inflammation and restore balanced crosstalk between the human genome and the microbiome are then recapitulated, including dietary measures, active lifestyle, and other potential approaches to manipulate the resident microbial community. To date, evidence from high-quality human studies is sparse to allow the unconditioned inclusion of understudied, though plausible solutions against inflammation into public health strategies for global wellness. This gap claims further focused, well-designed research targeted at unravelling the mechanisms behind future personalized medicine.

Keywords: Inflammation, immune system, gastrointestinal microbiome, diet, food, nutrition, exercise, oral hygiene, probiotics, prebiotics.

[1]
Williams B, Mancia G, Spiering W, et al. ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J 2018; 39: 3021-104.
[2]
Ross R. Atherosclerosis--an inflammatory disease. Eur Heart J 1999; 340: 115-26.
[3]
Grant PJ, Cosentino F. The 2019 ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD: New features and the ‘Ten Commandments’ of the 2019 Guidelines are discussed by Professor Peter J. Grant and Professor Francesco Cosentino, the Task Force chairmen. Eur Heart J 2019; 40: 3215-17.
[4]
Bozkurt B, Aguilar D, Deswal A, et al. Contributory risk and management of comorbidities of hypertension, obesity, diabetes mellitus, hyperlipidemia, and metabolic syndrome in chronic heart failure: a scientific statement from the american heart association. Circulation 2016; 134: e535-78.
[5]
Bassi N, Karagodin I, Wang S, et al. Lifestyle modification for metabolic syndrome: a systematic review. Am J Med 2014; 127: 1242.e1-0-.
[http://dx.doi.org/10.1016/j.amjmed.2014.06.035]
[6]
Fanouriakis A, Kostopoulou M, Alunno A, et al. update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis 2019; 78: 736-45.
[7]
Combe B, Landewe R, Daien CI, Hua C, et al. 2016 update of the EULAR recommendations for the management of early arthritis 2017; 76(6): 948-59.
[8]
Matsuoka K, Kobayashi T, Ueno F, et al. Evidence-based clinical practice guidelines for inflammatory bowel disease. J Gastroenterol 2018; 53: 305-53.
[http://dx.doi.org/10.1007/s00535-018-1439-1]
[9]
Forbes A, Escher J, Hébuterne X, et al. ESPEN guideline: Clinical nutrition in inflammatory bowel disease. Clin Nutr 2017; 36: 321-47.
[10]
Del Pinto R, Ferri C. Hypertension management at older age: an update. high blood press. Cardiovasc Prev 2019; 26(1): 27-36.
[http://dx.doi.org/10.1007/s40292-018-0290-z] [PMID: 30467638]
[11]
Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Clin Periodontol 2018; 45(Suppl. 20): S68-77.
[12]
Del Pinto R, Pagliacci S, De Feo M, Grassi D, Ferri C. Italian Society of Hypertension and Federfarma. Prevalence of hypertension and associated cardiovascular risk factors among pharmacies customers: an Italian nationwide epidemiological survey. Eur J Prev Cardiol 2019. 2047487319851301
[13]
Sattar N, McCarey DW, Capell H, McInnes IB. Explaining how “high-grade” systemic inflammation accelerates vascular risk in rheumatoid arthritis. Circulation 2003; 108: 2957-63.
[http://dx.doi.org/10.1161/01.CIR.0000099844.31524.05]
[14]
Pietropaoli D, Del Pinto R, Ferri C, et al. Association between periodontal inflammation and hypertension using periodontal inflamed surface area and bleeding on probing. J Clin Periodontol 2020; 47: 160-72.
[http://dx.doi.org/10.1111/jcpe.13216]
[15]
Nasef NA, Mehta S, Ferguson LR. Susceptibility to chronic inflammation: an update. Arch Toxicol 2017; 91: 1131-41.
[http://dx.doi.org/10.1007/s00204-016-1914-5]
[16]
Popa C, Netea MG, van Riel PLCM, van der Meer JWM, Stalenhoef AFH. The role of TNF-alpha in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk. J Lipid Res 2007; 48: 751-62.
[17]
Waterer GW, Wunderink RG. Science review: Genetic variability in the systemic inflammatory response. Care 2003; 7: 1-7.
