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1.  ACUTE INFLAMMATION AND TISSUE MAST CELLS IN ADRENALECTOMIZED RATS WITH CUTANEOUS MUCORMYCOSIS 
The effects of the absence of adrenal tissues on the inflammatory reaction and on the relationship of the tissue mast cells to the inflammatory process have been studied histologically in rats with cutaneous Rhizopus oryzae infection. Degranulation and regranulation of the tissue mast cells at the site of injury have been found to correlate respectively with the onset and subsidence of the exudative cellular phase of inflammation. In the adrenalectomized animals regranulation of these cells and correspondingly termination of the exudative phase are delayed. In the lesions of these rats the numbers of eosinophiles are increased. The proliferative cellular processes of inflammation, although delayed in onset, progress in essentially normal manner but result in some increased collagen deposition. The lack of adrenal secretions does not enhance fungus proliferation and is not associated with spread of the infection. In the present experiments the effectiveness of inflammation does not differ in normal and adrenalectomized rats.
PMCID: PMC2137709  PMID: 14074382
2.  TISSUE MAST CELLS AND ACUTE INFLAMMATION IN EXPERIMENTAL CUTANEOUS MUCORMYCOSIS OF NORMAL, 48/80-TREATED, AND DIABETIC RATS 
The Journal of Experimental Medicine  1960;112(6):1069-1084.
The role of the tissue mast cells in relation to the acute inflammatory reaction to experimental cutaneous mucormycosis was studied histologically in normal rats, in animals whose tissue mast cells had been depleted of their cytoplasmic granules prior to infection by the administration of compound 48/80 and in others in whom acute alloxan diabetes with acidosis had been produced before injection of the fungus. The discharge of the tissue mast cell granules in normal rats occurred within minutes at the site of infection and appeared to initiate the rapid onset of acute inflammation. The degranulation of the tissue mast cells subsided in a short time and the cells reassumed a normal histologic appearance while inflammation progressed with the formation of circumscribed lesions. In animals pretreated with compound 48/80 in which the tissue mast cells contained no granules, the onset of inflammation was briefly delayed, the intensity of the process was somewhat decreased, fibroblastic proliferation was retarded, and the fungus growth in the early lesions was increased. However, the infection did not spread and the lesions were well localized. The tissue mast cells in the diabetic and acidotic rats completely failed to discharge their cytoplasmic granules, the onset and intensity of the acute inflammatory response were markedly delayed and decreased and the infection progressed rapidly with massive fungus growth invading adjacent tissues. A relationship between the discharged tissue mast cell granules and eosinophilic granulocytes was noted since the latter were numerous among the inflammatory cell exudate in normal rats and scarce in the lesions of the diabetic animals. It is concluded that a function of the tissue mast cells in the normal rat is the rapid initiation of acute inflammation at the site of injury and that degranulation of these cells prior to infection somewhat delays the inflammatory response and therefore slightly diminishes host resistance. Furthermore, a severe metabolic disorder such as acute alloxan diabetes with acidosis, inhibits the normal function of the tissue mast cells, delays and decreases inflammation, and in this manner contributes to the greatly increased susceptibility of the host to infection.
PMCID: PMC2137316  PMID: 19867183
3.  THE DEVELOPMENT OF THE ACUTE INFLAMMATORY RESPONSE TO EXPERIMENTAL CUTANEOUS MUCORMYCOSIS IN NORMAL AND DIABETIC RABBITS 
The histologic changes associated with the development of the acute inflammatory response to experimental cutaneous mucormycosis were studied at various times from 5 minutes to 24 hours after inoculation into normal rabbits and in rabbits with acute alloxan diabetes and acidosis. In normal animals the response by polymorphonuclear leukocytes began within a few minutes after inoculation, increased rapidly in extent and intensity and reached its peak within 6 to 12 hours. By that time there was also early proliferation of fibroblasts and of large mononuclear cells and these cellular reactions, together with the accumulated granulocytes, began to produce a demarcation of the lesions. Beginning 4 to 6 hours after inoculation the fungus showed some growth but this remained confined to the necrotic center of the lesions. In the diabetic rabbits the onset of the response by polymorphonuclear leukocytes was delayed by several hours, reduced in intensity and was apparently less effective. There was no proliferation of fibroblasts and the lesions were spreading rather than circumscribed. Fungus growth in the tissues began shortly after inoculation, was marked, progressed rapidly, and soon extended beyond the site of inoculation. The large mononuclear cells, however, appeared at about the same time and in equal number in the lesions of both diabetic and non-diabetic animals and showed no morphologic changes. It is concluded that a significant delay and impaired effectiveness of the response by polymorphonuclear leukocytes, a lack of fibroblastic proliferation and an enhanced growth of the fungus lower host resistance to infection with it and are directly consequent on severe alterations in host metabolism.
