Tissue Mast Cells and Acute Inflammation in Experimental Cutaneous Mucormycosis of Normal, 48/80-Treated, and Diabetic Rats

Abstract

The tissue mast cells in the rat have been shown to play a part in the development of hyperemia, vascular permeability, edema formation, and wound healing (1-3). It appears that these processes, which are essential components of the normal inflammatory and reparative reaction, are elicited by the release of substances located in or on the cytoplasmic granules of the tissue mast cells. In the rat these substances have been identified as histamine, heparin, and serotonin (5-hydroxytryptamine) (4, 5). It has also been shown that the tissue content of histamine closely parallels the number and granularity of the tissue mast cells and that histamine, heparin, and serotonin are released into the tissues when the tissue mast cells are depleted of their granules by various experimental means (1, 4).The following experiments were devised to study in three different biologic settings the role of the tissue mast cells in the development of acute inflammation. The first experiment was designed to obtain information in normal rats regarding the behavior of these cells within the general framework of acute inflammation in response to a localized infection. In the second experiment the relation between the inflammatory reaction and infection was investigated in animals pretreated with a compound which temporarily depletes the tissue mast cells of their granules and chemical constituents but is not otherwise toxic for the rat. In the third experiment the influence of a severe, general alteration of host metabolism on the susceptibility to this infection in general and on the tissue mast cells in particular was studied and for this purpose acute alloxan diabetes with acidosis was produced. The same infection was employed in all animals and consisted of the subcutaneous injection of the fungus Rhizopus ory~ae since previous studies had shown that in the normal host mucormycotic infection is self-limiting and remains confined to the site of inoculation while in animals with acute alloxan diabetes and acidosis the infection progresses rapidly and spreads widely (6, 7). The results of the experiments were evaluated by histologic examination of the mucormycotic skin lesions.

Role of Mast Cells and Eosinophils in Tissue Injury Caused by Injection of Ascaris Fluid in the Rat

“…The findings obtained by Sheldon and Bauer [1960] on mucomycosis and by A rcher and McG overn [1968] on Amplicaecum robertsi infec-tion, i.e., the relationship between damage to mast cells and occurrence of eosinophils in rat tissues, seem to agree with the above-suggested hypothesis.…”

Histochemical Studies of Tissue Forms and of Perifungal Substance in Subcutaneous Phycomycosis

“…The latter affects various especially visceral organs, commonly as a secondary mycosis, in patients with considerably reduced immunological activity 12,6,8,9,18,19,[34][35][36][37][38][45][46][47] and others|. In these visceral phycomycoses, necroses and polymorphonuclear reactions with thrombangitis is usually elicited by the fungus, whereas subcutaneous phycomycosis causes predominantly an eosinophilic, lymph-and plasmacellular re action.…”

Eosinophils and Dietary Histamine in the Rat

“…Mast cell granules contain most of the histamine in the body [24] and these granules may be released in the immediate hypersensitivity reaction [25] or in acute inflammation [26], thus producing a local eosinophilia. Sheldon and Bauer [26] showed that damage to the skin of rats produced by experimental mucormycosis caused degranulation of local mast cells within half an hour followed by a local eosinophilia in about 6 h ; pretreatment with compound 48/80 (a histamine libera tor) caused degranulation of the mast cells, and inflammation was then not associated with a local eosinophilia.…”

“…Sheldon and Bauer [26] showed that damage to the skin of rats produced by experimental mucormycosis caused degranulation of local mast cells within half an hour followed by a local eosinophilia in about 6 h ; pretreatment with compound 48/80 (a histamine libera tor) caused degranulation of the mast cells, and inflammation was then not associated with a local eosinophilia. Since local eosinophilia is an uncommon accompaniment to acute inflammation, perhaps the mechanism in this case involved a hypersensitivity reaction.…”