Ein TLR5-Polymorphismus ist mit dem Verlauf der COPD assoziiert

The aetiology of chronic obstructive pulmonary disease (COPD) is unclear. It is supposed to be the product of an exogenous antigenic stimulus, such as tobacco smoke, and an endogenous genetic susceptibility. It is possible that the individual genetic pattern determines the onset as well as the course of COPD. Toll-like receptors (TLR) are signal molecules, essential for the cellular response to bacterial cell wall components. TLR5 is the receptor for flagellin, a constituent of Gram-positive and -negative bacterial flagella. A functional relevant TLR5 polymorphism (TLR5^392STOP) has been identified.

We genotyped 193 Caucasian patients with COPD and 193 healthy controls (matched by age, sex and smoking habits) for the TLR5^392STOP polymorphism with polymerase chain reaction (PCR) followed by restriction fragment length polymorphism analysis (RFLP).

Among COPD patients the prevalence for the TLR5 mutant allele was 8.81% (34/386). In the control group the TLR5 mutation prevalence was 6.74% (26/386) (p=0.326). In the group of 76 patients with a stable course of the disease, defined as less than three hospitalizations over the last three years due to COPD, we found a significant association with the prevalence of TLR5^392STOP gene polymorphism (13.16%, 20/152, p=0.032).

These data suggest that the TLR5^392STOP polymorphism is associated with a stable course of COPD. A possible explanation for this finding could be a diminished immune response normally caused by chronic colonization with flagellated bacteria.