Please click on one of the flags to reset Reading-Direction if you consider the current setting invalid


Views  280
Rating  0

 زينب خضر احمد المهدي الامين
23/03/2018 11:06:51
تصفح هذه الورقة الالكترونية بتقنية Media To Flash Paper
Zainab Al-Mahdi*, Roqia Ewad**, Haider Qassim Raheem **, Israa Adnan Ibraheam***, Nada Khalid Abo-Khumra**
*Collage of Dentistry, Babylon University, Iraq.
**DNA Research center, Babylon University, Hilla City, Iraq. ***College of Science for Women, Babylon University, Hilla City, Iraq.
Article received 17.6.2017, Revised 18.9.2017, 23.9.2017
The occurrence of obesity has augmented fast through new year. Our previous study showed obesity was related with diseases and or infections recorded, adipose tissue mediates immune system. Present study aim is evaluation some immune aspect related with IL-1- Beta as pro-inflammatory cytokine and IL-6 cytokine as both pro and anti- inflammatory cytokine) production in obese versus normal weight women. Enzyme-linked immune sorbent assay (ELISA) used for detecting and quantifying cytokines. Results shows that the concentration of the IL-1Beta as pro inflammatory cytokine stood greater in obese and overweight women (186.2 ± 58.54, n=17) than in normal weight women (control group (20.41 ± 9.387, n=3), (F=220.4, P < 0.05) while here stayed not any substantial variances in IL-6 concentrations between test group (198.5 ± 34.93, n=15) in compare with control group (212.6 ± 122.9, n=3), (F=2.475, P=0.240). In conclusion, our result improved that obesity responsible in elevation level of pro- inflammatory cytokine IL-1 Beta and interleukin 6 play important role as both anti and proinflammatory cytokine.
Key words: Obesity, IL-1Beta, IL-6, pro inflammatory cytokines.
The occurrence of obesity has amplified fast thro- ugh recent years. Obesity affect immune system. [Marti et al., 2001]. Cells of Immune system and adipocytes show resemblances trendy configure- tion and role in the creation of several inflamma- tory intermediaries. [Marti et al., 2001, Nave et al., 2011]. Adipose tissue facilitates immune system and adipose tissue relations by the excretion of adi- pokines, such as, leptin [Nave et al., 2011]. The variation of macrophages takes by exposed toward exist precious through the existence of fatness [Marti et al., 2001, Nave et al., 2011]. Adipose tissue alte- ring happens in obesity, considered through adipo- cyte hypertrophy then enlarged penetration of mac- rophages which furthermore change to phenotype of a proinflammatory. IL-1? a main cytokine crea- ted mainly in macrophages, is occupied trendy the progress of obesity-related insulin conflict [Chen, 2015].
Our previous study showed obesity was related with diseases and or infection recorded, in height pressure of blood, diabetes type 2, cancer, include- ing breast cancer, breathing disorders, including sleep apnea, infertility, non-alcoholic fatty liver disease, osteoarthritis, cellulitis and skin condition, gallbladder, gallstone, headache, teeth problems, hair fall, skin blackness, varicose veins, recurrent urinary tract infection, Atopic Dermatitis) Eczema, susceptibility to influenza infection, tuberculosis, stomach ulcer (Helicobacter pylori), pneumonia [Al-Mahdi et al., 2016].
Adipocytokines representative mostly soluble hor- mones created typically but not wholly by adipocytes have been exposed to have specific parts through immune responses. Leptin and adiponectin are the greatest profusely produced adipocytokines through distinct imports on immune responses and metabolism. Leptin has been related with chiefly pro inflammatory traits and the capability to encourage the making of ‘classical’ pro inflamma- tory cytokines for example IL12, TNF-? and IL1, all ensuing into a Th1-ruled pro-inflammatory immune response [Gainsford et al.,1996]. Obesity exists clear in a ceremonial of prolonged substan- dard inflammation named inflammation of meta- bolic in which the cells of immune, specially monocytes stay triggered penetrate the increasing adipose tissue then convert distinguished as occu- pant adipose tissue macrophages. ATMs remain categorized through the appearance of M1 or proin- flammatory markers (MCP-1, TNF-?, IL-6, CD11) [Michaud et al., 2013]. Interleukin IL-6 is a signi- ficant cytokine is concealed in adipocytes, macro- phages then further causes containing emaciated muscle, endothelial cells [Febbraio et al., 2002, Sundararaj et al., 2009]. It exists a general manager mass organization and metabolism of lipid [Shoe- lson et al.,2006., Mohamed-Ali et al.,1997]. It remains too related through fatness then resistance of insulin; nevertheless, it is uncertain whether it shows a risky [Eder et al., 2009, Senn et al., 2002] or a protecting part [Mauer et al.,2014., Pedersen et al., 2007]. Our present study aim is an evaluation the concentration of together IL-1 Beta then IL-6 in both obese and normal weight women in Hilla city in middle of Iraq.
