Familial and genetic determinants of systemic markers of inflammation: The NHLBI family heart study

James S. Pankow; Aaron R. Folsom; Mary Cushman; Ingrid B. Borecki; Paul N. Hopkins; John H. Eckfeldt; Russell P. Tracy

doi:10.1016/S0021-9150(00)00586-4

Familial and genetic determinants of systemic markers of inflammation: The NHLBI family heart study

James S. Pankow, Aaron R. Folsom, Mary Cushman, Ingrid B. Borecki, Paul N. Hopkins, John H. Eckfeldt, Russell P. Tracy

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334 Scopus citations

Abstract

Inflammation is thought to play a central role in the etiology and outcome of atherosclerosis. Animal studies as well as in vitro and in vivo human studies suggest that host factors modulate the magnitude and extent of inflammatory responses. We investigated familial aggregation of three systemic markers of inflammation (C-reactive protein (CRP), white blood cell count (WBC), and albumin) in a large, cross-sectional study conducted in four US communities. We found evidence of substantial heritability (35-40%) for CRP levels as well as for WBC and albumin levels. Negligible spouse correlations suggested little influence of shared household environment on these traits. The combination of sociodemographic factors (age, center, education), behavioral and lifestyle factors (cigarette smoking, alcohol intake, hormone replacement therapy), obesity and fat patterning, and prevalent diabetes explained 13-30% the interindividual variability of these traits. There was no evidence that these inflammation phenotypes were linked to a microsatellite marker in the interleukin-1 gene cluster on chromosome 2q, a region that includes several candidate genes for chronic inflammatory diseases. Our findings suggest that CRP levels, albumin levels, and WBC are determined at least partially by genetic factors. Further efforts to identify gene loci affecting these traits are warranted.

Original language	English (US)
Pages (from-to)	681-689
Number of pages	9
Journal	Atherosclerosis
Volume	154
Issue number	3
DOIs	https://doi.org/10.1016/S0021-9150(00)00586-4
State	Published - Feb 15 2001

Bibliographical note

Funding Information:
This paper is presented on behalf of the Investigators of the NHLBI Family Heart Study. Participating Institutions and Principal Staff of the study are as follows, Forsyth County/University of North Carolina/Wake Forest University, Gerardo Heiss, Stephen Rich, Greg Evans, James Pankow; H.A. Tyroler, Jeannette T. Bensen, Catherine Paton, Delilah Posey, and Amy Haire; University of Minnesota Field Center, Donna K. Arnett, Aaron R. Folsom, Larry Atwood, James Peacock, Greg Feitl; Boston University/Framingham Field Center, R. Curtis Ellison, Richard H. Myers, Yuqing Zhang, Andrew G. Bostom, Luc Djoussé, Jemma B. Wilk, and Greta Lee Splansky; University of Utah Field Center: Steven C. Hunt, Roger R. Williams (deceased), Paul N. Hopkins, Jan Skuppin and Hilary Coon; Coordinating Center, Washington University, St. Louis, Michael A. Province, D.C. Rao, Ingrid B. Borecki, Yuling Hong, Mary Feitosa, Jeanne Cashman, and Avril Adelman; Central Biochemistry Laboratory, University of Minnesota, John H. Eckfeldt, Greg Rynders, Catherine Leiendecker-Foster, and Michael Y. Tsai; Central Molecular Laboratory, University of Utah, Mark F. Leppert, Jean-Marc Lalouel, Tena Varvil, Lisa Baird; National Heart, Lung, & Blood Institute-Project Office, Phylliss Sholinsky, Millicent Higgins (retired), Jacob Keller (retired), Sarah Knox, and Lorraine Silsbee. This work was supported by National Heart, Lung, and Blood Institute cooperative agreement grants N01-HC-25104, N01-HC-25105, N01-HC-25106, N01-HC-25107, N01-HC-25108, and N01-HC-25109.

