Abstract
A model for the study of granulomatous inflammation has been developed, employing bentonite particles (65 μm in diameter) coated with soluble antigens derived from Mycobacterium tuberculosis, Histoplasma capsulatum and Schistosoma mansoni. These particles are injected i v. into the micro-vasculature of the lungs of unsensitized mice or mice sensitized to the above antigens in a variety of ways. Uncoated particles or those coated with heterologous antigens elicit rapidly forming small foci of inflammatory cells composed mainly of macrophages. In contrast, particles coated with homologous antigens elicit large hypersensitivity-type granulomas composed of lymphocytes, macrophages, eosinophils and occasionally epithelioid cells. The occurrence of hypersensitivity-type granulomas correlates well with delayed footpad swelling also elicited by homologous antigen. In addition, the florid specific granulomatous inflammation is transferrable to syngeneic recipients with immune lymphoid cells but not with antiserum. Finally, when bare or heterologous antigen-coated particles are injected into sensitized mice which are simultaneously injected i.v. with homologous antigen, hypersensitivity granulomas appear around the particles. This bentonite model thus facilitates the study of both the foreign body and hypersensitivity granulomas and suggests mechanisms by which they might be formed.
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