Materials and Methods
Assessment of obesity: Body mass index (BMI) is a modest index of weight for height that is used to categorize weighty and obesity in grownups. It is distinct as individual s weight in kilograms allo- cated by the square of his height in meters (kg/m2) [WHO, 1997].
BMI= [ ????????h??????????
(????????h?? ???? ??????????)2
. a BMI more than or equivalent to 25 is overweight
. a BMI more than or equivalent to 30 is obesity (table-1).
BMI delivers the greatest beneficial public level ration of obesity and weighty as it is the similar for together sexes and for wholly ages of adults. But, it must be reflected a rough guide since it might not agree to the similar grade of obesity in diverse persons.
Blood Sampling: Samples collection for present work was performed from Merjan Hospital during 2016. Blood were collected from obese and over- weight women as well as from normal weightwomen using sterile disposable syringes. Each tas- ter minus anticoagulant for parting of sera to study ELIZA cytokines, cytokine IL-1 beta, IL-6 grit stayed executed as in creation orders.
Cytokine Score: The cytokine reactions existed valued as immune enzyme color responses in rela- tionships of picograms per milliliters.
Biometric Analysis: Statistical analysis and gra- phing was accompanied with Graph Pad Prism software (Graph Pad Software, Inc, La Jolla, CA).
Results shows that the concentration of the pro inflammatory cytokine IL-1B was greater in obese and overweight women (186.2 ± 58.54, n=17) than in normal weight women (control group (20.41 ± 9.387, n=3), (F=220.4, P < 0.05)and results are pre- sented in table-1 & fig. 1, while there stayed no sig- nificant variances in concentrations of IL-6 among test group (198.5±34.93, n=15) in comparison with control group (212.6 ± 122.9, n=3), (F=2.475, P=0.240).
Through the progress of obesity, there is incre- ase of macrophages and additional immune cells in adipose tissue [Shoelson et al., 2007]. Adipose tiss- ue, usually conceptualized as inert storage for triglycerides and energy has been connected to the creation of numerous hormones, pro-inflammatory cytokines and chemokines. Documentation of the main causes that intermediate the harmful influ- ence of macrophages on adipocytes is acute forevolving actual therapeutic aims. IL-1? has been occupied as a basic manager in the conversion of obesity-related inflammation into insulin resista- nce in rodent types [Ehses et al., 2009, Jager et al., 2007].
Our results shows that the concentration of the pro inflammatory cytokine IL-1 Beta was higher in obese and overweight women (186.2 ± 58.54, n= 17) than in normal weight women (control group (20.41 ± 9.387, n=3), (F=220.4, P < 0.05), this results were similar with other papers which also shows that the proinflammatory cytokine IL-1B was higher in obese people than in control group [Aygun et al., 2005], however our results shows ten obese samples with very high IL-1B and higher than the values recorded by others, may be those patients suffer from other diseases such as type 2 diabetic patients[Mojtaba et al., 2011] . Interleukin-1?, a main cytokine of proinflamma- tory made mostly via macrophages, monocytes, is triggered over caspase-1 via the NLRP3 inflamma- some difficult [Agostini et al.,2004]. Modern educations propose IL-1? as a supposed contestant in the progress in type 2 diabetes and insulin resis- tance [Tack et al., 2012]. A promotion in flowing planes of IL-1? composed through IL-6 has stayed exposed toward rise the danger of diabetes kind 2 [Spranger et al., 2003]. IL-1? reserve decreases tissue inflammation then hyperglycemia in diabetic rats and overweight mice [Ehses et al., 2009]. Also, IL-1? might establish mediator of cell-cell in meta inflammation, as IL-1? manufactured in TNF?-ins- pired adipocytes of mouse consumes stayed exposed to prompt confrontation of insulin in cell of liver [Nov et al., 2010].
