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Infection and Immunity, January 2000, p. 303-309, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Seroreactivity to Chlamydia trachomatis Hsp10
Correlates with Severity of Human Genital Tract Disease
David
LaVerda,1,
Lisa N.
Albanese,1
Paul E.
Ruther,2
Sandra G.
Morrison,3
Richard P.
Morrison,3
Kevin A.
Ault,2 and
Gerald I.
Byrne1,*
Department of Medical Microbiology and Immunology,
University of Wisconsin
Madison, Madison, Wisconsin
537061; Department of Obstetrics and
Gynecology, University of Iowa Hospitals and Clinics, Iowa City, Iowa
522422; and Department of
Microbiology, Montana State University, Bozeman, Montana
597173
Received 23 August 1999/Returned for modification 20 September
1999/Accepted 20 October 1999
We have identified the chlamydial heat shock protein Hsp10 as a
potential correlate to the immunopathogenic process in women with tubal
factor infertility (TFI). The human serologic response to chlamydial
Hsp10, Hsp60, and major outer membrane protein (MOMP) was measured by
enzyme-linked immunosorbent assay. Three populations of women were
studied: uninfected controls (CU), acutely infected (AI) women, and
women with TFI. Sera from women in the AI and TFI groups both
recognized Hsp10 more frequently and at a higher overall level than
sera from healthy uninfected controls. Moreover, the infertile women
had significantly greater Hsp10 seroreactivity than acutely infected
women, indicating a concomitant increase of Hsp10 recognition in
populations with increasing levels of disease severity. Hsp60
reactivity showed a similar correlation in these populations, while
MOMP reactivity peaked at the same level in both AI and TFI populations
but did not increase with disease severity. Test populations were
standardized by level of reactivity to formalin-fixed Chlamydia
trachomatis elementary bodies (EBs) to address whether these
associations were reflections of increased overall chlamydial exposure
rather than a property specific to Hsp10. Associations between Hsp10
seropositivity and TFI were greater in the EB+ subgroup
while associations among the EB
subgroup were diminished.
When restricted to the EB+ subgroups, Hsp60 and MOMP
responses in the TFI population did not increase significantly over the
level of AI group responses. Thus, among women with similar exposure to
chlamydiae, the serologic response to Hsp10 exhibited a stronger
correlation with TFI than did the response to Hsp60 or MOMP. These
findings support the hypothesis that the serological response to
C. trachomatis heat shock proteins is associated with the
severity of disease and identifies Hsp10 as an antigen recognized by a
significant proportion of women with TFI.
*
Corresponding author. Mailing address: University of
Wisconsin
Madison, Department of Medical Microbiology and Immunology, 1300 University Ave., Madison, WI 53706. Phone: (608) 263-2494. Fax:
(608) 265-0683. E-mail: gibyrne{at}facstaff.wisc.edu.

Present address: The Maxwell Finland Institute for Infectious
Diseases, Boston Medical Center, Boston, MA
02118.
Infection and Immunity, January 2000, p. 303-309, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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