Is interleukin-22 a possible indicator of chronic heart failure's progression?

Gangemi, Sebastiano; Parisi, Pina; Ricciardi, L; Saitta, Salvatore; Minciullo, Paola Lucia; Cristani, Mariateresa; Nicita-Mauro, Vittorio; Saija, Antonella; Basile, Giorgio

doi:10.1016/j.archger.2009.05.003

Cited by 13 publications

(8 citation statements)

References 19 publications

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“…In the untreated SWMC mice, up-regulation of inflammatory mediator genes (IL-19, IL-22, MPO), antioxidant enzymes, and NADPH oxidases (Nox) family of enzymes generating reactive oxygen species (ROS) supports the view that healthy mice under extreme exposure conditions have an imbalance between inflammation and production of ROS and defensive mechanisms against oxidative damage (Dominguez-Rodriguez et al 2009; Gangemi et al, 2009; Kamata, 2009; Polytarchou et al, 2008) (Table 4). The up-regulation of genes such as IL-22, a potential indicator of chronic heart failure progression is likely to further harm the myocardium in these highly exposed animals (Gangemi et al, 2009).…”

Section: Resultsmentioning

confidence: 69%

“…The up-regulation of genes such as IL-22, a potential indicator of chronic heart failure progression is likely to further harm the myocardium in these highly exposed animals (Gangemi et al, 2009). Chocolate treated mice had a significant up-regulation of powerful antioxidant enzymes including glutathione peroxidase-3 (Gpx3) and a catalase (Cat) that protects cells from the toxic effects of hydrogen peroxide.…”

Section: Resultsmentioning

confidence: 99%

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Urban air pollution produces up-regulation of myocardial inflammatory genes and dark chocolate provides cardioprotection

Villarreal-Calderon

Reed

Palacios‐Moreno

et al. 2012

Experimental and Toxicologic Pathology

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Air pollution is a serious environmental problem. Elderly subjects show increased cardiac morbidity and mortality associated with air pollution exposure. Mexico City (MC) residents are chronically exposed to high concentrations of fine particulate matter (PM 2.5 ) and PM-associated lipopolysaccharides (PM-LPS). To test the hypothesis that chronic exposure to urban pollution produces myocardial inflammation, female Balb-c mice age 4 weeks were exposed for 16 months to two distinctly different polluted areas within MC: Southwest (SW) and Northwest (NW). SW mice were given either no treatment or chocolate 2g/9.5 mg polyphenols/3 times per week. Results were compared to mice kept in clean air. Key inflammatory mediator genes: cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and the LPS receptor CD14 (cluster of differentiation antigen 14) were measured by real time polymerase chain reaction. Also explored were target NFκB (Nuclear Factor κ B), oxidative stress and antioxidant defense genes.TNF-α, IL-6, and COX-2 were significantly increased in both NW and SWMC mice (p=0.0001). CD14 was up-regulated in SW mice in keeping with the high exposures to particulate matter associated endotoxin. Chocolate administration resulted in a significant down-regulation of TNF-α (p<0.0001), IL-6 (p=0.01), and IL-1β (p=0.02). The up-regulation of antioxidant enzymes and the down-regulation of potent oxidases, toll-like receptors, and pro-apoptotic signaling genes completed the protective profile.Exposure to air pollution produces up-regulation of inflammatory myocardial genes and endotoxin plays a key role in the inflammatory response. Regular consumption of dark chocolate may reduce

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Section: Resultsmentioning

confidence: 69%

Section: Resultsmentioning

confidence: 99%

Urban air pollution produces up-regulation of myocardial inflammatory genes and dark chocolate provides cardioprotection

Villarreal-Calderon

Reed

Palacios‐Moreno

et al. 2012

Experimental and Toxicologic Pathology

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“…Although clinical data have demonstrated that compared to the control group, higher serum IL-22 levels were observed in CHF patients with an NYHA class of II and III [ 14 ], the involvement of IL-22 in cardiac hypertrophy is still unknown, and the pathogenesis remains to be clarified. Therefore, this study aimed to investigate the role of IL-22 in cardiac hypertrophy mice.…”

