Compromisedhostにおける実験的尿路感染症の病態研究 ―感染局所における免疫応答の分析―

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Various compromised host models were created in mice for use in pathological studies of urinary tract infections (UTI) in compromised hosts which are likely to be encountered in the clinic, and studies were carried out of the local immune response at the site of infection. 1. Creation of Compromised Host Mouse Models Colchicine was administered to mice by intraperitoneal injection of 4 doses of 0.02 mg/mouse, thereby preparing an impaired neutrophilic chemotaxis group. Streptozotocin was administered to mice by intraperitoneal injection at a dosage of 280 mg/kg, thereby preparing a severe diabetic group with impaired neutrophilic phagocytosis. Cyclosporine was administered 4 times to mice in a dosage of 100 mg/kg by subcutaneous injection, thus creating an impaired T cell function group. These three mouse groups were employed in experiments. 2. Study of Experimental Ascending Pyelonephritis in Compromised Host Mice. Ascending pyelonephritis due to Pseudomonas aeruginosa or Escherichia coli was caused in each of the compromised host mouse models, and the infection rate and the mortality rate due to the infections were determined. The results showed that, in each of the compromised host mouse models, the mortality rate was significantly higher than in the control group (mice with normal immune functions). It was thus surmised that these models were infectible. In addition, the infection rate was significantly higher in the impaired neutrophilic chemotaxis group and the diabetic group than in the control group. The infection rate was also elevated in the impaired T cell function group. 3. Study of Local Immune Response at Infection Sites in Compromised Host Mice A time-course study was carried out of the local immune response to infection in the various compromised host mouse models having functional impairment of various cell types that are involved in immunity. In the impaired neutrophilic chemotaxis group, chemotaxis of neutrophils-which are at the heart of nonspecific defense mechanisms against infections-at infection sites was impaired. As a result, it was observed that the infiltration of the infection sites by neutrophils within the 3rd day of infection was reduced in this impaired neutrophilic chemotaxis group compared with the control group. However, the responses of macrophages and helper T cells were enhanced, and infiltration of IgG-positive B cells during the early period of the infection was noted. In the diabetic group, whose mice showed impaired neutrophilic phagocytosis, the results revealed not only impaired neutrophil function but also decreased infiltration of the infection sites by T cells and accompanying weakening of the B cell response. However, the neutrophil and macrophage responses were enhanced. In the impaired T cell function group, the functions of T cells-which are at the heart of specific defense mechanisms against infections-were impaired. In addition to that defect, the infiltration of the infection sites by T cells was decreased, and there was accompanying weakening of the B cell response. However, the neutrophil response was found to be enhanced. On the basis of the above findings, it was found that, in general, the cell infiltration of infection sites is comprised of a sequence starting with neutrophils and macrophages, followed by T cells and B cells. However, depending on the status of the host's immune functions against infections, there are variations in the degree of cell infiltration. That is, it is surmised that the response of cells involved in immunity varies as a function of modification of the defenses against infections, and there is a possibility of compensatory responses.
1994-04-01

Compromisedhostにおける実験的尿路感染症の病態研究 ―感染局所における免疫応答の分析―

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