# LYME DISEASE--DEVELOPMENT OF SKIN LESIONS AND ARTHRITIS

> **NIH NIH R01** · STATE UNIVERSITY NEW YORK STONY BROOK · 1990 · $127,420

## Abstract

Lyme disease is caused by infection with a spirochete, Borrelia
burgdorferi which is transmitted by the bite of Ixodes ticks.  It is
characterized by an annular skin lesion, usually starting at the site of
tick attachment, known as erythema chronicum migrans (ECM) and, in
decreasing order of frequency, by arthritis usually of the large joints,
neurological and cardiac complications.  The pathogenic relationships
between infection with the Lyme disease spirochete and the development of
lesions in the skin, heart, brain and joints are just beginning to be
understood.  Although the disease has many symptoms and may become
chronic, very few spirochetes are found in Lyme disease patients.  The
hypothesis that the pathogenesis of this disease results from biological
amplification of the effects of small numbers of organisms through the
release of highly active spirochetal products or from the production of
endogenous mediators of tissue injury, or both, will be investigated.  In
the present studies pathogenic components of B. burgdorferi will be
examined.  In so doing a more general understanding of bacterial
pathogenesis and especially of bacteria-induced arthritis should result.

Bacterial lipopolysaccharides (LPS) and peptidoglycans (PG) from the cell
wall have been shown to mediate tissue damage.  B. burgdorferi LPS and PG
will be extracted and characterized with respect to their
physicochemical, immunological and biological properties.  Sugar and
lipid moieties of the LPS will be identified as will the amino acid
composition of the PG.  LPS from cultured and freshly isolated
spirochetes will be compared.  Antibodies specific for LPS and PG will be
used to neutralize the biological activities of these molecules.
Monoclonal anti-LPS antibodies will be used to identify the epitopes
responsible for the inflammatory actions of LPS and to locate the LPS
using immunogold labeling and electron microscopy.  Inflammatory lesions
produced in animal skins following injection of PG or LPS will be
characterized with respect to morphology and induction of endogenous
mediators of inflammation.  A rat model of Lyme arthritis will be
investigated for the roles of LPS and PG in arthritogenesis.

## Key facts

- **NIH application ID:** 3157450
- **Project number:** 5R01AR036028-05
- **Recipient organization:** STATE UNIVERSITY NEW YORK STONY BROOK
- **SAM.gov UEI:** M746VC6XMNH9
- **Principal Investigator:** GAIL S HABICHT
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $127,420
- **Award type:** 5
- **Project period:** 1985-09-23 → 1994-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157450

## Citation

> US National Institutes of Health, RePORTER application 3157450, LYME DISEASE--DEVELOPMENT OF SKIN LESIONS AND ARTHRITIS (5R01AR036028-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3157450. Licensed CC0.

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