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العنوان
Study of cellular immune defense & T cell subsets among apparently healthy obese subjects /
المؤلف
Fouad, Shaimaa Hani Mohamed.
هيئة الاعداد
باحث / Shaimaa Hani Mohamed Fouad
مشرف / Fawzia Hassan Ahmed Abo Ali
مشرف / Asmaa Saber Abdel Rehim
مشرف / Nesrine Ali Mohamed
مشرف / Hoda Mohamed El Sayed
مشرف / Amira Ramadan Elmahdi
تاريخ النشر
2016.
عدد الصفحات
185 p. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب الباطني
تاريخ الإجازة
1/1/2016
مكان الإجازة
جامعة عين شمس - كلية الطب - Internal Medicine
الفهرس
Only 14 pages are availabe for public view

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from 185

Abstract

Overweight and Obesity are defined as ”abnormal accumulation offat that may negatively affects health.Globally, the number of obese individuals has reached alarming proportions. According to the WHO latest estimates, about 13% of the world’s adult populations were obese and 39% were overweight in 2014.
Several co morbidities are associated with this disease, especially immune dysfunction. Many studies demonstrated the negative impact of excess adiposity on immune function, provingthat changes in fat mass and the immune system are intimately linked. Studies have reported that White Adipose Tissue (WAT) is not only a storage organ, but produces close to 100 cytokines. These secreted adipokines are directly correlated to the increased adipose tissue mass and play an intricate role in various aspects of the innate and adaptive immune response and participate in a wide variety ofphysiological or physiopathological processes including food intake, insulin sensitivity and inflammation. In the obese status, secretion of these adipokinessuch as leptin and the proinflammatory cytokines like TNFα, IL-6 and IL-1β are bound to increase. When such pro inflammatory cytokines are secreted into blood, they are likely to produce disastrous condition for the host. This pro inflammatory excess energy milieu could have a definite impact on immune cell function under obesity. Such heightened pro-inflammatory cytokine expression, associated with increased tissue inflammation leading to increased mortality upon infection was seen in diet induced obesity(DIO) animals. Further, enhanced pro inflammatory cytokine expression was also associated with lower memory response in DIO animals. However, more studies are needed to delineate the mechanism by which this excess inflammatory response desensitizes the immune cells during an antigenic exposure.
Leptin is the keyadipokine, which indirectly affects immune responses.The pleiotropic effects of leptin on immune cell activity are highly diverse and complicated. Leptin bears striking similarity to cytokines and modulates immune responses. Leptin is structurally similar to Class I helical cytokines and shares the same JAK–STAT pathway downstream of its receptor. Leptin increases thymic secretion of acute phase reactants and TNFa and promotes T helper 1 cell differentiation. Leptin acts on T cell, macrophages, and other immune cells to stimulate the production of a wide spectrum of cytokines.
Several reports evince obesity to be a risk factor for post operative and surgical site, periodontitisand respiratory infections.Retrospective and prospective studies showed obesity to be an independent risk factor for infection after trauma. A recent study in diet-induced obese mice infected with A (H1N1) pandemic in 2009 suggested preexisting high levels of circulating leptin to be involved in mediating lung injury by producing excess proinflammatory cytokines and chemokines. In infected DIO mice, administration of antileptin antibody led to decrease in pro inflammatory cytokines and lung pathology and improved the survival rate.
Our study aimed atstudyingthe cellular immune defense &t cell sub classes CD4& CD8amongapparently healthy obese subjects.It wasconducted on 50 patients as a case control study divided into two group. It included 30 obese (BMI = 30) adult subjects patients attending the outpatient Obesity clinic at Ain Shams University Hospitals between October 2014and February 2016.Twenty controls (BMI 18.5-24.9) with matched age and sex were also included .All participants were subjected to full detailed history, thorough clinical examination including Blood pressure, BMI, WC, Routine biochemical tests, CRP, -Flow cytometric analysis for cellular immunity (CD4- CD8) and serum leptin.
In all participants we found that age has positive correlation with CD4/CD8 ratio. In addition there was positive correlation betweenBMI, WC and CD4.As they increased there was parallel increase in CD4.More over, there was positive correlation between, BMI, WC and CD4/CD8 ratio. Regarding serum Leptin, we found that as serum Leptin increases there was parallel increase in CD4/CD8 ratio. On the other hand, the increase in serum TGs had negative correlation with CD4/CD8 ratio level and positive correlation with CD8 level.Diastolic blood pressure also had negative correlation with CD4, and CD4/CD8 ratio.
On studying the obese group, we also found that there was positive correlation between age and CD4/CD8 ratio and negative correlation between Blood pressure and CD4 and CD4/CD8 ratio.On comparing obese and control groups we found that the obese group had statistically higher levels of monocytes, serum cholesterol level, LDL, serum Leptin, and CD4/CD8 ratio.