Abstract
Background Chlamydia trachomatis, an obligate intracellular pathogen, is a leading worldwide cause of ocular and urogenital diseases. Advances have been made in our understanding of the nine-member polymorphic membrane protein (Pmp) gene (pmp) family of C. trachomatis. However, there is only limited information on their biologic role, especially for biological variants (biovar) and clinical strains.Methodology/Principal FindingsWe evaluated expression for pmps throughout development for reference strains E/Bour and L2/434, representing different biovars, and for clinical E and L2 strains. Immunoreactivity of patient sera to recombinant (r)Pmps was also determined. All pmps were expressed at two hours. pmpA had the lowest expression but was up-regulated at 12 h for all strains, indicating involvement in reticulate body development. For pmpD, expression peaked at 36 h. Additionally, 57.7% of sera from infected and 0% from uninfected adolescents were reactive to rPmpD (p = 0.001), suggesting a role in immunogenicity. pmpF had the highest expression levels for all clinical strains and L2/434 with differential expression of the pmpFE operon for the same strains. Sera were nonreactive to rPmpF despite immunoreactivity to rMOMP and rPmpD, suggesting that PmpF is not associated with humoral immune responses. pmpFE sequences for clinical strains were identical to those of the respective reference strains. We identified the putative pmpFE promoter, which was, surprisingly, 100% conserved for all strains. Analyses of ribosomal binding sites, RNase E, and hairpin structures suggested complex regulatory mechanism(s) for this >6 Kb operon.Conclusions/SignificanceThe dissimilar expression of the same pmp for different C. trachomatis strains may explain different strain-specific needs and phenotypic distinctions. This is further supported by the differential immunoreactivity to rPmpD and rPmpF of sera from patients infected with different strains. Furthermore, clinical E strains did not correlate with the E reference strain at the gene expression level, reinforcing the need for expansive studies of clinical strains.
Highlights
Chlamydia trachomatis is an obligate intracellular pathogen that is responsible for significant worldwide morbidity associated with ocular and sexually transmitted diseases (STD)
The reference strains had significant gene expression differences where E/Bour had relatively lower mRNA levels and generally sustained expression from 24 to 48 h compared with L2/ 434 (Fig. 1)
In contrast to clinical L2, the three clinical E strains showed a dissimilar pmp expression profile to E/ Bour (Fig. 2). These remarkable expression dissimilarities are generally supported by our recent comparative genomics findings where the laboratory adapted reference strains did not reflect the same genetic make-up of strains that are circulating among human populations today and currently exposed to immune selection [28]
Summary
Chlamydia trachomatis is an obligate intracellular pathogen that is responsible for significant worldwide morbidity associated with ocular and sexually transmitted diseases (STD). C. trachomatis serological variants (serovars) are grouped within two human biological variants (biovars) according to characteristics of disease presentation: the trachoma biovar, including serovars A to C and Ba, which cause conjunctivitis and trachoma, and serovars D to K and Ba, Da, Ia and Ja, which cause conjunctivitis, urogenital infections and infant pneumonitis, and the lymphogranuloma venereum (LGV) biovar (serovars L1 to L3 and L2a). The dissimilar expression of the same pmp for different C. trachomatis strains may explain different strain-specific needs and phenotypic distinctions. This is further supported by the differential immunoreactivity to rPmpD and rPmpF of sera from patients infected with different strains. Clinical E strains did not correlate with the E reference strain at the gene expression level, reinforcing the need for expansive studies of clinical strains
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