Identification and characterization of immunogenic proteins of mycoplasma genitalium.

Mycoplasma genitalium causes nonchlamydial nongonococcal urethritis. M. genitalium was detected by PCR in 17 urethral swabs obtained from 99 men with and without urethritis (J. S. Jensen, R. Orsum, B. Dohn, S. Uldum, A. M. Worm, and K. Lind, Genitourin. Med. 69:265-269, 1993), and later, four M. genitalium strains were isolated (J. S. Jensen, H. T. Hansen, and K. Lind, J. Clin. Microbiol. 34:286-291, 1996). The objective of this study was to characterize immunogenic proteins of M. genitalium by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting by using a hyperimmune rabbit serum against M. genitalium G37, determine their identity by mass spectrometry, and develop an M. genitalium-specific enzyme-linked immunosorbent assay (ELISA) free from cross-reactivity with M. pneumoniae antibodies. Using recombinant fragments of the C-terminal part of MgPa (rMgPa), we developed a specific ELISA for detection of M. genitalium antibodies. This antigen did not bind M. pneumoniae antibodies. Using serum samples from the 99 men with and without urethritis, we found that 26 had immunoglobulin G (IgG) antibodies to M. genitalium. There was a strong statistically significant correlation between PCR and IgG antibodies to M. genitalium (odds ratio [OR], 5.9; 95% confidence interval [CI], 2.3 to 21.5; P = 0.002). Furthermore, men with recurrent urethritis were more likely to have antibodies to M. genitalium than were those without recurrent urethritis (OR, 4.0; 95% CI, 1.1 to 14.5; P = 0.0383) and they had significantly higher antibody titers. By use of the rMgPa ELISA, this study further substantiates the importance of M. genitalium as a cause of male urethritis.

Cell-mediated immunity in trachomatous scarring. Evidence from a leprosy population.

BACKGROUND: There is limited understanding of the mechanisms that mediate immunity after infection by Chlamydia trachomatis. Since it is known that the clinical course of leprosy is related to cell-mediated immunity and that such immunity contributes to the development of trachomatous conjunctival scarring, the authors examined patients to determine if there might be an association between leprosy status and trachomatous conjunctival scarring. METHODS: Leprosy patients registered at Shashemane Hospital were interviewed, examined, and patients with siblings residing in the vicinity were asked to return for further clinical examination. A subsample of sibships was selected for laboratory evaluation of cell-mediated immunity, measured by lymphocyte proliferative responses in vitro to stimulation by mycobacterial antigens. RESULTS: Conjunctival scarring was less severe in multibacillary leprosy patients (with suppressed cell-mediated immunity) than in their healthy siblings and more severe in paucibacillary leprosy patients (with enhanced cell-mediated immunity) than in their healthy siblings. The mean lymphocyte proliferative responses to mycobacterial antigens were greater in the sibling (whether leprous or healthy) with more severe conjunctival scarring, regardless of type of leprosy. CONCLUSION: The specific cellular immune responses to Mycobacterium leprae and p65 antigen in patients with increased conjunctival scarring provide evidence that early in the course of infection with C. trachomatis, factors related to an individual's cellular response are crucial to the development of conjunctival scarring. A delayed-type hypersensitivity reaction ("reversal reaction") found in paucibacillary leprosy patients could contribute to the increased trachomatous conjunctival scarring in these patients.