Characterization of <i>Actinobacillus actinomycetemcomitans</i> Hemolysin

Kimizuka, Ryuta; Miura, Tadashi; Okuda, K

doi:10.1111/j.1348-0421.1996.tb01132.x

Cited by 30 publications

(26 citation statements)

References 30 publications

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“…A likely explanation for this conclusion, which conflicts with the work that we de- (24). However, they found that their hemolysin had a molecular mass of 12 kDa, which is much less than the molecular mass of LtxA (ϳ114 kDa).…”

Section: Discussioncontrasting

confidence: 53%

“…We have also shown previously that breakdown of LtxA is common in older cultures of A. actinomycetemcomitans (19). Thus, we suggest that Kimizuka et al (24) may have indeed isolated LtxA as the hemolysin but that the 12-kDa protein represented one of leukotoxin's major breakdown products (19).…”

Section: Discussionmentioning

confidence: 77%

“…Previously, A. actinomycetemcomitans has usually been reported to be an organism that is not beta-hemolytic (1, 4); however, in two previous reports workers claimed that certain strains of A. actinomycetemcomitans can be beta-hemolytic. Kimizuka et al (24) showed that approximately 60% of the strains that they tested were beta-hemolytic on horse blood agar. In 1997, Haubek et al (14) reported that only highly leukotoxic strains showed betahemolysis on blood agar.…”

Section: Discussionmentioning

confidence: 99%

“…However, in a few reports workers have suggested that a hemolysin may be present in A. actinomycetemcomitans. In 1996, Kimizuka et al (24) reported that approximately 60% of the A. actinomycetemcomitans strains that they tested formed beta-hemolytic colonies on blood agar. A year later, Haubek et al (14) noted that only serotype b strains of A. actinomycetemcomitans formed beta-hemolytic colonies on blood agar after prolonged incubation.…”

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confidence: 99%

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Leukotoxin Confers Beta-Hemolytic Activity to Actinobacillus actinomycetemcomitans

et al. 2006

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Actinobacillus actinomycetemcomitans is the etiologic agent of localized aggressive periodontitis, a rapidly progressing oral disease that occurs in adolescents. A. actinomycetemcomitans can also cause systemic disease, including infective endocarditis. In early work on A. actinomycetemcomitans workers concluded that this bacterium is not beta-hemolytic. More recent reports have suggested that A. actinomycetemcomitans does have the potential to be beta-hemolytic. While growing A. actinomycetemcomitans on several types of growth media, we noticed a beta-hemolytic reaction on media from one manufacturer. Beta-hemolysis occurred on Columbia agar from Accumedia with either sheep or horse blood, but not on similar media from other manufacturers. A surprising result was that mutants of A. actinomycetemcomitans defective for production of leukotoxin, a toxin that is reportedly highly specific for only human and primate white blood cells, are not beta-hemolytic. Purified leukotoxin was able to lyse sheep and human erythrocytes in vitro. This work showed that in contrast to the accepted view, A. actinomycetemcomitans leukotoxin can indeed destroy erythrocytes and that the production of this toxin results in beta-hemolytic colonies on solid medium. In light of these results, the diagnostic criteria for clinical identification of A. actinomycetemcomitans and potentially related bacteria should be reevaluated. Furthermore, in studies on A. actinomycetemcomitans leukotoxin workers should now consider this toxin's ability to destroy red blood cells.

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Section: Discussioncontrasting

confidence: 53%

Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Leukotoxin Confers Beta-Hemolytic Activity to Actinobacillus actinomycetemcomitans

et al. 2006

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“…Numerous A. actinomycetemcomitans strains express cx-hemolysin activity, but the significance of this is not known (Avila-Campos, 1995). Another study, describing two distinct A. actinomycetemcomitans hemolytic activities (against human, horse, sheep, and rabbit), suggests that A. actinomycetemcomitans may possess multiple hemolysins (Kimizuka et al, 1996). Others have been unable to demonstrate A. actinomycetemcomitans' hemolytic activity toward sheep or rabbit blood cells (Slots, 1982).…”

Section: Escape From the Vacuole: Phospholipase C Activity Is A Candimentioning

confidence: 96%

Models of Invasion of Enteric and Periodontal Pathogens Into Epithelial Cells: A Comparative Analysis

Meyer

Mintz

Fives-Taylor

1997

Critical Reviews in Oral Biology & Medicine

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Bacterial invasion of epithelial cells is associated with the initiation of infection by many bacteria. To carry out this action, bacteria have developed remarkable processes and mechanisms that co-opt host cell function and stimulate their own uptake and adaptation to the environment of the host cell. Two general types of invasion processes have been observed. In one type, the pathogens (e.g., Salmonella and Yersinia spp.) remain in the vacuole in which they are internalized and replicate within the vacuole. In the other type, the organism (e.g., Actinobacillus actinomycetemcomitans, Shigella flexneri, and Listeria monocytogenes) is able to escape from the vacuole, replicate in the host cell cytoplasm, and spread to adjacent host cells. The much-studied enteropathogenic bacteria usurp primarily host cell microfilaments for entry. Those organisms which can escape from the vacuole do so by means of hemolytic factors and C type phospholipases. The cell-to-cell spread of these organisms is mediated by microfilaments. The investigation of invasion by periodontopathogens is in its infancy in comparison with that of the enteric pathogens. However, studies to date on two invasive periodontopathogens. A actinomycetemcomitans and Porphyromonas (Bacteroides) gingivalis, reveal that these bacteria have developed invasion strategies and mechanisms similar to those of the enteropathogens. Entry of A. actinomycetemcomitans is mediated by microfilaments, whereas entry of P. gingivalis is mediated by both microfilaments and microtubules. A. actinomycetemcomitans, like Shigella and Listeria, can escape from the vacuole and spread to adjacent cells. However, the spread of A. actinomycetemcomitans is linked to host cell microtubules, not microfilaments. The paradigms presented establish that bacteria which cause chronic infections, such as periodontitis, and bacteria which cause acute diseases, such as dysentery, have developed similar invasion strategies.

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