Cytokines family of IL-1 require designated to be eminent in adults weighty. A family contains amo- ngst others, IL-1 receptor antagonist, IL-18 and IL- 1. Together proinflammatory cytokines, IL-1 then IL18, are higher in adult fatness and part a like sign transduction way [Osborn et al., 2008].
Obesity is identified danger reason in the progress of Spartan asthma. Modern documents reported that the inflammation connected with obesity, possibly intermediated through the cytokine IL6, shows a part in initiating lowly role of lung and amplified danger for evolving asthma exacerbations [Peters et al., 2016].
IL-6 is too created by adipocytes then is assumed to be a cause why obese persons need greater pla- nes of endogenous CRP [Bastard et al., 1999]. mRNA appearance trainings display that adipocy- tes container synthesis together tumor necrosis fac- tor alpha and several interleukins, particularly IL- 1beta also IL-6 [Coppack, 2001]. While there were no significant variances in IL-6 deliberationsamong test group (198.5 ± 34.93, n=15) in compare with control group (212.6 ± 122.9, n=3), (F=2.475, P=0.240)
Adipose tissue is an essential basis of partying IL- 6 then the increasing adipose tissue in obesity might pay great plains of IL-6 in the exchange. It existed distinctly described in two diverse readings of plasma [Kern et al., 2001] and adipose tissue [Bastard et al., 2000] planes of IL-6 connected improved than TNF-? through obesity and insulin resistance.
By way of an anti-inflammatory cytokine, IL-6 was stated to obstruct the things of proinflammatory TNF-? [Pedersen et al., 2001], support M2 macro- phage polarity, and progress resistance of insulin [Mauer et al.,2014]. General the part of IL-6 in insulin sympathy and glucose homeostasis ruins divisive [Jansson et al., 2007] and we risk that the obesity-related alarms in IL-6 and its receptor expected require various things in diverse tissues and organs.
Resent documents provision a ideal in which human obesity clues toward the high appearance of IL-6R, IL-6 in the adipose tissue, with improved tissue expression of TNF-?, IP-10, MCP-1and penetration by CD11b, CD163 and macrophages as the primary types of meta-inflammation [Sardar et al., 2015].
In conclusion, our result improved that obesity responsible in elevation level of pro-inflammatory cytokine IL-1 Beta and interleukin 6 play important role as both anti and proinflammatory cytokine. Acknowledgment
The authors would like to thanks Babylon Univer- sity for providing facilities and support to finish this study. Also, we would thank Dr. Alaa Tariq at collage of science. Babylon University for doing ELISA test.
Agostini L., Martinon F., Burns K., McDermott M.F., Hawkins P.N., Tschopp J., NALP3 forms an IL-1beta-processing inflammasome with in- creased activity in Muckle-Wells autoinflamm- atory disorder. Immunity 20: 319–325 (2004).
Al-mahdi Z. and Yasir A., Obese and Over Weight Women and Public Health Issues in Hilla City, Iraq. International Journal of Medical, Health, Biomedical, Bioengineering and Pharmaceu- tical Engineering. 10 (3):164-9 (2016).
Aygun D., Gungor S., Ustundag B., Gurgoze M. K. and Sen Y., Proinflammatory Cytokines and Leptin Are Increased in Serum of Prepubertal Obese Children. Mediators of Inflammation 3:180–183 (2005).
Bastard J., Jardel C., Delattre J., Hainque B., et al.,Evidence for a Link Between Adipose Tissue Interleukin-6 Content and Serum C-Reactive Protein Concentrations in Obese Subjects. Circulation 99 (16): 2219–2222 (1999).
Bastard J.P., Jardel C., Bruckert E., Blondy P., Capeau J., Laville M., et al., Elevated levels of interleukin 6 are reduced in serum and subcuta- neous adipose tissue of obese women after weight loss. J. Clin. Endocrinol. Metab. 85: 3338–3342 (2000).
