Association between resistance to superinfection and patterns of surface protein labeling in mouse fibroblasts (L cells) persistently infected with Chlamydia psittaci.

When mouse fibroblasts (L cells) were persistently infected with Chlamydia psittaci strain 6BC, they became immune to superinfection because they no longer associated with exogenous C. psittaci in a way that led to ingestion and intracellular multiplication. At the same time, the persistently infected L cells also exhibited changes in surface structure as revealed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiographic visualization of the surface-exposed plasma membrane proteins that had been labeled with 125I by lactoperoxidase-catalyzed iodination.

Fatal misonidazole-induced encephalopathy: an RTOG case report.

A case of fatal encephalopathy following administration of misonidazole (MISO) is reported. Anorexia and dehydration preceded signs of encephalopathy after a cumulative dose of 18 g (11 g/m2) of MISO in five weekly doses. Serum MISO levels four hours after weekly administrations were markedly elevated.

The relation of basic biology to pathogenic potential in the genus Chlamydia.

Chlamydiae are obligately intracellular procaryotic parasites, and their activities as agents of human disease are determined to a large degree by their intracellular way of life. The inside of a host cell is a hostile environment, and few microorganisms survive and multiply intracellularly. Those that do have evolved adaptations that fit them for life inside other cells.

Attachment defect in mouse fibroblasts (L cells) persistently infected with Chlamydia psittaci.

Almost all the cells in populations of mouse fibroblasts (L cells) persistently infected with the 6BC strain of Chlamydia psittaci were immune to superinfection with high multiplicities of C. psittaci, whether or not the L cells contained visible chlamydial inclusions. As ascertained by experiments with 14C-labeled C.

Persistent infection of mouse fibroblasts (McCoy cells) with a trachoma strain of Chlamydia trachomatis.

An in vitro model of persistent infection of mouse fibroblasts (McCoy cells) with a trachoma strain (G17) of Chlamydia trachomatis has been developed. Persistently infected cultures were established by infecting McCoy cells with high multiplicities of chlamydiae. After the first cycle of chlamydial replication, the host cells multiplied more rapidly than the parasites, so that the fraction of inclusion-bearing cells declined to less than 1%.

Persistent infection of mouse fibroblasts (L cells) with Chlamydia psittaci: evidence for a cryptic chlamydial form.

When monolayers of mouse fibroblasts (L cells) were infected with enough Chlamydia psittaci (strain 6BC) to destroy most of the host cells, 1 in every 10(5) to 10(6) originally infected cells gave rise to a colony of L cells persistently infected with strain 6BC. In these populations, the density of L cells and 6BC fluctuated periodically and reciprocally as periods of host cell increase were followed by periods of parasite multiplication. Successive cycles of L-cell and 6BC reproduction were sustained indefinitely by periodic transfer to fresh medium.

Tumour response endpoints in the BA1112 rat sarcoma.

The rat rhabdomyosarcoma BA1112 has a number of features which make it a useful model for the study of tumour response to radiation therapy. It is a transplantable tumour, isologous to an inbred line of WAG/Rij rats and it elicits no demonstrable host immune response. The tumour grows locally at the implantation site and rarely metastasizes.

Cytochalasin B does not inhibit ingestion of Chlamydia psittaci by mouse fibroblasts (L cells) and mouse peritoneal macrophages.

Cytochalasin B did not inhibit ingestion of Chlamydia psittaci by either mouse fibroblasts (L cells) or mouse peritoneal macrophages in concentrations that produced distinctive morphological changes and inhibited phagocytosis of polystyrene latex beads and Escherichia coli K-12.

The cell as an extreme environment.

Living cells and their intracellular parasites show many of the characteristics ascribed to extreme environments and their dominant species. The diversity of species colonizing intracellular habitats is low, and successful inhabitants exhibit special fitness traits that often render them obligately dependent on residence within a host cell. However, the diversity-limiting factor in the extreme environment of the host cell interior is not abiotic, as it is in conventional extreme environments.

Arrays of hemispheric surface projections on Chlamydia psittaci and Chlamydia trachomatis observed by scanning electron microscopy.

Scanning microscopy of two strains of Chlamydia psittaci and four strains of Chlamydia trachomatis representative of the wide diversity in origin and behavior of members of the genus revealed patches of regular arrays of hemispheric projections on the surfaces of elementary bodies of all six strains. These distinctive and perhaps unique surface structure are probably present in all populations of chlamydiae.

Flagellar elongation and shortening in Chlamydomonas. IV. Effects of flagellar detachment, regeneration, and resorption on the induction of flagellar protein synthesis.

Synthesis of new proteins is required to regenerate full length Chlamydomonas flagella after deflagellation. Using gametes, which have a low basal level of protein synthesis, it has been possible to label and detect the synthesis of many flagellar proteins in whole cells. The deflagellation-induced synthesis of the tubulins, dyneins, the flagellar membrane protein, and at least 20 other proteins which co-migrate with proteins in isolated axonemes, can be detected in gamete cytoplasm, and the times of initiation and termination of synthesis for each of the proteins can be studied.

Effect of combined metronidazole and DMSO on tumour control and skin tolerance in the rat.