[18]
Price P, Witt C, Allcock R, et al. The genetic basis for the association of the 8.1 ancestral haplotype (A1, B8, DR3) with multiple immunopathological diseases. Immunol Rev 1999; 167: 257-74.
[19]
Louis E, Franchimont D, Piron A, et al. Tumour necrosis factor (TNF) gene polymorphism influences TNF-alpha production in lipopolysaccharide (LPS)-stimulated whole blood cell culture in healthy humans. Immunol Rev 1998; 113: 401-6.
[20]
Kroeger KM, Carville KS, Abraham LJ. The -308 tumor necrosis factor-α promoter polymorphism effects transcription. Mol Immunol 1997; 34: 391-9.
[21]
Mira JP, Cariou A, Grall F, et al. Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study. JAMA 1999; 282: 561-8.
[22]
McGuire W, Hill AV, Allsopp CE, Greenwood BM, Kwiatkowski D. Variation in the TNF-alpha promoter region associated with susceptibility to cerebral malaria. Nature 1994; 371: 508-10.
[23]
Knight JC, Udalova I, Hill AV, et al. A polymorphism that affects OCT-1 binding to the TNF promoter region is associated with severe malaria. Nat Genet 1999; 22: 145-50.
[http://dx.doi.org/10.1038/9649]
[24]
Grove J, Daly AK, Bassendine MF, Day CP. Association of a tumor necrosis factor promoter polymorphism with susceptibility to alcoholic steatohepatitis. Hepatology 1997; 26: 143-6.
[http://dx.doi.org/10.1002/hep.510260119]
[25]
Stüber F, Petersen M, Bokelmann F, Schade U. A genomic polymorphism within the tumor necrosis factor locus influences plasma tumor necrosis factor-alpha concentrations and outcome of patients with severe sepsis. Crit Care Med 1996; 24: 381-4.
[http://dx.doi.org/10.1097/00003246-199603000-00004]
[26]
Heesen M, Kunz D, Bachmann-Mennenga B, Merk HF, Bloemeke B. Linkage disequilibrium between tumor necrosis factor (TNF)-alpha-308 G/A promoter and TNF-beta NcoI polymorphisms: Association with TNF-alpha response of granulocytes to endotoxin stimulation. Crit Care Med 2003; 31: 211-4.
[27]
Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev 2018; 281: 8-27.
[http://dx.doi.org/10.1111/imr.12621]
[28]
Mantovani A, Dinarello CA, Molgora M, Garlanda C. Interleukin-1 and related cytokines in the regulation of inflammation and immunity. Immunity 2019; 50: 778-95.
[29]
Ma L, Chu W-M, Zhu J, Wu Y-N, Wang Z-L. Interleukin-1β (3953/4) C→T polymorphism increases the risk of chronic periodontitis in Asians: evidence from a meta-analysis of 20 case-control studies. Arch Med Sci 2015; 11: 267-73.
[30]
Karimbux NY, Saraiya VM, Elangovan S, et al. Interleukin-1 gene polymorphisms and chronic periodontitis in adult whites: a systematic review and meta-analysis. J Periodontol 2012; 83: 1407-19.
[31]
Azevedo PM, Merriman TR, Topless RK, Wilson NJ, Crengle S, Lennon DR. Association study involving polymorphisms in IL-6, IL-1RA, and CTLA4 genes and rheumatic heart disease in New Zealand population of Māori and Pacific ancestry. Cytokine 2016; 85: 201-6.
[32]
Buraczynska M, Zukowski P, Drop B, Baranowicz-Gaszczyk I, Ksiazek A. Effect of G(-174)C polymorphism in interleukin-6 gene on cardiovascular disease in type 2 diabetes patients. Cytokine 2016; 79: 7-11.
[33]
Zhao L, Cheng G, Jin R, et al. Deletion of interleukin-6 attenuates pressure overload-induced left ventricular hypertrophy and dysfunction. Circ Res 2016; 118: 1918-29.
[http://dx.doi.org/10.1161/CIRCRESAHA.116.308688]
[34]
Xia L, Chen M, Bi D, et al. Combined analysis of interleukin-10 gene polymorphisms and protein expression in children with cerebral palsy. Front Neurol 2018; 9 Available from:https://www.frontiersin.org/articles/10.3389/fneur.2018.00182/pdf
[http://dx.doi.org/10.3389/fneur.2018.00182]
[35]
Bianchi E, Rogge L. The IL-23/IL-17 pathway in human chronic inflammatory diseases-new insight from genetics and targeted therapies. Genes Immun 2019; 20: 415-25.