Chen Bing C., Interleukin-1? a culprit in macro- phage-adipocyte crosstalk in obesity. Adipocyte 4(2): 149–152 (2015).
Coppack S. W., Pro-inflammatory cytokines and adipose tissue. Proc. Nutr. Soc. 60(3): 349-56 (2001.)
Eder K., Baffy N., Falus A., Fulop A.K., The major inflammatory mediator interleukin-6 and obesity. Inflamm. Res. 58: 727–736 (2009).
Ehses J.A., Lacraz G., Giroix M.H., Schmidlin F., Coulaud J., Kassis N., Irminger J.C., Kergoat M., Portha B., Homo-Delarche F., Donath M. Y., IL-1 antagonism reduces hyperglycemia and tissue inflammation in the type 2 diabetic GK rat. Proc. Natl. Acad. Sci. USA 106: 13998– 4003 (2009).
Febbraio M.A., Pedersen B.K. Muscle-derived interleukin-6: mechanisms for activation and possible biological roles. FASEB J. 16: 1335– 1347 (2002).
Gainsford T., Willson T.A., Metcalf D., Handman E., McFarlane C., Ng A. et al., Leptin can induce proliferation, differentiation, and functi- onal activation of hemopoietic cells. Proc. Natl. Acad. Sci. USA 93: 14564–14568 (1996).
Jager J., Gremeaux T., Cormont M., Le Marchand- Brustel Y., Tanti J.F.,Interleukin-1beta-induced insulin resistance in adipocytes through down- regulation of insulin receptor substrate-1 expre- ssion. Endocrinology 148: 241–251 (2007).
Jansson J.O., Wallenius V., Point-counterpoint: Interleukin-6 does/does not have a beneficial role in insulin sensitivity and glucose homeo- stasis. J. Appl. Physiol. 102: 821 (1985).
Juge-Aubry C.E., Somm E., Chicheportiche R., Burger D., Pernin A., Cuenod-Pittet B., Quino- doz P., Giusti V., Dayer J.M., Meier C.A., Regulatory effects of interleukin (IL)-1, inter- feron-beta, and IL-4 on the production of IL-1 receptor antagonist by human adipose tissue. J. Clin. Endocrinol. Metab. 89: 2652–2658 (2004)
Kern P.A., Ranganathan S., Li C., Wood L., Rang- anathan G., Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. Am. J. Physiol. Endo- crinol. Metab. 280: E745–751 (2001).
Koenen T.B., Stienstra R., van Tits L.J., Joosten L.A., van Velzen J.F., Hijmans A., Pol J.A., van der Vliet J.A., NeteaM.G.,TackC.J., Stalenhoef A.F., de Graaf J., The inflammasome and casp- ase-1 activation: a new mechanism underlying increased inflammatory activity in human visceral adipose tissue. Endocrinology 152: 3769–3778 (2011).
Marti A., Marcos A., Martinez J.A., Obesity and immune function relationships. Obes. Rev. 2: 131–140 (2001).
Mauer J., Chaurasia B., Goldau J., Vogt M.C., Ruud J., Nguyen K.D., et al., Signaling by IL-6 promotes alternative activation of macrophages to limit endotoxemia and obesity-associated resistance to insulin. Nat Immunol 15: 423–430 (20014).
Michaud A., Pelletier M., Noel S., Bouchard C., Tchernof A., Markers of macrophage infiltra- tion and measures of lipolysis in human abdo- minal adipose tissues. Obesity (Silver Spring) 21: 2342–2349 (2013).
Mohamed-Ali V., Goodrick S., Rawesh A., Katz D.R., Miles J.M., Yudkin J.S., et al., Subcuta- neous adipose tissue releases interleu-kin-6, but not tumor necrosis factor-alpha, in vivo. J. Clin. Endocrinol. Metab. 82: 4196–4200 (1997).
Mojtaba E., Mahdi K., Mehdi J.R., Amir S., Serum interleukin-1 beta plays an important role in insulin secretion in type II diabetic. Inter- national J. Biosc. 1(3): 93-99 (2011).