A combination of the radiosensitizer, metronidazole, and the radioprotector, dimethyl sulfoxide (DMSO), was tested for its effects on the radiation tolerance of rat skin and on the radiosensitivity of the BA1112 rhabdomyosarcoma. The simplest interpretation of the effects of the combined treatment is that: metronidazole radiosensitizes BA1112 in one-fraction but not in five-fraction treatments; metronidazole slightly increases the radiosensitivity of skin in one-fraction treatments; metronidazole radiosensitization is independent of the radioprotection produced by DMSO.

Effect of actinomycin D and neoarsphenamine on tumor control and skin tolerance in the rat.

Actinomycin D and neoarsphenamine were tested for their ability to produce therapeutically favorable radiosensitization in the WAG/Rij rat. Acute and late skin reactions and control of the BA1112 rhabdomyosarcoma were examined in drug-treated and untreated animals irradiated in single- and five-fraction schedules. Actinomycin D was found to protect skin and tumors when added 15 minutes before irradiation.

Loss of inorganic ions from host cells infected with Chlamydia psittaci.

Mouse fibroblasts (L cells) infected with the 6BC strain of Chlamydia psittaci released potassium ion (K(+)) into the extracellular milieu in a way that depended on size of inoculum and time after infection. When the multiplicity of infection was 500 to 1,000 50% infectious units (ID(50)) per L cell, loss of intracellular K(+) was first apparent 4 to 10 h after infection and was nearly complete at 6 to 20 h. Magnesium ion and inorganic phosphate (P(i)) were also released.

Parasite-specified phagocytosis of Chlamydia psittaci and Chlamydia trachomatis by L and HeLa cells.

Phagocytosis of the 6BC strain of Chlamydia psittaci and the lymphogranuloma venereum 440L strain of Chlamydia trachomatis by L cells and HeLa 229 cells occurred at rates and to extents that were 10 to 100 times greater than those observed for the phagocytosis of Escherichia coli and polystyrene latex spheres. Both species of Chlamydia were efficiently taken up by host cells of a type they had not previously encountered. Phagocytosis of chlamydiae was brought about by the interaction of parasite surface ligands with elements of the host cell surface.

Division of single host cells after infection with chlamydiae.

Mouse fibroblasts (L cells) were infected in suspension with Chlamydia psittaci (6BC) and then plated out on a solid substrate at a density of 80 cells per cm2 so that the effect of chlamydial infection on the division of single host cells and their progeny could be determined. Uninfected L cells multiplied with a mean generation time of 15 h. The generation time of single L cells infected with 1.

Toxicity of low and moderate multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).

When mouse fibroblasts (L cells) were infected in suspension or in monolayer with 10 to 100 50% infectious doses (ID(50)) of Chlamydia psittaci (6BC) per host cell, they showed signs of damage 24 to 48 h later. Host-cell injuries were termed multiplication dependent when both the ingestion and subsequent reproduction of C. psittaci were required; when only ingestion but not replication was needed, the injuries were considered to be multiplication independent.

Effect of the radioprotective drugs MEA, DMSO, and WR-2721 on tumor control and skin tolerance in the rat.

Mercaptoethylamine (MEA), dimethylsulfoxide (DMSO), and S-2-(3-aminopropylamino)ethylphosphorothioate (WR-2721) were tested for their protective effects against single and fractionated doses of 250 kv X-rays. Acute and late skin reactions and control of the BA-1112 rhabdomyosarcoma were examined in protected and unprotected WAG/Rij rats. All drugs protected skin in both single and fractionated treatment regimens, with MEA giving the most protection and DMSO the least.

Immediate toxicity of high multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).

One hour after suspensions of mouse fibroblasts (L cells) were exposed to 500 to 1,000 L-cell 50% infectious doses of Chlamydia psittaci (6BC), the L cells failed to attach to and spread out on solid substrates, phagocytosed polystyrene latex spheres at reduced rates, incorporated less [14C]isoleucine into protein, and had smaller soluble pools of nucleoside triphosphates. The infected L cells began to die at 8 h and were all dead by 20 h. Lower multiplicities of infection took correspondingly longer to kill the L cells.

Radiation reaction of rat skin. The role of the number of fractions and the overall treatment time.

Acute skin reactions resulting from orthovoltage x-irradiation were measured in the WAG/Rij rat. A wide range of combination of fraction number and overall time were used in an attempt to determine their relative importance. There appeared to be little effect of prolongation of overall treatment time until periods of over 2 weeks were reached.

The steepness of the dose-response curve in radiation therapy. Theoretical considerations and experimental results.

The random nature of cell killing by ionizing radiations sets an upper limit on the steepness of the dose-response (D-R) curve for tumor cure. This theoretical limit was approached but not reached in a carefully controlled experimental system. It would seem unlikely that this result could be achieved in clinical practice because of the potential importance of tumor heterogeneity and treatment error in decreasing the slope of the D-R curve.

Dose-time relationships for skin reactions and structural damage in rat feet exposed to 250-kVp x rays.

The effects of fractionated irradiation on the feet of rats were the subjects of a time-dose study. The doses required to produce various levels of early skin damage, late skin damage, and late structural damage were determined for single doses and for treatments employing three fractions per week and lasting up to 50 days. The data did not follow the relationship first proposed by strandqvist, in which dose is proportional to time-n; rather, when the normal-tissue reactions were plotted on a linear-coordinate graph, they formed parallel time-dose isoeffect curves with distinct positive curvatures.