[36]
Mokry LE, Zhou S, Guo C, et al. Interleukin-18 as a drug repositioning opportunity for inflammatory bowel disease: A Mendelian randomization study. Sci Rep 2019; 9: 1-7.
[37]
Abate E, Blomgran R, Verma D, et al. Polymorphisms in CARD8 and NLRP3 are associated with extrapulmonary TB and poor clinical outcome in active TB in Ethiopia. Sci Rep 2019; 9: 1-6.
[http://dx.doi.org/10.1038/s41598-019-40121-8]
[38]
Schweiger DS, Goricar K, Hovnik T, et al. Dual role of PTPN22 but not NLRP3 inflammasome polymorphisms in type 1 diabetes and celiac disease in children. Front Pedriat 2019; 7
[http://dx.doi.org/10.3389/fped.2019.00063]
[39]
Heap GA, van Heel DA. The genetics of chronic inflammatory diseases. Hum Mol Genet 2009; 18: R101-6.
[http://dx.doi.org/10.1093/hmg/ddp001]
[40]
Ellinghaus D, Jostins L, Spain SL, et al. Analysis of five chronic inflammatory diseases identifies 27 new associations and highlights disease-specific patterns at shared loci. Nat Genet 2016; 48: 510-8.
[http://dx.doi.org/10.1038/ng.3528]
[41]
van der Laan SW, Siemelink MA, et al. Genetic susceptibility loci for cardiovascular disease and their impact on atherosclerotic plaques. Circ Genom Precis Med 2018; 11 e002115
[42]
Ligthart S, Vaez A, Võsa U, et al. Genome analyses of >200,000 individuals identify 58 loci for chronic inflammation and highlight pathways that link inflammation and complex disorders. Am J Hum Genet 2018; 103: 691-706.
[43]
Del Pinto R, Ferri C. Inflammation-accelerated senescence and the cardiovascular system: mechanisms and perspectives. Int J Mol Sci 2018; 19
[http://dx.doi.org/10.3390/ijms19123701]
[44]
Pont AR, Sadri N, Hsiao SJ, Smith S, Schneider RJ. mRNA decay factor AUF1 maintains normal aging, telomere maintenance, and suppression of senescence by activation of telomerase transcription. Mol Cell 2012; 47: 5-15.
[45]
Stylianou E. Epigenetics of chronic inflammatory diseases. J Inflamm Res 2019; 12: 1-14.
[46]
Wood IC. Contribution and therapeutic potential of epigenetic modifications in Alzheimer’s disease. Neurosci 2018; 12: 649.
[47]
Ciechomska M, van Laar JM, O’Reilly S. Emerging role of epigenetics in systemic sclerosis pathogenesis. Genes Immun 2014; 15: 433-9.
[http://dx.doi.org/10.1038/gene.2014.44]
[48]
Whayne TF. Epigenetics in the development, modification, and prevention of cardiovascular disease. Mol Biol Rep 2015; 42: 765-76.
[http://dx.doi.org/10.1007/s11033-014-3727-z]
[49]
Gilbert JA, Blaser MJ, Caporaso JG, Jansson JK, Lynch SV, Knight R. Current understanding of the human microbiome. Nat Med 2018; 24: 392-400.
[http://dx.doi.org/10.1038/nm.4517]
[50]
Ursell LK, Metcalf JL, Parfrey LW, Knight R. Defining the human microbiome. Nutr Rev 2012; 70(Suppl. 1): S38-44.
[http://dx.doi.org/10.1111/j.1753-4887.2012.00493.x]
[51]
Del Pinto R, Ferri C, Cominelli F. Vitamin D axis in inflammatory bowel diseases: role. current uses and future perspectives. Int J Mol Sci 2017; 18
[http://dx.doi.org/10.3390/ijms18112360]
[52]
Tang WHW, Bäckhed F, Landmesser U, Hazen SL. Intestinal microbiota in cardiovascular health and disease: JACC state-of-the-art review. J Am Coll Cardiol 2019; 73(16): 2089-105.
