Systemic <i>Aggregatibacter actinomycetemcomitans</i> Leukotoxin‐Neutralizing Antibodies in Periodontitis

Johansson, Anders; Buhlin, Kåre; Sorsa, Timo; Pussinen, Pirkko J.

doi:10.1902/jop.2016.160193

Cited by 12 publications

(11 citation statements)

References 38 publications

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“…All antibody levels were remarkably stable during the 6‐month periodontal treatment. This has also been observed in other studies, whether comprising treatment or not . The levels of antibody to A. actinomycetemcomitans and P. gingivalis are determined primarily by the presence of the bacterium and secondly by the signs of periodontitis .…”

Section: Molecular Mimicrysupporting

confidence: 79%

Mediators between oral dysbiosis and cardiovascular diseases

Pietiäinen

Liljestrand

Kopra

et al. 2018

European J Oral Sciences

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Clinical periodontitis is associated with an increased risk for cardiovascular diseases (CVDs) through systemic inflammation as the etiopathogenic link. Whether the oral microbiota, especially its quality, quantity, serology, and virulence factors, plays a role in atherogenesis is not clarified. Patients with periodontitis are exposed to bacteria and their products, which have access to the circulation directly through inflamed oral tissues and indirectly (via saliva) through the gastrointestinal tract, resulting in systemic inflammatory and immunologic responses. Periodontitis is associated with persistent endotoxemia, which has been identified as a notable cardiometabolic risk factor. The serology of bacterial biomarkers for oral dysbiosis is associated with an increased risk for subclinical atherosclerosis, prevalent and future coronary artery disease, and incident and recurrent stroke. In addition to species-specific antibodies, the immunologic response includes persistent, cross-reactive, proatherogenic antibodies against host-derived antigens. Periodontitis may affect lipoprotein metabolism at all levels, and all lipoprotein classes are affected. Periodontitis or its bacterial signatures may be involved not only in increased storage of proatherogenic lipids but also in attenuation of the anti-atherogenic processes, thereby putatively increasing the net risk of atherosclerosis. In this review we summarize possible molecular mediators between the dysbiotic oral microbiota and atherosclerotic processes.

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Section: Molecular Mimicrysupporting

confidence: 79%

Mediators between oral dysbiosis and cardiovascular diseases

Pietiäinen

Liljestrand

Kopra

et al. 2018

European J Oral Sciences

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“…The differences in the neutrophil function between individuals with and without AgP could also be due to a variability in anti-Ltx antibody production and clonality. These antibodies can inactivate Ltx (45), but interindividual differences have not been investigated yet. Moreover, it is likely that other host factors, such as serum components, play a role in enhancing Ltx systemically and, thus, modify the virulence of this toxin (46, 47).…”

Section: Discussionmentioning

confidence: 99%

Effects ofAggregatibacter actinomycetemcomitansleukotoxin on neutrophil migration and extracellular trap formation

Hirschfeld

Roberts

Chapple

et al. 2016

Journal of Oral Microbiology

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BackgroundAggressive periodontitis is associated with the presence of Aggregatibacter actinomycetemcomitans, a leukotoxin (Ltx)-producing periodontal pathogen. Ltx has the ability to lyse white blood cells including neutrophils.ObjectivesThis study was aimed at investigating the interactions between neutrophils and Ltx with regard to the chemotactic properties of Ltx and the release of neutrophil extracellular traps (NETs).MethodsNeutrophils from healthy blood donors were isolated and incubated for 30 min and 3 h with increasing concentrations of Ltx (1, 10, and 100 ng/mL) as well as with A. actinomycetemcomitans strains (NCTC 9710 and HK 1651) producing different levels of Ltx. Formation of NETs and cell lysis were assessed by microscopy, fluorescence-based assays, and measurement of released lactate dehydrogenase. Neutrophil migration in response to different Ltx gradients was monitored by real-time video microscopy, and image analysis was performed using ImageJ software.ResultsAlthough Ltx (10 and 100 ng/mL) and the leukotoxic A. actinomycetemcomitans strain HK 1651 lysed some neutrophils, other cells were still capable of performing NETosis in a concentration-dependent manner. Low doses of Ltx and the weakly leukotoxic strain NCTC 9710 did not lead to neutrophil lysis, but did induce some NETosis. Furthermore, all three concentrations of Ltx enhanced random neutrophil movement; however, low directional accuracy was observed compared with the positive control (fMLP).ConclusionsThe results indicate that Ltx acts both as a neutrophil activator and also causes cell death. In addition, Ltx directly induces NETosis in neutrophils prior to cell lysis. In future studies, the underlying pathways involved in Ltx-meditated neutrophil activation and NETosis need to be investigated further.

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“…However, the study by Johansson et al. (2016) concluded that the presence and levels of systemic immunoreactivity against Aa leukotoxin are associated with a decreased remission after otherwise successful treatment [78]. These results show that periodontal destruction in periodontitis patients especially JP (aggressive periodontitis) is associated with infection by and an immune response to Aggregatibacter actinomycetemcomitans .…”

Section: The Isolation and Studies Of Super‐leukotoxic Strain Aa Jp2mentioning

confidence: 96%

Aggregatibacter (Actinobacillus) actimycetemcomitans leukotoxin and human periodontitis – A historic review with emphasis on JP2

Tsai

Chou

et al. 2018

The Kaohsiung J of Med Scie

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Aggregatibacter (Actinobacillus) actimycetemcomitans (Aa) is a gram-negative bacterium that colonizes the human oral cavity and is causative agent for localized aggressive (juvenile) periodontitis (AgP). In the middle of 1990s, a specific JP2 clone of belonging to the cluster of serotype b strains of Aa with highly leukotoxicity (leukotoxin, LtxA) able to kill human immune cells was isolated. JP2 clone of Aa was strongly associated with in particularly in rapidly progressing forms of aggressive periodontitis. The JP2 clone of Aa is transmitted through close contacts. Therefore, AgP patients need intense monitoring of their periodontal status as the risk for developing severely progressing periodontitis lesions are relatively high. Furthermore, timely periodontal treatment, including periodontal surgery supplemented by the use of antibiotics, is warranted. More importantly, periodontal attachment loss should be prevented by early detection of the JP2 clone of Aa by microbial diagnosis testing and/or preventive means.

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Systemic Aggregatibacter actinomycetemcomitans Leukotoxin‐Neutralizing Antibodies in Periodontitis

Abstract: Presence and levels of systemic immunoreactivity against A. actinomycetemcomitans Ltx are associated with decreased remission after otherwise successful periodontal treatment.

Cited by 12 publications

References 38 publications

Mediators between oral dysbiosis and cardiovascular diseases

Mediators between oral dysbiosis and cardiovascular diseases

Effects ofAggregatibacter actinomycetemcomitansleukotoxin on neutrophil migration and extracellular trap formation

Aggregatibacter (Actinobacillus) actimycetemcomitans leukotoxin and human periodontitis – A historic review with emphasis on JP2

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