Section: Introductionmentioning

confidence: 99%

Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice

Liu

et al. 2017

Mediators of Inflammation

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Background Interleukin- (IL-) 22 is considered a proinflammatory cytokine. Recent evidence has demonstrated that it plays a role in cardiovascular diseases. In the recent study, we investigate whether IL-22 is involved in cardiac hypertrophy. Methods Angiotensin II was used to build hypertrophy model and the IL-22 and IL-22 receptor 1 (IL-22R1) levels in heart tissue were measured. In addition, angiotensin II-treated mice received an injection of anti-IL-22-neutralizing antibody (nAb) to investigate the effects of IL-22 nAb on myocardial hypertrophy, cardiac function, and cardiac fibrosis; the activation of the signaling pathway and the prohypertrophic inflammatory cytokine mRNA levels was detected. Furthermore, the effect of IL-22 nAb on angiotensin II-induced hypertrophy in vitro was also determined. Results IL-22 and IL-22R1 levels were significantly increased after angiotensin II infusion. Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1β, IFN-γ, and TNF-α. In addition, IL-22 nAb attenuated angiotensin II-induced hypertrophy in H9C2 cells. Conclusion Our data demonstrated that neutralization of IL-22 alleviated angiotensin II-induced cardiac hypertrophy. The downregulation of IL-22 may be a novel therapeutic strategy to prevent cardiac hypertrophy.

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“…We also found increased IL-22 serum levels in older patients with chronic heart failure [ 26 ] and in healthy centenarians [ 27 ]. In particular, only the II and III NYHA class had IL-22 values significantly higher than the controls, whereas there was no difference between the IL-22 levels of NYHA class IV and the controls [ 26 ]. The reason may be the decline of immune function in patients with chronic heart failure.…”

Section: Introductionmentioning

confidence: 95%

“…The reason may be the decline of immune function in patients with chronic heart failure. In fact we can hypothesize that the reduction of IL-22 levels with the progression of NYHA class can be responsible of the impaired ability of these patients to respond to infections, as IL-22 has anti-microbial properties [ 26 ]. Therefore, it is likely that the pro-inflammatory condition sustained by IL-22 is protective against infection, promoting the longevity of these subjects [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Allergic diseases in the elderly: biological characteristics and main immunological and non-immunological mechanisms

et al. 2017

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Life expectancy and the number of elderly people are progressively increasing around the world. Together with other pathologies, allergic diseases also show an increasing incidence in geriatric age. This is partly due to the growing emphasis on a more accurate and careful diagnosis of the molecular mechanisms that do not allow to ignore the real pathogenesis of many symptoms until now unknown, and partly to the fact that the allergic people from 20 years ago represent the elderly population now. Moreover, environmental pollution predisposes to the onset of allergic asthma and dermatitis which are the result of internal pathologies more than the expression of allergic manifestations. At the same time the food contamination permits the onset of allergic diseases related to food allergy. In this review we provide the state of the art on the physiological changes in the elderly responsible for allergic diseases, their biological characteristics and the major immunological and extra immunological mechanisms. Much emphasis is given to the management of several diseases in the elderly, including anaphylactic reactions. Moreover, some new features are discussed, such as management of asthma with the support of physical activity and the use of the AIT as prevention of respiratory diseases and for the purpose of a real and long lasting benefit. The mechanisms of adverse reactions to drugs are also discussed, due to their frequency in this age, especially in polytherapy regimens. Study of the modifications of the immune system is also of great importance, as regards to the distribution of the lymphocytes and also the presence of a chronic inflammatory disease related to the production of cytokines, especially in prevision of all the possible therapies to be adopted to allow an active and healthy aging.

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Is interleukin-22 a possible indicator of chronic heart failure's progression?

Cited by 13 publications

References 19 publications

Urban air pollution produces up-regulation of myocardial inflammatory genes and dark chocolate provides cardioprotection

Urban air pollution produces up-regulation of myocardial inflammatory genes and dark chocolate provides cardioprotection

Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice

Allergic diseases in the elderly: biological characteristics and main immunological and non-immunological mechanisms

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