[http://dx.doi.org/10.1016/j.jacc.2019.03.024] [PMID: 31023434]
[53]
Wilkins LJ, Monga M, Miller AW. Defining dysbiosis for a cluster of chronic diseases. Sci Rep 2019; 9: 12918.
[54]
Kozarov EV, Dorn BR, Shelburne CE, Dunn WA Jr, Progulske-Fox A. Human atherosclerotic plaque contains viable invasive Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Vasc Biol 2005; 25: e17-8.
[http://dx.doi.org/10.1161/01.ATV.0000155018.67835.1a]
[55]
Kuo CC, Shor A, Campbell LA, Fukushi H, Patton DL, Grayston JT. Demonstration of Chlamydia pneumoniae in atherosclerotic lesions of coronary arteries. J Infect Dis 1993; 167: 841-9.
[http://dx.doi.org/10.1093/infdis/167.4.841]
[56]
Koizumi Y, Kurita-Ochiai T, Oguchi S, Yamamoto M. Nasal immunization with Porphyromonas gingivalis outer membrane protein decreases P. gingivalis-induced atherosclerosis and inflammation in spontaneously hyperlipidemic mice. Infect Immun 2008; 76: 2958-65.
[57]
O’Brien-Simpson NM, Holden JA, et al. A therapeutic gingipain vaccine induces neutralising IgG1 antibodies that protect against experimental periodontitis NJP vaccines 2016; 1 16022
[http://dx.doi.org/10.1038/npjvaccines.2016.22]
[58]
Andraws R, Berger JS, Brown DL. Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials. JAMA 2005; 293: 2641-7.
[http://dx.doi.org/10.1001/jama.293.21.2641]
[59]
Lam V, Su J, Koprowski S, et al. Intestinal microbiota determine severity of myocardial infarction in rats. FASEB J 2012; 26: 1727-35.
[http://dx.doi.org/10.1096/fj.11-197921]
[60]
Jie Z, Xia H, Zhong S-L, et al. The gut microbiome in atherosclerotic cardiovascular disease. Nat Commun 2017; 8: 845.
[http://dx.doi.org/10.1038/s41467-017-00900-1]
[61]
Pietropaoli D, Del Pinto R, Ferri C, Ortu E, Monaco A. Definition of hypertension-associated oral pathogens in NHANES. J Periodontol 2019; 90: 866-76.
[http://dx.doi.org/10.1002/JPER.19-0046]
[62]
Neuman H, Forsythe P, Uzan A, Avni O, Koren O. Antibiotics in early life: dysbiosis and the damage done. FEMS Microbiol Rev 2018; 42: 489-99.
[http://dx.doi.org/10.1093/femsre/fuy018]
[63]
Sun S, Lulla A, Sioda M, et al. Gut microbiota composition and blood pressure. Hypertension 2019; 73: 998-1006.
[64]
Luedde M, Winkler T, Heinsen F-A, et al. Heart failure is associated with depletion of core intestinal microbiota. ESC Heart Fail 2017; 4: 282-90.
[http://dx.doi.org/10.1002/ehf2.12155]
[65]
Kummen M, Mayerhofer CCK, Vestad B, et al. Gut microbiota signature in heart failure defined from profiling of 2 independent cohorts. J Am Coll Cardiol 2018; 71: 1184-6.
[66]
Pedersen HK, Gudmundsdottir V, et al. Human gut microbes impact host serum metabolome and insulin sensitivity. Nature 2016; 535: 376-81.
[http://dx.doi.org/10.1038/nature18646]
[67]
Wilck N, Matus MG, Kearney SM, et al. Salt-responsive gut commensal modulates TH17 axis and disease. Nature 2017; 551: 585-89.
[68]
Kleinewietfeld M, Manzel A, Titze J, et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature 2013; 496: 518-22.
[http://dx.doi.org/10.1038/nature11868]
[69]
Rogler G, Rosano G. The heart and the gut. Eur Heart J 2014; 35: 426-30.
[http://dx.doi.org/10.1093/eurheartj/eht271]
[70]
Hill C, Guarner F, Reid G, et al. Expert consensus document. The International Scientific Association for Probiotics and Prebiotics consensus statement on the scope and appropriate use of the term probiotic. Gastroenterol Hepatol 2014; 11: 506-14.
