Chronic Inflammation Is Correlated with Percentage of Body Fat Independent of the Burden of Infection Katayoun Vahdat, 1 Fatemeh Azizi, 1 Keivan Zandi, 1 Majid Assadi, 2 and Iraj Nabipour 3,4 Abstract—The aim of this population-based study was to investigate the association of the percentage of body fat (BF) and high-sensitivity C-reactive protein (hs-CRP) when the infectious burden was adjusted for. A total of 1,546 subjects were randomly selected. BF was determined using bioelectrical impedance analysis. Sera were analyzed for IgG antibodies to Chlamydia pneumoniae, herpes simplex virus type 1, Helicobacter pylori, and cytomegalovirus using ELISA. Measurement of C-reactive protein (CRP) by a high-sensitivity CRP assay was performed. A linear relationship between an increase in the number of pathogens and CRP concentrations was observed (p =0.007). Age-adjusted serum hs-CRP levels were correlated with percentage of BF in men (r =0.28, p <0.0001) and women (r =0.37, p <0.0001). In multiple regression analyses, hs-CRP showed significant correlations with percentage of BF after controlling for age, sex, cardiovascular risk factors, and the infectious burden was divided into two, three, and four pathogens [(β =0.24, p <0.0001), (β =0.2 1, p <0.0001), and (β =0.23, p =<0.0001), respectively]. In conclusion, there was a strong association between hs-CRP and percentage of body fat independent of viral and bacterial pathogens that had been previously associated with coronary artery disease as well as carotid atherosclerosis. KEY WORDS: obesity; body fat; C-reactive protein; burden of infection; adipose tissue. INTRODUCTION Recent research has pinpointed adipose tissue as an active organ in modulating glucose and energy metab- olism, insulin sensitivity, bone metabolism, immunity, and inflammation. This dynamic endocrine tissue pro- duces a variety of proinflammatory and anti-inflamma- tory molecules, including leptin, adiponectin, resistin, visfatin, monocyte chemoattractant protein 1 as well as cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6 [1]. It has been proposed that adipose tissue-derived proinflammatory cytokines contribute to the progression of multiple cardiometabolic risk factors independently of the body mass index (BMI) through production of chronic low-grade inflammation [2, 3]. Numerous studies in various parts of the world have clearly established that the C-reactive protein (CRP), as a blood biomarker for low-grade inflammation, predicts myocar- dial infarction, coronary artery disease death, stroke, peripheral artery disease, sudden death, etc.[4]. Thus, the Centers for Disease Control and the American Heart Association have issued a statement recommending that patients at intermediate risk of coronary artery disease might benefit from measurement of CRP [5]. The direct association between adiposity and low- grade inflammation has been under close investigation in both cross-sectional [6, 7] and longitudinal studies [8, 9]. In the medical literature, the correlation between subcuta- neous and visceral adipose tissue and markers of chronic low-grade inflammation, in particular the presence of the highly sensitive C-reactive protein (hs-CRP), is well described [10–13]. Visceral fat thickness was reported to be the strongest contributor to circulating hs-CRP in 1 Department of Infectious Diseases, The Persian Gulf Tropical Medicine Research Center, Bushehr University of Medical Sciences, Bushehr, Iran 2 The Persian Gulf Nuclear Medicine Research Center, Bushehr University of Medical Sciences, Bushehr, Iran 3 Department of Biochemistry, The Persian Gulf Marine Biotechnology Research Center, Bushehr University of Medical Sciences, Boostan 19 Alley, Imam Khomeini St, Bushehr, IR, Iran 7514763448 4 To whom correspondence should be addressed at Department of Biochemistry, The Persian Gulf Marine Biotechnology Research Center, Bushehr University of Medical Sciences, Boostan 19 Alley, Imam Khomeini St, Bushehr, IR, Iran 7514763448. E-mail: inabipour@gmail.com 0360-3997/12/0400-1322/0 # 2012 Springer Science+Business Media, LLC Inflammation, Vol. 35, No. 4, August 2012 ( # 2012) DOI: 10.1007/s10753-012-9445-6 1322