Experimental infection of mouse peritoneal mesothelium with scrub typhus rickettsiae: an ultrastructural study

Ewing, Edwin P.; Takeuchi, Akio; Shirai, Akira; Osterman, J V

doi:10.1128/iai.19.3.1068-1075.1978

Cited by 87 publications

(41 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The rickettsiae released by budding are covered with host cell membrane and infection of other cells with these covered rickettsiae was demonstrated by Ewing et al (2). However naked rickettsiae without host cell membrane are definitely released by lysis of the host cells at a later stage of infection as shown in the present study (Fig.…”

Section: Discussionsupporting

confidence: 78%

Electron Microscopic Studies on Intracellular Multiplication of Rickettsia tsutsugamushi in L Cells

Urakami

Tsuruhara

Tamura

1984

Microbiology and Immunology

View full text Add to dashboard Cite

The mechanism and kinetics of intracellular growth of Rickettsia tsutsugamushi were investigated by electron microscopic observations, parallel with quantitative analysis by counting the rickettsiae seen in electron micrographs and by plaque assay for infectivity of the culture. The observations demonstrated the existence of electron‐less dense and ‐dense types of rickettsiae in the early stage of infection, binary fission and the process of release of the microorganisms in the host cell cytoplasm and from the cell surface, formation of abnormally long rickettsiae, and the process of lysis of the host cell in the later stage of infection with vacuole formation between the inner and outer leaflets of the host cell nuclear membrane. Separate titrations of infectivity of the cells and the culture fluid showed a very slow increase in infectivity in the culture fluid compared with the intracellular titer, suggesting that the progeny rickettsiae stay in the cell or at the cell surface for a relatively long period. Doubling time of the rickettsia was found to be about 9 hr.

show abstract

Section: Discussionsupporting

confidence: 78%

Electron Microscopic Studies on Intracellular Multiplication of Rickettsia tsutsugamushi in L Cells

Urakami

Tsuruhara

Tamura

1984

Microbiology and Immunology

View full text Add to dashboard Cite

show abstract

“…Ultrastructural studies of the rickettsial penetration process, and direct demonstration of phagocytosis and entry, were reported by Ewing et al (2), and Rikihisa and Ito (5,6), both with R. tsutsugamushi. This species of rickettsia is released from host cells in the budding form and the budding rickettsiae are surrounded outside of their own cell wall and cell membrane by an additional host cell cytoplasmic membrane (3,9).…”

mentioning

confidence: 72%

“…No other modes of penetration were found. Ewing et al (2) observed in an in vivo system, the phagocytosis and escape of R. tsutsugamushi which were enclosed by the host cell membrane obtained in the egress stage. The inoculum used in the present study, however, contained only naked rickettsiae purified by Percoll density gradient centrifugation, by which one could separate the naked rickettsiae from those surrounded by a host cell membrane.…”

Section: Discussionmentioning

confidence: 99%

“…This species of rickettsia is released from host cells in the budding form and the budding rickettsiae are surrounded outside of their own cell wall and cell membrane by an additional host cell cytoplasmic membrane (3,9). Ewing et al (2) observed that in vivo these budding rickettsiae, still enclosed by the host cell membrane, were phagocytized in the phagosomes of other cells, and then the outermost membrane of the rickettsiae and the phagosomal membranes fused together, resulting in the release of the rickettsiae into the host cell cytoplasm. Rikihisa and Ito (5) showed a similar phagocytotic mechanism in cultured polymorphonuclear leukocytes by using electron-dense tracer particles to label the sequential events of rickettsial phagocytosis and escape.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Penetration of Rickettsia tsutsugamushi into Cultured Mouse Fibroblasts (L Cells): An Electron Microscopic Observation