[71]
Kumar M, Nagpal R, Verma V, et al. Probiotic metabolites as epigenetic targets in the prevention of colon cancer. Nutr Rev 2013; 71: 23-34.
[http://dx.doi.org/10.1111/j.1753-4887.2012.00542.x]
[72]
Food and Agriculture Organization of the United Nations, World Health Organization. Report of the Joint FAO/WHO Expert Consultation on Evaluation of Health and Nutritional Properties of Probiotics in Food Including Powder Milk with Live Lactic Acid Bacteria, Córdoba, Argentina, 1-4 October 2001; 30
[73]
Guo Q, Goldenberg JZ, Humphrey C, El Dib R, Johnston BC. Probiotics for the prevention of pediatric antibiotic-associated diarrhea. Cochrane Database Syst Rev 2019; 4CD004827
[http://dx.doi.org/10.1002/14651858.CD004827.pub5]
[74]
Goldenberg JZ, Yap C, Lytvyn L, et al. Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. Cochrane Database Syst Rev 2017; 12
[http://dx.doi.org/10.1002/14651858.CD006095.pub4]
[75]
Rondanelli M, Faliva MA, Perna S, Giacosa A, Peroni G, Castellazzi AM. Using probiotics in clinical practice: Where are we now? A review of existing meta-analyses. Gut Microbes 2017; 8: 521-43.
[76]
Parker EA, Roy T, D’Adamo CR, Wieland LS. Probiotics and gastrointestinal conditions: An overview of evidence from the Cochrane Collaboration. Nutrition 2018; 45: 125- 134.e11.
[77]
Maldonado Galdeano C, Cazorla SI, Lemme Dumit JM, Vélez E, Perdigón G. Beneficial effects of probiotic consumption on the immune system. Ann Nutr Metab 2019; 74: 115-24.
[78]
Mantis NJ, Rol N, Corthésy B. Secretory IgA’s complex roles in immunity and mucosal homeostasis in the gut. Mucosal Immunol 2011; 4: 603-11.
[http://dx.doi.org/10.1038/mi.2011.41]
[79]
Sichetti M, De Marco S, Pagiotti R, Traina G, Pietrella D. Anti-inflammatory effect of multistrain probiotic formulation (L. rhamnosus, B. lactis, and B. longum). Nutrition 2018; 53: 95-102.
[80]
Furrie E, Macfarlane S, Kennedy A, et al. Synbiotic therapy (Bifidobacterium longum/Synergy 1) initiates resolution of inflammation in patients with active ulcerative colitis: a randomised controlled pilot trial. Gut 2005; 54: 242-9.
[81]
Velez EMM, Maldonado Galdeano C, Carmuega E, Weill R, Bibas Bonet ME, Perdigón G. Probiotic fermented milk consumption modulates the allergic process induced by ovoalbumin in mice. Br J Nutr 2015; 114: 566-76.
[http://dx.doi.org/10.1017/S0007114515001981]
[82]
Gibson GR, Hutkins R, Sanders ME, et al. Expert consensus document: The International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of prebiotics. Nat Rev Gastroenterol Hepatol 2017; 14: 491-502.
[83]
De Leoz MLA, Kalanetra KM, Bokulich NA, et al. Human milk glycomics and gut microbial genomics in infant feces show a correlation between human milk oligosaccharides and gut microbiota: a proof-of-concept study. J Proteome Res 2015; 14: 491-502.
[http://dx.doi.org/10.1021/pr500759e]
[84]
He Y, Lawlor NT, Newburg DS. Human milk components modulate toll-like receptor-mediated inflammation. Adv Nutr 2016; 7: 102-11.
[85]
Connolly ML, Tuohy KM, Lovegrove JA. Wholegrain oat-based cereals have prebiotic potential and low glycaemic index. Br J Nutr 2012; 108: 2198-206.
[http://dx.doi.org/10.1017/S0007114512000281]
[86]
Tuohy KM, Fava F, Viola R. ‘The way to a man’s heart is through his gut microbiota’--dietary pro- and prebiotics for the management of cardiovascular risk. Proc Nutr Soc 2014; 73: 172-85.
[87]
Chun RF, Liu PT, Modlin RL, Adams JS, Hewison M. Impact of vitamin D on immune function: lessons learned from genome-wide Frontiers Physiol analysis 2014.
