TY - JOUR
T1 - The influence of persistent pathogens on circulating levels of inflammatory markers
T2 - A cross-sectional analysis from the Multi-Ethnic Study of Atherosclerosis
AU - Nazmi, Aydin
AU - Diez-Roux, Ana V.
AU - Jenny, Nancy S.
AU - Tsai, Michael Y.
AU - Szklo, Moyses
AU - Aiello, Allison E.
N1 - Funding Information:
AN, AEA and ADR, were supported by a grant from the Center for Integrative Approaches to Health Disparities P60-MD00249-01. In addition, AEA was supported by the University of Michigan-Medical School, Institute of Gerontology RCDC Fellowship and by R21-NR011181-01 from National Institute of Nursing Research. This work was also supported in part by R01 HL076831 from the National Heart Lung and Blood Institute to ADR. The Multi-Ethnic Study of Atherosclerosis is supported by contracts N01-HC-95159 through N01-HC-95165 and N01-HC-95169 from the National Heart, Lung, and Blood Institute. The authors thank the investigators, staff, and participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org.
PY - 2010
Y1 - 2010
N2 - Background: Systemic inflammation is linked to cardiovascular risk, but the influence of persistent pathogens, which are conventionally dichotomously categorized, on circulating levels of inflammatory markers is not clear. Antibody levels of pathogens have not been examined in relation to inflammation. Methods. Using data from a subsample of the Multi-Ethnic Study of Atherosclerosis, we examined circulating levels of interleukin-6 (IL-6), C-reactive protein (CRP) and fibrinogen in relation to five common persistent pathogens: cytomegalovirus, herpes simplex virus-1, Hepatitis A virus, Helicobacter pylori and Chlamydia pneumoniae. We tested the hypothesis that the number of seropositive pathogens (based on conventional cut-off points) would not be as sensitive a marker of inflammation as immune response measured by antibody levels to pathogens. Results. High antibody response to multiple pathogens showed graded and significant associations with IL-6 (p < 0.001), CRP (p = 0.04) and fibrinogen (p = 0.001), whereas seropositive pathogen burden did not. In multiple linear regression models, high antibody response to multiple pathogens maintained a positive association only with IL-6 (4.4% per pathogen exhibiting high antibody response, 95% CI 0.0-8.9). Conclusions. High antibody response to pathogens was a more consistent marker of inflammatory outcomes compared to seropositivity alone and high antibody response to multiple pathogens was a stronger marker compared to any single pathogen.
AB - Background: Systemic inflammation is linked to cardiovascular risk, but the influence of persistent pathogens, which are conventionally dichotomously categorized, on circulating levels of inflammatory markers is not clear. Antibody levels of pathogens have not been examined in relation to inflammation. Methods. Using data from a subsample of the Multi-Ethnic Study of Atherosclerosis, we examined circulating levels of interleukin-6 (IL-6), C-reactive protein (CRP) and fibrinogen in relation to five common persistent pathogens: cytomegalovirus, herpes simplex virus-1, Hepatitis A virus, Helicobacter pylori and Chlamydia pneumoniae. We tested the hypothesis that the number of seropositive pathogens (based on conventional cut-off points) would not be as sensitive a marker of inflammation as immune response measured by antibody levels to pathogens. Results. High antibody response to multiple pathogens showed graded and significant associations with IL-6 (p < 0.001), CRP (p = 0.04) and fibrinogen (p = 0.001), whereas seropositive pathogen burden did not. In multiple linear regression models, high antibody response to multiple pathogens maintained a positive association only with IL-6 (4.4% per pathogen exhibiting high antibody response, 95% CI 0.0-8.9). Conclusions. High antibody response to pathogens was a more consistent marker of inflammatory outcomes compared to seropositivity alone and high antibody response to multiple pathogens was a stronger marker compared to any single pathogen.
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U2 - 10.1186/1471-2458-10-706
DO - 10.1186/1471-2458-10-706
M3 - Article
C2 - 21083905
AN - SCOPUS:78349271302
SN - 1471-2458
VL - 10
JO - BMC public health
JF - BMC public health
M1 - 706
ER -