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Biomedical subjects

H Isogai

Publications and source records attributed to H Isogai.

At least 91 records · Page 5Linked to original sources
PubMed1988

Histological changes and some in vitro biological activities induced by lipopolysaccharide from Bacteroides gingivalis.

The biological activities of lipopolysaccharide from Bacteroides gingivalis 381 (B-LPS) were examined in vivo and in vitro. Intra-oral mucosal injection of B-LPS induced an acute inflammation at the injection site. Intravenous injection of B-LPS induced necrotic lesions with many thrombi in the liver and lymphocytic reduction in the spleen. By immunohistochemical examination, B-LPS was detected in macrophages in the liver, spleen and lymph nodes. In vitro analysis showed that B-LPS was a potent activator of both neutrophils and macrophages in luminol-dependent response and IL-1 secretion from macrophages and was mitogenic to the spleen cells not only from BALB/c mice but also from LPS-non-responder C3H/HeJ mice. Interferon production from human peripheral mononuclear leucocytes was induced, in vitro, by stimulation with B-LPS but not with the other enterobacterial LPS. These findings clarified the various biological activities of B-LPS affecting various cells and tissues, especially neutrophils, macrophages and lymphocytes. The potent inflammability of B-LPS shown in the present study indicates that it is one of the effective agents to induce periodontitis.

Animals↗
PubMed1986

Biological activities of leptospiral lipopolysaccharide.

Lipopolysaccharide extracted with phenol-water from Leptospira interrogans serovar copenhageni strain Shibaura (L-LPS) showed various biological activities. In lethality for mice, L-LPS was active (LD 50, 3.4 mg/mouse) but about 12 times less potent than Escherichia coli LPS (E-LPS) per weight basis. L-LPS had pyrogenicity for rabbits, and the fever curves showed no evidence of the classical biphasic fever produced by E-LPS. In the bone marrow of mice, L-LPS caused hemorrhages and necrosis but less severe than those caused by E-LPS. Histopathologically, fresh hemorrhages were found in the intestine, spleen, lung and the other organs at 24 h after inoculation of L-LPS. Necrosis was also found in these organs and was particularly severe in mice inoculated with more than 2 mgL-LPS. Liver necrosis was found at 7th day after inoculation of L-LPS but not after inoculation of E-LPS. L-LPS had adjuvant activity just like E-LPS. L-LPS enhanced non-specific resistance to Salmonella infection and activated mouse peritoneal macrophages to kill these organisms. L-LPS was positive in limulus test just like E-LPS. These results demonstrated similarities of L-LPS and E-LPS. Some toxic effects of L-LPS were less than those of E-LPS, but some effects of L-LPS were more than those of E-LPS. L-LPS was antigenically active and the specificity was serogroup-associated. L-LPS was composed of carbohydrate (54%), lipid (12%), protein (5%). Arabinose, xylose and rhamnose were major sugars as detected by gas chromatography. 2-keto-deoxyoctanate (KDO) was not detectable.

Animals↗
PubMed1986

Phagocytosis as a defense mechanism against infection with leptospiras.

The role of macrophages in host defense was studied in vivo and in vitro. The intravenous administration of silica, an agent reported to selectively inactivate macrophages, increased the sensitivity to leptospiral infection and inhibited bacterial clearance. Active immunization with killed organisms or with leptospiral lipopolysaccharide (L-LPS), and passive immunization with a monoclonal antibody showed powerful protective effects against infection in mice. The effect of immunization decreased in silica-treated mice. These findings were supported by electron microscopic examination and observation of killing by macrophages in vitro.

Animals↗
PubMed1986

Decreased lipopolysaccharide content and enhanced susceptibility of leptospiras to serum leptospiricidal action and phagocytosis after treatment with diphenylamine.

Growth of leptospiras in the presence of diphenylamine (DPA) caused a decrease in the content of leptospiral lipopolysaccharide (LPS). In association with this decrease of LPS, leptospiras became susceptible to anti-leptospiral action of normal rabbit serum (NRS), leptospiricidal action of antibody and complement, and killing by phagocytes. DPA-treated leptospiras were eliminated rapidly from the blood of infected mice and could not grow in the animals.

Aniline Compounds↗
PubMed1986

Bacterial adherence to gingival epithelial cells of rats with naturally occurring gingivitis.

Bacterial adherence to gingival cells was compared in rats with spontaneous gingivitis (SUS rat) and in control rats (RES rat). In the SUS rat, the number of adherent bacteria in gingival cells changed according to the progression of gingival inflammation. There was a correlation between the change of the number of adherent bacteria, progress of inflammation and pH in the pocket. In the RES rat, the number of adherent bacteria was constant and very small. In the adherence assay, adherence of Bacteroides intermedius to epithelial cells was dependent on the pH. Adherence of B. intermedius was better than that of other species. B. gingivalis and B. macacae showed good adherence but B. levii showed poor adherence. Adherence to the epithelial cells of the SUS rat was always better than that of the RES rat. These results were supported by scanning electron microscopic studies.

Adhesiveness↗
PubMed1985

Microbial ecology of plaque in rats with naturally occurring gingivitis.

The microbial ecology of adherent plaque was investigated in relation to the pathological findings of gingivitis in plaque-susceptible rats. Plaque developed in the gingiva of the lower incisor in plaque-susceptible rats, but not in plaque-resistant rats, after they were fed a commercial powder diet. With increase in plaque volume, the total counts of bacteria increased 10(9) to 10(11)/g. In the first 3 months, Bacteroides species increased and became the predominant population. Streptococcus species also increased at the same time. After 9 months, Fusobacterium species and oral Treponema species were recognized in increasing numbers. The anaerobic bacteria increased in proportion with the progression of plaque development. Bacteroides intermedius, Fusobacterium nucleatum, Streptococcus salivarius, and other species were isolated. Acute gingivitis was observed within 3 months, and subacute-chronic gingivitis was observed between 2 and 12 months. These findings suggest that proportional changes in the gingival plaque flora may uniquely contribute to the development of gingival inflammation in this experimental model.

Animals↗