[http://dx.doi.org/10.3389/fphys.2014.00151]
[88]
Wang T-T, Dabbas B, Laperriere D, et al. Direct and indirect induction by 1,25-dihydroxyvitamin D3 of the NOD2/CARD15-defensin β2 innate immune pathway defective in Crohn disease. J Biol Chem 2010; 285: 2227-31.
[89]
Kong J, Zhang Z, Musch MW, et al. Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Am J Physiol Gastrointest Liver Physiol 2008; 294: G208-16.
[http://dx.doi.org/10.1152/ajpgi.00398.2007]
[90]
Liu W, Chen Y, Golan MA, et al. Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis. J Clin Invest 2013; 123: 3983-96.
[http://dx.doi.org/10.1172/JCI65842]
[91]
Waterhouse JC, Perez TH, Albert PJ. Reversing bacteria-induced vitamin D receptor dysfunction is key to autoimmune disease. Ann N Y Acad Sci 2009; 1173: 757-65.
[http://dx.doi.org/10.1111/j.1749-6632.2009.04637.x]
[92]
Xue L-N, Xu K-Q, Zhang W, Wang Q, Wu J, Wang X-Y. Associations between vitamin D receptor polymorphisms and susceptibility to ulcerative colitis and Crohn’s disease: a meta-analysis. Inflamm Bowel Dis 2013; 19: 54-60.
[93]
Del Pinto R, Wright JT, Monaco A, Pietropaoli D, Ferri C. Vitamin D and blood pressure control among hypertensive adults: results from NHANES 2001-2014. J Hypertens 2019.
[http://dx.doi.org/10.1097/HJH.0000000000002231]
[94]
Autier P, Mullie P, Macacu A, et al. Effect of vitamin D supplementation on non-skeletal disorders: a systematic review of meta-analyses and randomised trials. Lancet Diabetes Endocrinol 2017; 5: 986-1004.
[http://dx.doi.org/10.1016/S2213-8587(17)30357-1]
[95]
Marniemi J, Alanen E, Impivaara O, et al. Dietary and serum vitamins and minerals as predictors of myocardial infarction and stroke in elderly subjects. Nutr Metab Cardiovasc Dis 2005; 15: 188-97.
[http://dx.doi.org/10.1016/j.numecd.2005.01.001]
[96]
Manson JE, Cook NR, Lee I-M, et al. Vitamin D supplements and prevention of cancer and cardiovascular disease. N Engl J Med 2019; 380: 33-44.
[http://dx.doi.org/10.1056/NEJMoa1809944]
[97]
Akbaraly TN, Shipley MJ, Ferrie JE, et al. Long-term adherence to healthy dietary guidelines and chronic inflammation in the prospective Whitehall II study. Am J Med 2015; 128: 152- 160.e4.
[http://dx.doi.org/10.1016/j.amjmed.2014.10.002]
[98]
Ahluwalia N, Andreeva VA, Kesse-Guyot E, Hercberg S. Dietary patterns, inflammation and the metabolic syndrome. Diabetes Metab 2013; 39: 99-110.
[http://dx.doi.org/10.1016/j.diabet.2012.08.007]
[99]
Sureda A, Bibiloni MDM, Julibert A, et al. Adherence to the mediterranean diet and inflammatory markers. Nutrients 2018; 10(1)
[http://dx.doi.org/10.3390/nu10010062]
[100]
Mamalaki E, Anastasiou CA, Ntanasi E, et al. Associations between the mediterranean diet and sleep in older adults: Results from the hellenic longitudinal investigation of aging and diet study. Geriatr Gerontol Int 2018; 18: 1543-8.
[101]
Rees K, Takeda A, Martin N, et al. Mediterranean-style diet for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2019; 3 CD009825
[http://dx.doi.org/10.1002/14651858.CD009825.pub3]
[102]
Julia C, Meunier N, Touvier M, et al. Dietary patterns and risk of elevated C-reactive protein concentrations 12 years later. Br J Nutr 2013; 110: 747-54.
[http://dx.doi.org/10.1017/S0007114512005636]
[103]
Sudheendran S, Chang CC, Deckelbaum RJ. N-3 vs. saturated fatty acids: effects on the arterial wall. Prostaglandins Leukot Essent Fatty Acids 2010; 82: 205-9.
