# IMMUNOPATHOLOGY OF CHLAMYDIA--INDUCED REACTIVE ARTHRITIS

> **NIH NIH R01** · UNIV OF ARKANSAS FOR MED SCIS · 1990 · $98,170

## Abstract

Reactive arthritis has been found to result from gastrointestinal
infections with Yersinia enterocolitica, Salmonella, Shigella, and
Campylobacter and from genital tract infections with Chlamydia
trachomatis.  Despite a knowledge of the association of these
bacteria with reactive arthritis, little is known of the mechanism
by which the arthropathy develops.  It is the objective of this
proposal to investigate the mechanisms by which reactive arthritis
develops as a consequence of genital infections with Chlamydia
trachomatis.  An understanding of these mechanisms may help to
recognize susceptible patients and to develop prophylactic
strategies.  These studies will be conducted in a murine model of
reactive arthritis which is produced by inoculating inactivated
chlamydial antigen into mice which have been infected genitally
with the agent of mouse pneumonitis (MoPn), a C. trachomatis
biovar.  An immune response to the offending bacterium has been
implicated in humans as being a prerequisite for the production of
arthritis.  In the mouse model, previous studies have indicated
that cell mediated immunity is the effector mechanism; thus, this
study will characterize the T cell subpopulations which are
required.  This will be accomplished by separation of the
populations and adoptive transfer into naive mice in which antigen
will be inoculated intra-articularly.  The role of antibody and T
suppressor cells will be investigated using antibody and adoptive
cell transfer systems.  The nature of the chlamydial antigen
responsible for eliciting the arthritis will be determined by
challenging MoPn-infected animals in the joint with different
chlamydial serovars and species, other arthritis-inducing bacteria,
and purified outer membrane components of chlamydiae.  Potential
cross-reactivity of chlamydial antigens with host joint antigens
will also be studied.  Finally, strains of mice bearing different
H-2 antigens will be assessed for their arthritic potential to
determine if there is a relationship with histocompatibility
antigens as occurs in humans.

## Key facts

- **NIH application ID:** 3159941
- **Project number:** 5R01AR039726-02
- **Recipient organization:** UNIV OF ARKANSAS FOR MED SCIS
- **SAM.gov UEI:** VDFYLZPJEAV6
- **Principal Investigator:** Roger G Rank
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $98,170
- **Award type:** 5
- **Project period:** 1988-12-01 → 1991-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3159941

## Citation

> US National Institutes of Health, RePORTER application 3159941, IMMUNOPATHOLOGY OF CHLAMYDIA--INDUCED REACTIVE ARTHRITIS (5R01AR039726-02). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3159941. Licensed CC0.

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