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Biomedical subjects

E Kondo

Publications and source records attributed to E Kondo.

At least 217 records · Page 12Linked to original sources
PubMed1977

The relationship between the chemical structure of fatty acids and their mycobactericidal activity.

The bactericidal activity of long-chain fatty acids on mycobacteria was examined by exposing the organisms to these acids at 0.04 mM in 0.05 M acetate buffer (pH 5.6). The lethal effect of saturated fatty acids was related to the chain-length of hydrocarbon, C14:0 being the strongest in the activity and longer and shorter fatty acids being less active. Unsaturation, isomerism and the presence of alpha-hydroxy group were found to be other factors governing the activity. The lethal effect was greater in the order of C18:3 greater than C18:2 greater than C18:1(cis) greater than C18:1(trans) greater than alpha-OH C18:0 greater than C18:0. C20:4 was placed between C18:3 and C18:2 in this respect. Esterification of C14:0, C18:1 and C20:4 to methyl esters and cholesteryl esters abolished completely the bactericidal activity of these acids, suggesting the requirement of carboxyl group for the activity. The relationship between the fatty acid structure and the lethal effect was discussed in reference to these observations.

Chemical Phenomena↗
PubMed1976

An attempt to cultivate mycobacteria in simple synthetic liquid medium containing lecithin-cholesterol liposomes.

An attempt was made to cultivate mycobacteria in a simple synthetic liquid medium containing lecithin-cholesterol liposomes. This lipid complex showed a marked growth-promoting effect on the submerged growth of M. tuberculosis and M. bovis. The role of lecithin as nutrient was suggested. The bacillary growth in such environment retained good viability, strong acid-fastness, and high virulence in mice. An avirulent strain of tubercle bacilli, H37Ra, did not respond to lecithin-cholesterol liposomes unlike the parent virulent strain, H37Rv. However, this was not a general rule for virulence, as a highly virulent strain of M. bovis (Ravenel) and an attenuated strain (BCG) both grew well in the presence of lipsomes. Lipid analysis showed that cholesterol in the liposome medium was esterified to some extent during the bacterial growth. It was discussed that the culture in the liposome-containing medium may present an experimental model for the study of interaction between mycobacteria and the macrophage membrane.

Animals↗
PubMed1976

Accumulation of cholesterol esters in macrophages incubated with mycobacteria in vitro.

Macrophages separated from the granulomatous lungs of tuberculous mice had a high amount of cholesterol esters. Resident peritoneal macrophages of normal mice were very low in the ester content. However, when the cells were incubated with mycobacteria in Hanks' solution the ester content of the mixture increased greatly. Peritoneal macrophages harvested by induction with casein had a much larger amount of cholesterol esters than unstimulated resident cells. When such stimulated macrophages were incubated alone in Hanks' solution, the ester content went down probably due to hydrolysis into free form. This reduction was markedly inhibited by incubation with mycobacteria. These observations at a macrophage level presented a cytological explanation for our previous finding that cholesterol ester content increased in the mouse lungs with the development of granulomatous lesions.

Animals↗
PubMed1976

A suggested role of a host-parasite lipid complex in mycobacterial infection.

On the basis of our previous observations and related literatures, was assumed tht cholesterol esters of host origin and phthiocerol dimycocerosate of bacterial origin are located as a lipid mixture around the periphery of pathogenic mycobacteria growing in vivo, probably within the phagocytic vacuole of macrophages. To examine the role of such a postulated lipid complex in mycobacterial infection, a model experiment was made in which tubercle bacilli grown in vitro were "coated" with both lipids and then suspended homogenously in water to serve as an inoculum to infect mice intravenously. Their fate in mouse tissue was compared with that of untreated control bacilli. The results indicated that the lipid "coating" had an infection-promoting effect as revealed by the longer persistence of the treated avirulent bacilli at higher levels of viable counts. When virulent tubercle bacilli were "coated" with the lipid mixture, they became less sensitive to the protective mechanism of BCG-immunized mice.

Animals↗
PubMed1976

Further studies on the lethal effect of long-chain fatty acids on mycobacteria.

Mycobactericidal activity of long-chain fatty acids was confirmed by in vitro exposure of BCG. The killing effect was accompanied by inhibition of the membrane-bound acid phosphatase activity. Such active fatty acids were those having a stronger hemolytic activity (e.g., C12:0, C14:0, C18:1, C18:2). Heat-killed BCG cells or their cell walls adsorbed the toxic fatty acids, whereas the fatty acid-insensitive E. coli cells did not. It was suggested that the mycobactericidal action of long-chain fatty acids is due to their detergent-like action on the cytoplasmic membrane, and that the determinant factor for the fatty acid-sensitivitiy of bacteria is the property of the cell wall by which fatty acids are adsorbed so that the active site is brought into contact with the inner membrane.

Acid Phosphatase↗