# CANDIDA ADHERENCE & PENETRATION OF VASCULAR ENDOTHELIUM

> **NIH NIH R01** · LOS ANGELES COUNTY HARBOR-UCLA MED CTR · 1987 · $79,814

## Abstract

During the past two decades, there has been a considerable increase in
disseminated candidiasis, particularly in immunocompromised patients,
complicated postoperative patients, and neonates in intensive care settings.

These studies are designed to elucidate the process by which hematogenously
spread Candida organisms traverse the endothelium as they escape from the
vascular compartment to invade parenchymal tissues.  An in vitro assay has
been developed to quantify the adherence of C. albicans and other
non-albicans Candida species to human, bovine, and rabbit vascular
endothelium.  Rabbit antiserum to killed Candida cells has been found to
block adherence to rabbit endothelial cells:  this antiserum will be
absorbed by affinity chromatography to remove the blocking components for
indirect identification of Candida constituents responsible for adherence.
Further characterization of Candida adherence constituents will be
accomplished by removing cell wall (and possibly cell membrane) fractions,
selectively inactivating specific components, and coating carrier cells or
particles with the removed and treated fractions to quantify adherence.
Our blocking antiserum, subjected to affinity chromatography, will be
tested against these extracted cell wall fractions for substantiation and
further definition of components of Candida which mediate endothelial
adherence.

Candida adherence to vascular endothelium occurs in a milieu of circulating
cellular and humoral components; a unique environment when compared to
adherence on epithelial surfaces.  Complex interactions between the
organism, endothelial cells, and these blood elements are likely.  Further
studies will focus on four areas within this context:  a) exploration of
possible endothelial induced improvement in Candida phagocytosis and
killing by circulating PMNs and monocytes, b) development of a method to
quantify Candida and/or phagocytic cell induced endothelial damage, c)
characterization of leukocyte adherence to, and migration through,
endothelium invaded by Candida, d) possible modulation of Candida
endothelial adherence by specific leukocytic peptides recently defined in
amino acid sequence.

The long range goal of these studies is to elucidate the mechanisms of
Candida adherence and penetration of vascular endothelium, in vitro, so
that methods can be developed to modify the events of tissue invasion in
the rabbit model of hematogenous candidiasis and ultimately in patients
susceptible to invasive hematogenous Candida infections.

## Key facts

- **NIH application ID:** 3129448
- **Project number:** 5R01AI019990-03
- **Recipient organization:** LOS ANGELES COUNTY HARBOR-UCLA MED CTR
- **Principal Investigator:** John E Edwards
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $79,814
- **Award type:** 5
- **Project period:** 1984-09-01 → 1988-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3129448

## Citation

> US National Institutes of Health, RePORTER application 3129448, CANDIDA ADHERENCE & PENETRATION OF VASCULAR ENDOTHELIUM (5R01AI019990-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3129448. Licensed CC0.

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