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Background  Elevated circulating levels of C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen (FG) have been repeatedly associated with many adverse outcomes in patients with chronic obstructive pulmonary disease (COPD). To date, it remains unclear whether and to what extent systemic inflammation is primary or secondary in the pathogenesis of COPD.  The aim of this study was to examine the association between haplotypes of  CRP ,  IL6  and  FGB  genes, systemic inflammation, COPD risk and COPD-related phenotypes (respiratory impairment, exercise capacity and body composition).    Methods  Eighteen SNPs in three genes, representing optimal haplotype-tagging sets, were genotyped in 355 COPD patients and 195 healthy smokers. Plasma levels of CRP, IL-6 and FG were measured in the total study group. Differences in haplotype distributions were tested using the global and haplotype-specific statistics.    Results  Raised plasma levels of CRP, IL-6 and fibrinogen were demonstrated in COPD patients. However, COPD population was very heterogeneous: about 40% of patients had no evidence of systemic inflammation (CRP < 3 mg/uL or no inflammatory markers in their top quartile). Global test for haplotype effect indicated association of  CRP  gene and CRP plasma levels (P = 0.0004) and  IL6  gene and COPD (P = 0.003). Subsequent analysis has shown that  IL6  haplotype H2, associated with an increased COPD risk (p = 0.004, OR = 4.82; 1.64 to 4.18), was also associated with very low CRP levels (p = 0.0005). None of the genes were associated with COPD-related phenotypes.    Conclusion  Our findings suggest that common genetic variation in  CRP  and  IL6  genes may contribute to heterogeneity of COPD population associated with systemic inflammation.

IL6 and CRPhaplotypes are associated with COPD risk and systemic inflammation: a case-control study