# EOSINOPHILS IN HUMAN DISEASE

> **NIH NIH R01** · MAYO CLINIC ROCHESTER · 1991 · $204,815

## Abstract

Over the past two decades information regarding the eosinophilic
leukocyte has dramatically increased.  It is now appreciated that the
eosinophil has the ability to kill parasites in vitro and likely does so
in vivo and that eosinophils most probably serve as effector cells for
damage to tissues in hypersensitivity diseases.  Prior studies supported
by this grant resulted in the isolation of the major eosinophil granule
proteins, production of antibodies to these proteins and development of
methods to investigate the role of the eosinophil in disease.  Because
eosinophil granule proteins are potent toxins in vitro, their deposition
onto tissues in association with. damage to these tissues is a strong
argument for an effector role of the eosinophil and its toxic granule
proteins in disease.  Furthermore, in certain diseases, such as atopic
dermatitis, degranulation can occur without a marked increase in the
number of eosinophils in tissues.
     Eosinophilia is now recognized as being under the control of
cytokines, specifically interleukin (IL)-3, IL-5 and the
granulocyte/macrophage-colony stimulating factor (GM-CSF).  Thus, one can
argue that the proper characterization of an eosinophil associated
disease involves not only the identification of eosinophil degranulation
and deposition of toxic proteins onto damaged tissues, but also
elucidation of the mechanism of the eosinophilia.  This grant application
focuses on the elucidation of the mechanisms of eosinophilia and
eosinophilia associated diseases.  Four goals are identified. First, the
cytokines present in body fluids of individuals with eosinophilia will be
identified and quantitated using an exquisitely sensitive assay for
eosinophil activating cytokines, namely the eosinophil survival assay.
Second, cells producing cytokines will be investigated with particular
attention to T cells and mast cells by in situ hybridization and
immunofluorescence for the cellular localization of GM-CSF, IL-3 and
IL-5.  Third, T cell clones will be established from patients with
eosinophilia to test the hypothesis that clones producing eosinophil
active cytokines are disproportionately increased in number in the blood
of patients with eosinophilia.  Fourth and finally, patients with
eosinophilia will continue to be monitored in order to determine whether
or not novel syndromes can be identified.  Note that this grant served as
the "nidus" of investigations which resulted in the identification of the
eosinophilia-myalgia syndrome, an epidemic of disease which ultimately
has been traced to the ingestion of contaminated batches of L-tryptophan.
Thus, this grant supports investigations to further our understanding of
the pathophysiology of eosinophil associated disease, and it also
monitors these diseases in clinical practice.

## Key facts

- **NIH application ID:** 3126068
- **Project number:** 2R01AI015231-14
- **Recipient organization:** MAYO CLINIC ROCHESTER
- **SAM.gov UEI:** Y2K4F9RPRRG7
- **Principal Investigator:** Gerald J Gleich
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $204,815
- **Award type:** 2
- **Project period:** 1978-09-01 → 1996-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3126068

## Citation

> US National Institutes of Health, RePORTER application 3126068, EOSINOPHILS IN HUMAN DISEASE (2R01AI015231-14). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3126068. Licensed CC0.

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