Evidence for invasion of a human oral cell line by Actinobacillus actinomycetemcomitans

Meyer, Diane H.; Sreenivasan, Prem K.; Fives-Taylor, Paula

doi:10.1128/iai.59.8.2719-2726.1991

Cited by 179 publications

(142 citation statements)

References 28 publications

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“…Controls for this experiment included lktA encoding the well-studied leucotoxin gene, which is expressed during in vitro growth of the pathogen [16]. Under the infection conditions used, virtually every HeLa cell was infected at a level of 1-5 CFU per HeLa cell, or 0.1-0.5% of the inoculum, which is consistent with previously reported data [17]. The template amount used in the assay was normalized using the total count of viable bacteria (CFU) as a reference point, and done in duplicate in at least two independent experiments.…”

Section: Gene Expression Profile Analysissupporting

confidence: 85%

In vivo induced antigenic determinants of Actinobacillus actinomycetemcomitans

Cao

2004

FEMS Microbiology Letters

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Actinobacillus actinomycetemcomitans is a Gram-negative capnophilic rod and the etiological agent of localized aggressive periodontitis. The genome-wide survey of A. actinomycetemcomitans using in vivo induced antigen technology (IVIAT) has previously resulted in the discovery of antigenic determinants expressed specifically in diseased patients. The present study evaluated the potential of these antigens as putative disease markers, and investigating their contribution to the pathogenesis of the microorganism. Sera from patients had a significantly greater antibody titer than sera from healthy controls against six antigens, which supports the in vivo expression of these antigens, and suggests their usefulness as disease markers. A. actinomycetemcomitans invasion of epithelium-derived HeLa cells resulted in the induction of all three genes tested, as evidenced by real-time PCR. Isogenic mutants of these three genes were constructed and the adhesion and intracellular survival of the mutants was assayed in a competition assay with the wild-type strain. A significant defect in the intracellular survival of two of these mutant strains (orf1402 and orf859) was found. This defect could not be attributed to an adhesion defect. In contrast, a mutation in vapA, a homologue of a novel putative transcriptional regulator, out-competed the wild-type strain in the same assay. The virulent phenotype was restored for a mutant strain in orf859 upon complementation. This data provided new insight into the pathogenic personality of A. actinomycetemcomitans in vivo and supported the use of HeLa cells as a valid in vitro host-pathogen interactions model for that microorganism. IVIAT is applicable to most pathogens and will undoubtedly lead to the discovery of novel therapies, antibiotics and diagnostic tools.

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Section: Gene Expression Profile Analysissupporting

confidence: 85%

In vivo induced antigenic determinants of Actinobacillus actinomycetemcomitans

Cao

2004

FEMS Microbiology Letters

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“…The results of several in vitro studies also demonstrate that A. actinomycetemcomitans has invasive capabilities. Meyer et al [34] reported that 24% of 42 strains of the organism could invade KB cells (without affecting their viability) and, to a lesser extent, human laryngeal and intestinal epithelial cells. The ability to invade was strain-dependent with the most invasive being as invasive as entero-invasive Escherichia coli.…”

Section: Invasionmentioning

confidence: 99%

Virulence factors of Actinobacillus actinomycetemcomitans relevant to the pathogenesis of inflammatory periodontal diseases

Wilson¹

1995

FEMS Microbiology Reviews

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There is strong evidence implicating Actinobacillus actinomycetemcomitans as the causative agent of localised juvenile periodontitis (LJP), a disease characterised by rapid destruction of the tooth-supporting tissues. This organism possesses a large number of virulence factors with a wide range of activities which enable it to colonise the oral cavity, invade periodontal tissues, evade host defences, initiate connective tissue destruction and interfere with tissue repair. Adhesion to epithelial and tooth surfaces is dependent on the presence of surface proteins and structures such as microvesicles and fimbriae. Invasion has been demonstrated in vivo and in vitro although the mechanisms involved are poorly understood. The organism has a number of means of evading host defences which include: (i) inhibiting poloymorphonuclear leukocyte (PMN) chemotaxis; (ii) killing PMNs and monocytes; (iii) producing immunosuppressive factors; (iv) secreting proteases capable of cleaving IgG; and (v) producing Fc-binding proteins. Surface components of A. actinomycetemcomitans are potent stimulators of bone resorption and can induce the release of a range of cytokines which can initiate tissue destruction. A number of surface components can also inhibit the proliferation of fibroblasts and their production of components of the extracellular matrix. Little is known, however, regarding the way in which these factors operate in vivo to produce the pathological features of the disease.

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“…In the oral cavity, the virulence of the periodontal pathogens Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis is enhanced by their ability to invade epithelial cells. [1][2][3][4] Their tendency to invade soft tissue makes them difficult to eliminate by scaling and root planing alone.…”

mentioning

confidence: 99%