[104]
Serhan CN, Chiang N, Van Dyke TE. Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators. Nat Rev Immunol 2008; 8: 349-61.
[http://dx.doi.org/10.1038/nri2294]
[105]
Manson JE, Cook NR, Lee I-M, et al. Marine n-3 fatty acids and prevention of cardiovascular disease and cancer. N Engl J Med 2019; 380: 23-32.
[http://dx.doi.org/10.1056/NEJMoa1811403]
[106]
Aronson JK. Defining ‘nutraceuticals’: neither nutritious nor pharmaceutical. Br J Clin Pharmacol 2017; 83: 8-19.
[http://dx.doi.org/10.1111/bcp.12935]
[107]
Santini A, Cammarata SM, Capone G, et al. Nutraceuticals: opening the debate for a regulatory framework. Br J Clin Pharmacol 2018; 84: 659-72.
[http://dx.doi.org/10.1111/bcp.13496]
[108]
Kris-Etherton PM, Hecker KD, Bonanome A, et al. Bioactive compounds in foods: their role in the prevention of cardiovascular disease and cancer. Am J Med 2002; 113: 71-88.
[http://dx.doi.org/10.1016/S0002-9343(01)00995-0]
[109]
Cicero AFG, Grassi D, Tocci G, Galletti F, Borghi C, Ferri C. Nutrients and nutraceuticals for the management of high normal blood pressure: an evidence-based consensus document. High Blood Press Cardiovasc Prev 2019; 26(1): 9-25.
[110]
Vanhatalo A, Blackwell JR, L’Heureux JE, et al. Nitrate-responsive oral microbiome modulates nitric oxide homeostasis and blood pressure in humans. Free Radic Biol Med 2018; 124: 21-30.
[http://dx.doi.org/10.1016/j.freeradbiomed.2018.05.078]
[111]
Grassi D, Socci V, Tempesta D, et al. Flavanol-rich chocolate acutely improves arterial function and working memory performance counteracting the effects of sleep deprivation in healthy individuals. J Hypertens 2016; 34: 1298-308.
[http://dx.doi.org/10.1097/HJH.0000000000000926]
[112]
Desideri G, Kwik-Uribe C, Grassi D, et al. Benefits in cognitive function, blood pressure, and insulin resistance through cocoa flavanol consumption in elderly subjects with mild cognitive impairment: the Cocoa, Cognition, and Aging (CoCoA) study. Hypertension 2012; 60: 794-801.
[113]
Kim J, Kim J, Shim J, Lee CY, Lee KW, Lee HJ. Cocoa phytochemicals: recent advances in molecular mechanisms on health. Crit Rev Food Sci Nutr 2014; 54: 1458-72.
[http://dx.doi.org/10.1080/10408398.2011.641041]
[114]
Gleeson M, Bishop NC, Stensel DJ, Lindley MR, Mastana SS, Nimmo MA. The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol 2011; 11: 607-15.
[http://dx.doi.org/10.1038/nri3041]
[115]
Ford ES. Does exercise reduce inflammation? Physical activity and C-reactive protein among U.S. adults. Epidemiology 2002; 13(5): 561-8.
[http://dx.doi.org/10.1097/00001648-200209000-00012] [PMID: 10.1097/00001648-200209000-00012]
[116]
Ouchi N, Parker JL, Lugus JJ, Walsh K. Adipokines in inflammation and metabolic disease. Nat Rev Immunol 2011; 11: 85-97.
[http://dx.doi.org/10.1038/nri2921]
[117]
Pedersen BK. Edward F. Adolph distinguished lecture: muscle as an endocrine organ: IL-6 and other myokines. J Appl Physiol 2009; 107: 1006-14.
[http://dx.doi.org/10.1152/japplphysiol.00734.2009]
[118]
Steensberg A, Fischer CP, Keller C, Møller K, Pedersen BK. IL-6 enhances plasma IL-1ra, IL-10, and cortisol in humans. Am J Physiol Endocrinol Metab 2003; 285: E433.
[119]
Flynn MG, McFarlin BK. Toll-like receptor 4: link to the anti-inflammatory effects of exercise? Exerc Sport Sci Rev 2006; 34: 176-81.
