Related Experiment Video
Updated: Jun 19, 2026
05:18
A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
Published on: February 17, 2023
TISSUE MAST CELLS AND ACUTE INFLAMMATION IN EXPERIMENTAL CUTANEOUS MUCORMYCOSIS OF NORMAL, 48/80-TREATED, AND
1Department of Pathology, Emory University School of Medicine, Atlanta.
The Journal of Experimental Medicine
|October 30, 2009
Summary
Tissue mast cells rapidly initiate inflammation in normal rats during mucormycosis infection. Depleting mast cells or inducing diabetes delays inflammation, increasing susceptibility to fungal growth.
Area of Science:
- Immunology
- Pathology
- Mycology
Background:
- Tissue mast cells play a crucial role in acute inflammatory responses.
- Cutaneous mucormycosis is a fungal infection that can cause significant tissue damage.
Purpose of the Study:
- To investigate the role of tissue mast cells in the acute inflammatory reaction to experimental cutaneous mucormycosis in rats.
- To examine the effects of mast cell degranulation and metabolic disorders on the host's response to mucormycosis.
Main Methods:
- Histological examination of rat tissue.
- Experimental induction of cutaneous mucormycosis.
- Depletion of mast cells using compound 48/80.
- Induction of acute alloxan diabetes with acidosis.
Main Results:
- In normal rats, mast cell degranulation rapidly initiated acute inflammation at the infection site.
- Mast cell depletion delayed inflammation onset and intensity, increasing early fungal growth but localizing lesions.
- Diabetic rats showed inhibited mast cell degranulation, delayed/decreased inflammation, and rapid fungal invasion.
Conclusions:
- Tissue mast cells are critical for the rapid initiation of acute inflammation in response to injury.
- Mast cell degranulation influences host resistance to mucormycosis.
- Severe metabolic disorders like diabetes impair mast cell function, increasing susceptibility to fungal infections.