Keywords

Albumin
C-reactive protein
Inflammation
Interleukin-1
White blood cell count

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "Familial and genetic determinants of systemic markers of inflammation: The NHLBI family heart study",

abstract = "Inflammation is thought to play a central role in the etiology and outcome of atherosclerosis. Animal studies as well as in vitro and in vivo human studies suggest that host factors modulate the magnitude and extent of inflammatory responses. We investigated familial aggregation of three systemic markers of inflammation (C-reactive protein (CRP), white blood cell count (WBC), and albumin) in a large, cross-sectional study conducted in four US communities. We found evidence of substantial heritability (35-40%) for CRP levels as well as for WBC and albumin levels. Negligible spouse correlations suggested little influence of shared household environment on these traits. The combination of sociodemographic factors (age, center, education), behavioral and lifestyle factors (cigarette smoking, alcohol intake, hormone replacement therapy), obesity and fat patterning, and prevalent diabetes explained 13-30% the interindividual variability of these traits. There was no evidence that these inflammation phenotypes were linked to a microsatellite marker in the interleukin-1 gene cluster on chromosome 2q, a region that includes several candidate genes for chronic inflammatory diseases. Our findings suggest that CRP levels, albumin levels, and WBC are determined at least partially by genetic factors. Further efforts to identify gene loci affecting these traits are warranted.",

keywords = "Albumin, C-reactive protein, Inflammation, Interleukin-1, White blood cell count",

author = "Pankow, {James S.} and Folsom, {Aaron R.} and Mary Cushman and Borecki, {Ingrid B.} and Hopkins, {Paul N.} and Eckfeldt, {John H.} and Tracy, {Russell P.}",

note = "Funding Information: This paper is presented on behalf of the Investigators of the NHLBI Family Heart Study. Participating Institutions and Principal Staff of the study are as follows, Forsyth County/University of North Carolina/Wake Forest University, Gerardo Heiss, Stephen Rich, Greg Evans, James Pankow; H.A. Tyroler, Jeannette T. Bensen, Catherine Paton, Delilah Posey, and Amy Haire; University of Minnesota Field Center, Donna K. Arnett, Aaron R. Folsom, Larry Atwood, James Peacock, Greg Feitl; Boston University/Framingham Field Center, R. Curtis Ellison, Richard H. Myers, Yuqing Zhang, Andrew G. Bostom, Luc Djouss{\'e}, Jemma B. Wilk, and Greta Lee Splansky; University of Utah Field Center: Steven C. Hunt, Roger R. Williams (deceased), Paul N. Hopkins, Jan Skuppin and Hilary Coon; Coordinating Center, Washington University, St. Louis, Michael A. Province, D.C. Rao, Ingrid B. Borecki, Yuling Hong, Mary Feitosa, Jeanne Cashman, and Avril Adelman; Central Biochemistry Laboratory, University of Minnesota, John H. Eckfeldt, Greg Rynders, Catherine Leiendecker-Foster, and Michael Y. Tsai; Central Molecular Laboratory, University of Utah, Mark F. Leppert, Jean-Marc Lalouel, Tena Varvil, Lisa Baird; National Heart, Lung, & Blood Institute-Project Office, Phylliss Sholinsky, Millicent Higgins (retired), Jacob Keller (retired), Sarah Knox, and Lorraine Silsbee. This work was supported by National Heart, Lung, and Blood Institute cooperative agreement grants N01-HC-25104, N01-HC-25105, N01-HC-25106, N01-HC-25107, N01-HC-25108, and N01-HC-25109. ",

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doi = "10.1016/S0021-9150(00)00586-4",

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AU - Eckfeldt, John H.

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N2 - Inflammation is thought to play a central role in the etiology and outcome of atherosclerosis. Animal studies as well as in vitro and in vivo human studies suggest that host factors modulate the magnitude and extent of inflammatory responses. We investigated familial aggregation of three systemic markers of inflammation (C-reactive protein (CRP), white blood cell count (WBC), and albumin) in a large, cross-sectional study conducted in four US communities. We found evidence of substantial heritability (35-40%) for CRP levels as well as for WBC and albumin levels. Negligible spouse correlations suggested little influence of shared household environment on these traits. The combination of sociodemographic factors (age, center, education), behavioral and lifestyle factors (cigarette smoking, alcohol intake, hormone replacement therapy), obesity and fat patterning, and prevalent diabetes explained 13-30% the interindividual variability of these traits. There was no evidence that these inflammation phenotypes were linked to a microsatellite marker in the interleukin-1 gene cluster on chromosome 2q, a region that includes several candidate genes for chronic inflammatory diseases. Our findings suggest that CRP levels, albumin levels, and WBC are determined at least partially by genetic factors. Further efforts to identify gene loci affecting these traits are warranted.

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KW - Albumin

KW - C-reactive protein

KW - Inflammation

KW - Interleukin-1

KW - White blood cell count

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Familial and genetic determinants of systemic markers of inflammation: The NHLBI family heart study

Abstract

Bibliographical note

Keywords

UN SDGs

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