# PULMONARY AND SYSTEMIC KILLING OF OPPORTUNISTIC FUNGI

> **NIH NIH R01** · BOSTON UNIVERSITY MEDICAL CENTER HOSP · 1987 · $313,501

## Abstract

Candidiasis, aspergillosis, cryptococcosis and mucormycosis are the most
common opportunistic mycoses, and have been recognized with increasing
frequency in recent years.  In our past work, we developed new methods for
quantitating damage to hyphae, the tissue invasive forms of Candida,
Aspergillus and Rhizopus.  With in vitro systems, we have continued to
define some of the oxidative and nonoxidative mechanisms involved in
killing of fungi by human and murine neutrophils, monocytes and
macrophages.  Utilizing murine models of respiratory-acquired mycoses which
we developed, we compared factors related to the pathogenesis of
aspergillosis and mucormycosis.  As these mycoses prominently include
vascular invasion as a major factor in progression, we have begun studies
on interactions between fungi, vascular endothelial cells, and other host
cells.  We now intend to continue this combined approach with four major
areas of emphasis:  1) to determine the relative abilities of different
cell types (alveolar, peritoneal and tissue macrophages, neutrophils,
monocytes, natural killer cells, and antibody-dependent killer cells) to
mediate killing of hyphal and other forms of Aspergillus, Rhizopus and
Candida, as well as mechanisms of cell activation and killing by defining
events occurring at the leukocyte surface during activation stimulated by
contact with hyphae (compared with intracellular events occurring within
phagocytic vacuoles, after complete ingestion of particles - e.g.,
comparison of activation by Candida albicans hyphae vs. blastospores); 2)
to further define surface features of fungi which are involved in
attachment to and activation of neutrophils utilizing characterized fungal
products as well as existing monoclonal antibodies to neutrophil surface
features; 3) to continue studies of the role of endothelial cells in the
pathogenesis of these mycoses using systems we have developed for in vitro
tissue culture, as well as whole vessel, in situ perfusion to monitor
interactions of fungi with endothelial and other host cells (leukocytes and
platelets); and 4) interacting with the three above aims relating to in
vitro studies, to continue in vivo studies of opportunistic mycoses to
define the relative importance of specific host defects in the pathogenesis
of individual mycoses (e.g., aspergillosis vs. mucormycosis), and the
reasons for the association of one or another fungal infection with a
particular predisposing factor (e.g., diabetes mellitus, corticosteroids,
etc.).

## Key facts

- **NIH application ID:** 3126152
- **Project number:** 5R01AI015338-10
- **Recipient organization:** BOSTON UNIVERSITY MEDICAL CENTER HOSP
- **Principal Investigator:** RICHARD D DIAMOND
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $313,501
- **Award type:** 5
- **Project period:** 1978-09-01 → 1990-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3126152

## Citation

> US National Institutes of Health, RePORTER application 3126152, PULMONARY AND SYSTEMIC KILLING OF OPPORTUNISTIC FUNGI (5R01AI015338-10). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3126152. Licensed CC0.

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