[120]
Kawanishi N, Yano H, Yokogawa Y, Suzuki K. Exercise training inhibits inflammation in adipose tissue via both suppression of macrophage infiltration and acceleration of phenotypic switching from M1 to M2 macrophages in high-fat-diet-induced obese mice. Exerc Immunol Rev 2010; 16: 105-8.
[121]
Sahl RE, Andersen PR, Gronbaek K, et al. Repeated excessive exercise attenuates the anti-inflammatory effects of exercise in older men. Front Physiol 2017; 8: 1286.
[122]
Fischer CP. Interleukin-6 in acute exercise and training: what is the biological relevance? Exerc Immunol Rev 2006; 12: 6-33.
[123]
Tonetti MS, D’Aiuto F, Nibali L, et al. Treatment of periodontitis and endothelial function. N Engl J Med 2007; 356: 911-20.
[124]
Pietropaoli D, Del Pinto R, Ferri C, et al. Poor oral health and blood pressure control among us hypertensive adults: results from the national health and nutrition examination survey 2009 to 2014. Hypertension 2018; 72: 1365-73.
[125]
Nesse W, Abbas F, van der Ploeg I, Spijkervet FKL, Dijkstra PU, Vissink A. Periodontal inflamed surface area: quantifying inflammatory burden. J Clin Periodontol 2008; 35: 668-73.
[http://dx.doi.org/10.1111/j.1600-051X.2008.01249.x]
[126]
Orlandi M, Suvan J, Petrie A, et al. Association between periodontal disease and its treatment, flow-mediated dilatation and carotid intima-media thickness: a systematic review and meta-analysis. Atherosclerosis 2014; 236: 39-46.
[http://dx.doi.org/10.1016/j.atherosclerosis.2014.06.002]
[127]
Demmer RT, Squillaro A, Papapanou PN, et al. Periodontal infection, systemic inflammation, and insulin resistance: results from the continuous National Health and Nutrition Examination Survey (NHANES) 1999-2004. Diabetes Care 2012; 35: 2235-42.
[http://dx.doi.org/10.2337/dc12-0072]
[128]
Sanz M, Marco Del Castillo A, Gonzalez-Juanatey JR, et al. Periodontitis and cardiovascular diseases: Consensus report. J Clin Periodontol 2020; 47: 268-88.
[129]
van Nood E, Vrieze A, Nieuwdorp M, et al. Duodenal infusion of donor feces for recurrent Clostridium difficile. N Engl J Med 2013; 368: 407-15.
[130]
Shogbesan O, Poudel DR, Victor S, et al. A systematic review of the efficacy and safety of fecal microbiota transplant for infection in immunocompromised patients. Can J Gastroenterol Hepatol 2018; 2018 1394379
[131]
Hui W, Li T, Liu W, Zhou C, Gao F. Fecal microbiota transplantation for treatment of recurrent C. difficile infection: An updated randomized controlled trial meta-analysis. PLoS One 2019; 14 e0210016
[132]
Imdad A, Nicholson MR, Tanner-Smith EE, et al. Fecal transplantation for treatment of inflammatory bowel disease. Cochrane Database Syst Rev 2018; 11
[http://dx.doi.org/10.1002/14651858.CD012774.pub2]
[133]
Burrello C, Garavaglia F, Cribiù FM, et al. Therapeutic faecal microbiota transplantation controls intestinal inflammation through IL10 secretion by immune cells. Nat Commun 2018; 9: 5184.
[http://dx.doi.org/10.1038/s41467-018-07359-8]
[134]
Huber S, Gagliani N, Esplugues E, et al. Th17 cells express interleukin-10 receptor and are controlled by Foxp3− and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner. Immunity 2011; 34: 554-65.
[135]
Burrello C, Giuffrè MR, Macandog AD, et al. Fecal microbiota transplantation controls murine chronic intestinal inflammation by modulating immune cell functions and gut microbiota composition. Cells 2019; 8
[http://dx.doi.org/10.3390/cells8060517]
[136]
Centre for Biologies Evaluation, Research. Safety Communication on Use of SMD and MDROs. U. S. Food and Drug Administration 2019.http://www.fda.gov/vaccines-blood-biologics/safety-availability-biologics/important-safety-alert-regarding-use-fecal-microbiota-transplantation-and-risk-serious-adverse

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