Lung abscess caused by infection of <i>Actinobacillus actinomycetemcomitans</i>

Hagiwara, Shin-ichiro; Fujimaru, Takuya; Ogino, Aozora; Takano, Tadamasa; Sekijima, Toshio; Kagimoto, Seiichi; Eto, Yoshikatsu

doi:10.1111/j.1442-200x.2009.02899.x

Cited by 12 publications

(13 citation statements)

References 9 publications

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“…Aggregatibacter actinomycetemcomitans is a common inhabitant of the upper aerodigestive tract of humans and non‐human primates. Although the bacterium can be recovered from the subgingival sulcus, tongue, buccal mucosa, and saliva from 10–15% of healthy young individuals (Sirinian et al ., ), it is also, in certain cases, associated with disseminated infections, including lung and brain abscesses (Stepanovic et al ., ; Hagiwara et al ., ), pediatric infective endocarditis (Paturel et al ., ; Tang et al ., ), and localized aggressive periodontitis (Haubek et al ., ). The organism produces a variety of virulence factors that contribute to either bacterial colonization or pathogenesis of disease.…”

Section: Introductionmentioning

confidence: 99%

Membrane association and destabilization by Aggregatibacter actinomycetemcomitans leukotoxin requires changes in secondary structures

Walters

Brown

Edrington

et al. 2013

Molecular Oral Microbiology

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SUMMARY Aggregatibacter actinomycetemcomitans is a common inhabitant of the upper aerodigestive tract of humans and non-human primates and is associated with disseminated infections, including lung and brain abscesses, pediatric infective endocarditis in children, and localized aggressive periodontitis. A. actinomycetemcomitans secretes a repeats-in-toxin protein, leukotoxin, which exclusively kills lymphocyte function-associated antigen-1-bearing cells. The toxin's pathological mechanism is not fully understood; however, experimental evidence indicates that it involves the association with and subsequent destabilization of the target cell's plasma membrane. We have long hypothesized that leukotoxin secondary structure is strongly correlated with membrane association and/or destabilization. In this study, we tested this hypothesis by analyzing lipid-induced changes in leukotoxin conformation. Upon incubation of leukotoxin with lipids that favor leukotoxin-membrane association, we observed an increase in leukotoxin α-helical content that was not observed with lipids that favor membrane destabilization. The change in leukotoxin conformation after incubation with these lipids suggests that membrane binding and membrane destabilization have distinct secondary structural requirements, suggesting that they are independent events. These studies thus provide insight into the mechanism of cell damage that leads to disease progression by A. actinomycetemcomitans.

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Section: Introductionmentioning

confidence: 99%

Membrane association and destabilization by Aggregatibacter actinomycetemcomitans leukotoxin requires changes in secondary structures

Walters

Brown

Edrington

et al. 2013

Molecular Oral Microbiology

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“…In addition, A. actinomycetemcomitans causes disseminated infections, including lung and brain abscesses (Stepanović et al. , 2005; Hagiwara et al. , 2009), and it is also the most common HACEK ( Haemophilus spp., Aggregatibacter actinomycetemcomitans , Cardiobacterium hominis , Eikenella corrodens , and Kingella spp.)…”

Section: Introductionmentioning

confidence: 99%

“…Localized aggressive periodontitis affects approximately 0.5% of adolescents in the USA (Lö e & Brown, 1991). In addition, A. actinomycetemcomitans causes disseminated infections, including lung and brain abscesses (Stepanović et al, 2005;Hagiwara et al, 2009), and it is also the most common HACEK (Haemophilus spp., Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella spp.) microorganism associated with infective endocarditis (Paturel et al, 2004;Tang et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharides mediate leukotoxin secretion in Aggregatibacter actinomycetemcomitans

Tang

Kawai²,

Komatsuzawa

et al. 2011

Molecular Oral Microbiology

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SUMMARY We previously reported that lipopolysaccharide (LPS) related sugars are associated with the glycosylation of the collagen adhesin EmaA, a virulence determinant of Aggregatibacter actinomycetemcomitans. In this study, the role of LPS in the secretion of other virulence factors was investigated. The secretion of the epithelial adhesin Aae, the immunoglobulin Fc receptor Omp34 and leukotoxin were examined in a mutant strain with inactivated TDP-4-keto-6-deoxy-d-glucose 3,5-epimerase (rmlC), which resulted in altered O-antigen polysaccharides (O-PS) of LPS. The secretion of Aae and Omp34 was not affected. However, the leukotoxin secretion, which is mediated by the TolC-dependent Type I secretion system, was altered in the rmlC mutant. The amount of secreted leukotoxin in the bacterial growth medium was reduced 9-fold, with a concurrent 4-fold increase of the membrane-bound toxin in the mutant compared with the wild type strain. The altered leukotoxin secretion pattern was restored to the wild-type by complementation of the rmlC gene in trans. Examination of the ltxA mRNA levels indicated that the leukotoxin secretion was posttranscriptionally regulated in the modified O-PS containing strain. The mutant strain also showed increased resistance to vancomycin, an antibiotic dependent on TolC for internalization, indicating that TolC was affected. Overexpression of TolC in the rmlC mutant resulted in an increased TolC level in the outer membrane but did not restore the leukotoxin secretion profile to the wild-type phenotype. The data suggest that O-PS mediate leukotoxin secretion in A. actinomycetemcomitans.

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“…[4][5][6][7]9,10 The youngest patient was 9 years old. 7 This may be attributed to the predisposing dental status which can be noticed in most of the reports. 4,6-8 All pediatric cases reported are summarized in Table 1.…”

Section: Discussionmentioning

confidence: 99%