PMCID: PMC2137039  PMID: 14445772
4.  EXPERIMENTAL PULMONARY PNEUMOCYSTIS CARINII INFECTION IN RABBITS 
Moderate to marked interstitial pneumonitis with many Pneumocystis organisms was found in rabbits treated with cortisone and antibiotics and instilled intranasally with a suspension of lung tissue from either a patient or a rabbit with this infection. Organisms and pulmonary lesions of similar severity and frequency were present in controls treated in the same manner but instilled with either saline or a boiled suspension of normal human lung tissue. The administration of antibiotics and infected rabbit lung suspension only produced less marked lung changes with fewer organisms. Rare organisms and minute foci of pneumonitis were encountered in normal rabbits which had received neither hormone, antibiotics, nor inoculum. The pulmonary lesions in the cortisone-treated rabbits resembled closely the findings in patients with the subclinical form of Pneumocystis pneumonitis. They did not reproduce the massive lesions of widespread Pneumocystis pneumonia in infants. The findings indicate that latent pulmonary Pneumocystis infection was widespread in these rabbits but do not establish the transmission of the disease. The activation of latent infection was dependent on an impairment of host resistance which in these experiments was produced most effectively by the administration of cortisone. The differences between the experimental lesions and those of typical Pneumocystis pneumonia in infants suggest that in man an unknown defect of host defenses other than that induced by prolonged hormone administration accounts for the increased susceptibility to the infection. It is concluded that in the presence of widespread latent Pneumocystis infection the development of active disease is a manifestation of altered host resistance.
PMCID: PMC2136960  PMID: 13664876
5.  ACTIVATION OF QUIESCENT MUCORMYCOTIC GRANULOMATA IN RABBITS BY INDUCTION OF ACUTE ALLOXAN DIABETES 
In normal rabbits subcutaneous granulomata produced by the injection of a spore suspension of Rhizopus oryzae remained confined to the site of inoculation, showed no fungus proliferation, no longer yielded the agent on culture 10 weeks after inoculation, and eventually healed. Similar well established granulomata in rabbits with acute alloxan diabetes induced 8, 10, and 15 days after injection of the fungus uniformly showed activation of the infection. This occurred only in animals showing acetonuria. In these animals the skin lesions showed proliferation of the fungus frequently associated with invasion and early necrosis of the granuloma wall. In some instances, spread of the infection to adjacent tissues with invasion of blood vessels had occurred. These experiments illustrate that changes in host metabolism can activate a preexisting quiescent infection.
PMCID: PMC2136893  PMID: 13549649
6.  LEUKOPENIA WITH GRANULOCYTOPENIA IN EXPERIMENTAL MUCORMYCOSIS (RHIZOPUS ORYZAE INFECTION 
Mucormycosis was produced in rabbits with sustained, severe leukopenia and granulocytopenia induced by repeated injections of nitrogen mustard. Initially, these animals developed extensive fungus lesions at the site of inoculation which later became granulomatous and tended to heal. Only the early phases of host resistance appeared impaired by the virtual elimination of the polymorphonuclear leukocyte as a factor in the host response. Despite the persistent leukopenia and granulocytopenia, the later phases of host resistance resembled those of the normal animal. Thus, the behavior of the infection in this experiment differs greatly from the unchecked progression of mucormycosis in the metabolically abnormal animal with acute alloxan diabetes. The differences in the course of the disease and in the morphologic appearance of the lesions indicate that metabolic alterations in the host affect all phases of host resistance and not only the polymorphonuclear leukocytic response.
PMCID: PMC2136802  PMID: 13475609

Results 1-11 (11)