EVIDENCE OF GENETIC SUSCEPTIBILITY TO CHLAMYDIA TRACHOMATIS-INDUCED PELVIC INFLAMMATORY DISEASE IN THE PIG-TAILED MACAQUE

The macaque model of chlamydial pelvic inflammatory disease (PID) demo nstrates individual variability in the time of onset of intrapelvic ad hesions, Some animals develop adhesions rapidly, within 2 weeks after a single tubal inoculation with Chlamydia trachomatis, while in others , adhesions are not observed until 2 weeks after a second tubal inocul ation, To test whether this variability correlates with major histocom patibility complex (MHC) class I haplotype, we used macaque alloantise ra and mouse anti-HLA monoclonal antibodies to determine the MHC class I haplotypes of 44 C. trachomatis-infected macaques (Macaca nemestrin a). Macaques developing gross tubal adhesions after the first chlamydi al inoculation mere classified as susceptible (n = 29), while those no t developing adhesions until after the second chlamydial inoculation w ere classified as relatively resistant (n = 15), to adhesion formation , Three antibody specificities correlated with susceptibility (odds ra tio [OR] 5.2, P < 0.01; OR 6.1 and 4.3, P < 0.05), and two correlated with relative resistance to adhesions (OR 0.1, P < 0.05; OR 0.2, P < 0 .01), Because several of these antibodies are cross-reactive, as many as five different MHC class I alleles (three increasing and two decrea sing ORs) or as few as two different MHC class I alleles (one increasi ng and one decreasing OR) could be correlated with risk of adhesion fo rmation, We conclude that in macaques, susceptibility or relative resi stance to rapid formation of tubal adhesions is correlated with expres sion of MHC class I alleles, consistent with reports of MHC class I re striction of chlamydial immunopathology in humans.