Nave H., Beutel G., Kielstein J.T., Obesity-related immunodeficiency in patients with pandemic influenza H1N1. Lancet Infect. Dis. 11: 14–15 (2011).
Nov O., Kohl A., Lewis E.C., Bashan N., Dvir I., Ben-Shlomo S., Fishman S., Wueest S., Konrad D,, Rudich A., Interleukin-1beta may mediate insulin resistance in liver-derived cells in resp- onse to adipocyte inflammation. Endocrinology 151: 4247–4256 (2010).
Osborn. O., H. Gram, E.P. Zorrilla, B. Conti and T. Bartfai, Insights into the roles of the inflammatory mediators IL-1, IL-18 and PGE2 in obesity and insulin resistance,” Swiss Medi- cal Weekly 138(45-46): 665–673 (2008).
Pedersen B.K., Febbraio M.A. Point: Interleukin-6 does have a beneficial role in insulin sensitivity and glucose homeostasis. J. Appl. Physiol. 102: 814–816 (1985).
Pedersen B.K., Steensberg A., Schjerling P., Mus- cle derived interleukin-6: possible biological effects. J. Physiol. 536: 329–337 (2001).
Peters M.C., McGrath K.W., Hawkins G.A., Hastie A.T., Levy B.D., Israel E., Phillips B.R., Mauger D.T., Comhair S.A., Erzurum S.C.,
Johansson M.W., Jarjour N.N., Coverstone A. M., Castro M., Holguin F., Wenzel S.E., Woodruff P.G., Bleecker E.R., Fahy J.V., Plasma interleukin-6 concentrations, metabolic dysfunction, and asthma severity: a cross- sectional analysis of two cohorts. The Lancet. Respiratory Medicine 4(7): 574–84 (2016).
Sardar Sindhu, Reeby Thomas, Puthiyaveetil Shihab, Devarajan Sriraman, Kazem Behbehani and Rasheed Ahmad1, Obesity Is a Positive Modulator of IL-6R and IL-6 Expression in the Subcutaneous Adipose Tissue: Significance for Metabolic Inflammation. PLoS One 10(7): e0133494 (2015).
Schultz O., Oberhauser F., Saech J., Rubbert-Roth A., Hahn M., Krone W. et al., Effects of inhibi- tion of interleukin-6 signalling on insulin sensi- tivity and lipoprotein (a) levels in human subje- cts with rheumatoid diseases. PLoS One 5: e143 28 (2010)
Senn J.J., Klover P.J., Nowak I.A., Mooney R.A., Interleukin-6 induces cellular insulin resistance in hepatocytes. Diabetes 51: 3391–3399 (2002)
Shoelson S.E., Herrero L., Naaz A., Obesity, infla- mmation, and insulin resistance. Gastroente- rology 132: 2169–2180 (2007).
Shoelson S.E., Lee J., Goldfine A.B. (2006) Inflammation and insulin resistance. J. Clin. Invest. 116: 1793–1801 (2006).
Spranger J., Kroke A., Mohlig M., Hoffmann K., Bergmann M.M., Ristow M., Boeing H., Pfeiffer AF. Inflammatory cytokines and the risk to develop type 2 diabetes: results of the pros- pective population-based European Prospective Investigation into Cancer and Nutrition (EPIC)- Potsdam Study. Diabetes 52: 812–817 (2003).
Sundararaj K.P., Samuvel D.J., Li Y., Sanders J.J., Lopes-Virella MF, Huang Y., Interleukin-6 released from fibroblasts is essential for up- regulation of matrix metalloproteinase-1 expre- ssion by U937 macrophages in coculture: cross- talking between fibroblasts and U937 macro- phages exposed to high glucose. J. Biol. Chem. 284: 13714–13724 (2009).
Tack C.J., Stienstra R., Joosten L.A., Netea M.G., Inflammation links excess fat to insulin resistance: the role of the interleukin-1 family. Immunol. Rev. 249: 239–252 (2012).
WHO, Obesity: Preventing and managing the global epidemic. Report of a WHO consultation on Obesity, Geneva, 1-276 (1997).

  • وصف الــ Tags لهذا الموضوع
  • Obesity, IL-1Beta, IL-6, pro inflammatory cytokines.