Germfree F344 rats developed severe arthritis with 100% incidence after a single intradermal injection of either squalane containing 0.5 mg of heat-killed Mycobacterium bovis BCG or a water-in-oil emulsion containing 0.2 mg of peptidoglycan derived from Staphylococcus epidermidis. Conventional F344 rats developed less-severe arthritis with 20% incidence for heat-killed BCG and 0% incidence for peptidoglycan. Specific-pathogen-free rats showed an intermediate susceptibility between germfree and conventional rats. Interestingly, both unimmunized specific-pathogen-free and conventional rats, but not unimmunized germfree rats, showed weak delayed-type hypersensitivity reactions to peptidoglycans derived from either S. epidermidis or Lactobacillus plantarum, suggesting that a bacterial flora may furnish a stimulus for induction of cell-mediated immunity to ubiquitous bacterial peptidoglycans. It is thus possible that although a bacterial flora is not necessary for development of adjuvant arthritis, it may have some suppressive effect on the development of the disease in specific-pathogen-free and conventional F344 rats, possibly through modulation of the immune response. Adjuvant arthritis (AA) can be induced by a single injection of a water-in-oil emulsion containing mycobacterium (14), many other bacteria, and their cell walls (8, 11). A common factor among these bacterial cell walls responsible for promoting the development of AA was proved to be peptidoglycans (PGs) (12), which are found universally in all bacterial cell walls. This disease has been generally believed to be the result of a delayed-type hypersensitivity (DTH) response to components of bacterial cell walls (20), such as PGs (12). The precise mechanisms which underlie its development are still obscure. There
An investigation was undertaken to study the effects of germfree (GF) status and mild food restriction on life span in GF and specific pathogen-free (SPF) male ICR mice either full-fed (ad libitum) or on a restricted diet of 4.5 grams per day (equivalent to approximately 80% of full-fed intake) from five-week-old. The mean life span of the full-fed SPF and GF mice was 75.9 and 88.9 weeks respectively, whie the mean life span of the food-restricted SPF and GF mice was 117.5 and 109.6 weeks, respectively. Mice in both GF and SPF food-restricted groups were characterized by lower body weight and increased survival. These findings suggest that the cessation of growth may be importantly and perhaps causally related to longevity. The GF mice survived longer than the SPF mice, but the combination of GF status with food restriction did not seem to extend life span more than food restriction alone.
The cytopathic effects of extracts of pharyngeal cells from patients with IgA nephropathy on fibroblasts were determined. Autoradiographical analysis of antigens in the fibroblasts was also described. Freeze and thawed extracts of pharyngeal cells obtained from patients with IgA nephropathy, other glomerular diseases and healthy adults were cultured with fibroblasts such as Vero or Hel cells at 37°C for 1 or 2 weeks. The cytopathic effects of fibroblasts were examined with a light microscope. In addition, the eluate obtained from renal tissues of IgA nephropathy was labeled with iodine-125 by the chloramine-T method. These cultured fibroblasts were incubated with iodine-125-labeled eluate from the same or other patients with IgA nephropathy. The degree of cytopathic effects of extracts of pharyngeal cells from patients with IgA nephropathy on Vero or Hel cells was significantly increased compared with that from patients with other glomerular diseases or healthy adults without glomerular diseases. The cytopathic effects of such fibroblasts were not inhibited by filtration of extracts of pharyngeal cells obtained from patients with IgA nephropathy. It was shown that the antibodies eluted from renal tissues of patients with IgA nephropathy specifically bound with the nuclear regions of such fibroblasts. It was suggested that some antigenic substances might exist in the epithelial cells of the upper respiratory tracts of some patients with IgA nephropathy, and that such antigens were able to be transferred to cultured fibroblasts.
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