Urakami

Tsuruhara

Tamura

1983

Microbiology and Immunology

View full text Add to dashboard Cite

The mechanism of penetration of purified Rickettsia tsutsugamushi (Gilliam strain) into cultured mouse fibroblasts (L cells) was examined by electron microscopy. After 10-40 min of infection, rickettsiae in the process of being phagocytized were often seen on the cell surface. These were restricted to the rickettsiae which seemed to be intact in morphology, while heavily plasmolyzed ones were never phagocytized. Additionally, rickettsiae were taken up individually into a phagosome, and phagocytosis of several rickettsiae together was rarely observed, except in the case of heat-inactivated microorganisms. In the cells, phagosomes whose membranes enclosed rickettsiae either tightly or loosely were seen. Rickettsiae in the loose phagosomes often showed signs of plasmolysis and were rarely released into the cell cytoplasm. Partial disintegration of phagosomal membranes and the escape of rickettsiae from the phagosomes were seen only in tight phagosomes. Large phagosomes containing a clump of several rickettsiae were observed occasionally, in which case the microorganisms were deformed and seemed to be denatured. From the above observations and the frequency of appearance of these different penetration stages in the specimens 10, 20, and 40 min after infection, it was concluded that the rickettsiae enter initially into a tight phagosome by phagocytosis and are then released into the cell cytoplasm by disruption of the phagosomal membrane. No other mechanisms of penetration were found. On the other hand, rickettsiae inactivated by trypsin did not attach to host cells. Inactivation by heat or UV irradiation resulted in reduction of phagocytosis, and rickettsiae treated with rifamycin could penetrate into the host cell cytoplasm to the same extent as in the case of infection with intact rickettsiae.Although rickettsiae are recognized as obligatory intracellular microparasites which propagate in the host cell cytoplasm, studies on the mechanism of penetration of this microorganism across the host cell membrane are scarce. Cohn et al (I) first showed that the entrance of Rickettsia tsutsugamushi into cultured mouse MB III lymphoblasts requires active participation of both the rickettsiae and the host, and a similar result was reported by Walker and Winkler (10) in the R. protoazekiimouse fibroblast (L cell) system. Wisseman et al (13) indicated rapid, bidirectional traffic of R. rickettsii directly across the host cell membrane. However Wisse-251

show abstract

“…The bacteria (Liszeria, Rickettsia, and Shigella) can move to the cell surface where they push the plasma membrane out to form filopodia. Phagocytosis by uninfected cells of these filopodia, either after they are released from the infected cell or while they are still attached to it, is thought to be the mechanism for further infection [Ewing et al, 1978;Tilney and Portnoy , 19891. The directional polymerization of the actin monomers onto the barbed ends of the actin filaments near the bacterial surface appears to be responsible for the bacterial movement [Sanger et al, 1990b, 19921 with the tail remaining in place as actin polymerization apparently pushes the bacterium forward both in the cytoplasm [Sanger et al, 1990bTheriot et al, 19921 and in the undulating filopodia [Sanger et al, 1990b, 19921.…”

Section: Introductionmentioning

confidence: 99%

Intact alpha‐actinin molecules are needed for both the assembly of actin into the tails and the locomotion of Listeria monocytogenes inside infected cells

Dold

Sanger

1994

Cell Motil. Cytoskeleton

View full text Add to dashboard Cite

After the infectious bacterium, Listeria monocytogenes, is phagocytosed by a host cell, it leaves the lysosome and recruits the host cell's cytoskeletal proteins to assemble a stationary tail composed primarily of actin filaments cross-linked with alpha-actinin. The continual recruitment of contractile proteins to the interface between the bacterium and the tail accompanies the propulsion of the bacterium ahead of the elongating tail. When a bacterium contacts the host cell membrane, it pushes out the membrane into an undulating tubular structure or filopodium that envelops the bacterium at the tip with the tail of cytoskeletal proteins behind it. Previous work has demonstrated that alpha-actinin can be cleaved into two proteolytic fragments whose microinjection into cells interferes with stress fiber integrity. Microinjection of the 53 kD alpha-actinin fragment into cells infected with Listeria monocytogenes, induces the loss of tails from bacteria and causes the bacteria to become stationary. Infected cells that possess filopodia when injected with the 53 kD fragment lose their filopodia. These results indicate that intact alpha-actinin molecules play an important role in the intracellular motility of Listeria, presumably by stabilizing the actin fibers in the stationary tails that are required for the bacteria to move forward. Fluorescently labeled vinculin associated with the tails when it was injected into infected cells. Talin antibody staining indicated that this protein, also, is present in the tails. These observations suggest that the tails share properties of attachment plaques normally present in the host cells. This model would explain the ability of the bacterium (1) to move within the cytoplasm and (2) to push out the surface of the cell to form a filopodium. The attachment plaque proteins, alpha-actinin, talin, and vinculin, may bind and stabilize the actin filaments as they polymerize behind the bacteria and additionally could also enable the tails to bind to the cell membrane in the filopodia.

show abstract

Experimental infection of mouse peritoneal mesothelium with scrub typhus rickettsiae: an ultrastructural study

Cited by 87 publications

References 3 publications

Electron Microscopic Studies on Intracellular Multiplication of Rickettsia tsutsugamushi in L Cells

Electron Microscopic Studies on Intracellular Multiplication of Rickettsia tsutsugamushi in L Cells

Penetration of Rickettsia tsutsugamushi into Cultured Mouse Fibroblasts (L Cells): An Electron Microscopic Observation

Intact alpha‐actinin molecules are needed for both the assembly of actin into the tails and the locomotion of Listeria monocytogenes inside infected cells

Contact Info

Product

Resources

About