Background It is known that chlamydial species can propagate in hepatocyte cell lines. Moreover, some clinical cases of chlamydial infection involve liver abnormalities. This study was to clarify whether chlamydial markers (protein and nucleic acids) could be detected in liver biopsies from patients with calculous cholecystitis.
Material and Methods Liver biopsies were obtained from 39 patients during cholecystectomy and analysed with immunohistochemical, nucleic acid amplification and serological protocols. Liver specimens from 8 trauma victims served as controls.
Results It was shown that from 39 patients with cholecystitis 19 gave considerable signal generated by antibodies against C. trachomatis (15 patients) or C. pneumoniae (4 patients). 10.2% (4/39) of the samples contained detectable 16S rRNA genomic sequence from C. pneumoniae while amplifiable fragments of 16S rRNA and pLGV cryptic plasmid from C. trachomatis were found in 20.5% (8/39) of DNA specimens. The control group had a zero detection rate for chlamydial genetic markers in the liver. Simultaneous detection of genetic and immunohistochemical markers validated by positive serological status took place in a very limited number of the patients (4 cases for C. trachomatis and 2 cases for C. pneumoniae). Moreover, it was shown that C. trachomatis and C. pneumoniae can efficiently propagate in freshly isolated rat primary hepatocytes forming infectious progeny.
Conclusions Identification of chlamydial markers in liver biopsies along with the ability of the chlamydial pathogens to propagate in native hepatocytes may suggest the possible involvement of chlamydial species in inflammatory hepatobiliary disease. We have assumed previously that abnormalities of cholesterol homeostasis associated with the increase of ApoB-containing lipoproteins may promote enhanced uptake of chlamydial particles in the liver. Thus, it is conceivable that the appearance of chlamydial markers in hepatic biopsies of patients with cholelithiasis takes place due to proatherogenic changes in plasma lipoprotein profile.