Modeling experiments in an animal model of pulmonary granulomatous vasculitis

Summary

Pulmonary granulomatous vasculitis (pulmonary granulomatous vasculitis) is clinically rare, the specific etiology is still unclear, due to the fact that immune complex deposition in the lesion tissue is rare, but there is often an increase in complement, so it may be related to cellular immunity. When sensitized lymphocytes are re-exposed to the antigen, they can activate monocytes, transforming them into macrophages or histiocytes and multinucleated giant cells, which are involved in the formation of granulomas.

Principle

The basic principle of modeling experiments in an animal model of pulmonary granulomatous vasculitis is that dextran, the polysaccharide portion of the cell wall of Saccharomyces cerevisiae, stimulates the monocyte-phagocyte system and causes macrophage proliferation, which can significantly enhance both humoral and cellular immunity.

Operation method

Modeling experiments in an animal model of pulmonary granulomatous vasculitis

Principle

The basic principle of modeling experiments in an animal model of pulmonary granulomatous vasculitis is that dextran, the polysaccharide portion of the cell wall of Saccharomyces cerevisiae, stimulates the monocyte-phagocyte system and causes macrophage proliferation, which can significantly enhance both humoral and cellular immunity.

Materials and Instruments

Equipment:
① Syringe;
② Male SD rats, etc.
Reagents:
① Dextran.

Move

The basic process of modeling experiments in animal models of pulmonary granulomatous vasculitis can be divided into the following steps:
A. Rat: male SD rats, weighing 250-350 g, a single tail vein injection of dextran 5 mg induced pulmonary granulomatous vasculitis in rats.
B

. After a single injection of dextran, the animals rapidly developed lung lesions, and light microscopy showed the formation of scattered granulomatous lesions around the vasculature, which were found primarily around pulmonary arteries and small pulmonary arteries, with occasional involvement of alveolar capillaries and small veins.

Occlusion of larger vascular structures by large typical epithelioid cells is common; fibrinoid degeneration is absent in these lesions, but focal necrosis and vascular stenosis are evident. Such granulomas are characteristic of 'allergic' granulomas rather than foreign body reactions, and many of them contain large numbers of lymphocytes and typical epithelioid cells.

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