Interaction Between Salmonella Typhimurium and Phagocytic Cells in Cell Culture

Furness, G.

doi:10.1093/infdis/103.3.272

Cited by 51 publications

(32 citation statements)

References 11 publications

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“…typhimurium, on the other hand, apparently invaded the lamina propria mainly by passing through the intercellular junctions, in addition to incorporation by epithelial cells, and multiplied within mononuclear cells (9,10). The ability to survive or multiply within the cells played an important role for establishment of infection (1). In this respect, the pathogenicity of Y. enterocolitica was very similar to that of Sal.…”

Section: Discussionmentioning

confidence: 96%

Studies on the Pathogenicity ofYersinia enterocolitica

Une

1977

Microbiology and Immunology

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Analysis of the pathogenicity of Yersinia enterocolitica was performed by means of cell culture studies on the interaction of the organisms with HeLa cells and rabbit peritoneal macrophages based on observations of the pathogenic behavior of the organisms in vivo (11). The pathogenic strains, which successfully produced experimental enterocolitis in rabbits (11), had the ability to penetrate HeLa cells and to survive or multiply within the macrophages. The nonpathogenic strains, lacking the ability to produce pathological changes in rabbits (11), failed to penetrate HeLa cells, except for one strain, and also to survive totally or multiply within the macrophages. It was evident that the abilities of the organisms to penetrate epithelial linings which serve as the barrier of intestinal mucosa and to survive or multiply within the host cells appears to be closely related to the pathogenicity of Y. enterocolitica.

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Section: Discussionmentioning

confidence: 96%

Studies on the Pathogenicity ofYersinia enterocolitica

Une

1977

Microbiology and Immunology

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“…The technique appears preferable to that of adding antibiotics which are assumed to be ineffective against intracellular bacteria (Hart, 1974). Observations that bacteria gain protection from antibiotics by intracellular residence (Magoffin & Spink, 1951 ;Suter, 1952;Mackaness, 1952) led to widespread adoption of the use of antibiotics such as penicillin and streptomycin to selectively kill extracellular bacteria in vitro (Furness, 1958;Holmes et ul., 1966;Alexander & Good, 1968;Solberg, 1972;Ward et ul., 1972;Hsu & Mayo, 1973;Wilder & Edberg, 1973). It became clear that these antibiotics could enter phagocytes and kill intracellular bacteria (Richardson & Holt, 1962;Groschel & Jakubowitch, 1967;Cole & Brostoff, 1975;Veale et al, 1976) and therefore could interfere with estimates of cellular antimicrobial power.…”

Section: Discussionmentioning

confidence: 99%

“…Studies with macrophages in vitro show that virulent salmonellae are more capable than avirulent organisms of increasing intracellularly (Furness, 1958 ;Furness & Ferreira, 1959 ;Jenkin & Benacerraf, 1960) and that macrophages from immune animals are better able to restrict intracellular proliferation than those from susceptible animals (Jenkin & Benacerraf, 1960;Blanden, 1968;Maier & Oels, 1972). However, virulence might equate with either superior resistance to intracellular bactericidal mechanisms, or to faster multiplication on the nutrients available within the cell, or both.…”

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confidence: 99%

Division and Death Rates of Salmonella typhimurium Inside Macrophages: Use of Penicillin as a Probe

Lowrie

Aber

Carrol

1979

Journal of General Microbiology

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409In mouse peritoneal macrophages infected in vitro with Salmonella typhimurium the number of viable bacteria and the number of stainable bacteria detected by light microscopy both increased at similar rates with a doubling time of more than 1 h. Antibiotics were not present ; instead extracellular bacteria were removed by frequently rinsing the cells. The bacterial doubling time in the same medium in the absence of macrophages was about 20 min.Penicillin added to macrophage monolayers rapidly entered the macrophages, reaching a diffusion equilibrium. The penicillin-induced bacterial death rate appeared to depend on the bacterial division rate as well as on the penicillin concentration. These properties of penicillin were used to monitor intracellular bacterial division and death rates. The results indicated that intracellular killing, with the disappearance of stainable bacteria, did not contribute to the extended doubling time in macrophages. It was concluded that the intracellular environment of the bacteria was probably growth inhibitory but not bactericidal.

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“…typhimurium (7). Moreover, this ability might largely influence the bacterial retention in the foci and progressiveness of intestinal disorders.…”

Section: Discussionmentioning

confidence: 99%