Colonization and Persistence of Labeled and “Foreign” Strains of Aggregatibacter actinomycetemcomitans Inoculated into the Mouths of Rhesus Monkeys

Dh, Fine; Karched, Maribasappa; Furgang, David; SampathKumar,; Velusamy, Senthil Kumar; Godboley, Dipti

doi:10.13188/2377-987x.1000005

Cited by 10 publications

(7 citation statements)

References 39 publications

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“…In a screening effort to identify an optimal host for monitoring Aggregatibacter actinomycetemcomitans, the leading cause of periodontitis in humans, Macaca mulatta (rhesus [Rh] monkeys) ranked as the first choice. Rh monkeys provide an established oral habitat to validate A. actinomycetemcomitans-mediated periodontitis (365). Rh monkeys have also been tested for age-mediated apoptosis gene expression in oral mucosal tissues.…”

Section: Vertebrate Animal Modelsmentioning

confidence: 99%

Options and Limitations in Clinical Investigation of Bacterial Biofilms

et al. 2018

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Bacteria can form single- and multispecies biofilms exhibiting diverse features based upon the microbial composition of their community and microenvironment. The study of bacterial biofilm development has received great interest in the past 20 years and is motivated by the elegant complexity characteristic of these multicellular communities and their role in infectious diseases. Biofilms can thrive on virtually any surface and can be beneficial or detrimental based upon the community's interplay and the surface. Advances in the understanding of structural and functional variations and the roles that biofilms play in disease and host-pathogen interactions have been addressed through comprehensive literature searches. In this review article, a synopsis of the methodological landscape of biofilm analysis is provided, including an evaluation of the current trends in methodological research. We deem this worthwhile because a keyword-oriented bibliographical search reveals that less than 5% of the biofilm literature is devoted to methodology. In this report, we (i) summarize current methodologies for biofilm characterization, monitoring, and quantification; (ii) discuss advances in the discovery of effective imaging and sensing tools and modalities; (iii) provide an overview of tailored animal models that assess features of biofilm infections; and (iv) make recommendations defining the most appropriate methodological tools for clinical settings.

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Section: Vertebrate Animal Modelsmentioning

confidence: 99%

Options and Limitations in Clinical Investigation of Bacterial Biofilms

et al. 2018

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“…Supragingival plaque communities were examined in an interventional/experimental Rhesus (Rh) primate model (9). With respect to Aa , Rh primates are unique in that the overwhelming majority of healthy primates harbor Aa in their supragingival plaque (9). This consistent presence of Aa in supragingival plaque allows for examination of Aa 's role in early plaque formation (9).…”

Section: Misconception 2: Nutritional Fastidious Nature Of Aamentioning

confidence: 99%

“…In this review the disease provoking process has been divided into four steps as follows; Step 1: colonization above the gum-line, Step 2: integration and survival in the biofilm milieu, Step 3: migration to a new setting below the gumline, and Step 4: suppression of the mucosal host defenses below the gum-line. Many of these steps have been clarified in recent years by harmonizing; (a) clinical observational studies in humans (7), (b) studies using molecular approaches (8), and (c) interventional/experimental studies in animal models (9). As a result it is now possible to put forward a narrative that illustrates how Aa can actively participate in the disease process.…”

Section: Introductionmentioning

confidence: 99%

Aggregatibacter actinomycetemcomitans (Aa) Under the Radar: Myths and Misunderstandings of Aa and Its Role in Aggressive Periodontitis

2019

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Aggregatibacter actinomycetemcomitans (Aa) is a low-abundance Gram-negative oral pathobiont that is highly associated with a silent but aggressive orphan disease that results in periodontitis and tooth loss in adolescents of African heritage. For the most part Aa conducts its business by utilizing strategies allowing it to conceal itself below the radar of the host mucosal immune defense system. A great deal of misinformation has been conveyed with respect to Aa biology in health and disease. The purpose of this review is to present misconceptions about Aa and the strategies that it uses to colonize, survive, and evade the host. In the process Aa manages to undermine host mucosal defenses and contribute to disease initiation. This review will present clinical observational, molecular, and interventional studies that illustrate genetic, phenotypic, and biogeographical tactics that have been recently clarified and demonstrate how Aa survives and suppresses host mucosal defenses to take part in disease pathogenesis. At one point in time Aa was considered to be the causative agent of Localized Aggressive Periodontitis. Currently, it is most accurate to look at Aa as a community activist and necessary partner of a pathogenic consortium that suppresses the initial host response so as to encourage overgrowth of its partners. The data for Aa's activist role stems from molecular genetic studies complemented by experimental animal investigations that demonstrate how Aa establishes a habitat (housing), nutritional sustenance in that habitat (food), and biogeographical mobilization and/or relocation from its initial habitat (transportation). In this manner Aa can transfer to a protected but vulnerable domain (pocket or sulcus) where its community activism is most useful. Aa 's “strategy” includes obtaining housing, food, and transportation at no cost to its partners challenging the economic theory that “there ain't no such thing as a free lunch.” This “strategy” illustrates how co-evolution can promote Aa's survival, on one hand, and overgrowth of community members, on the other, which can result in local host dysbiosis and susceptibility to infection.

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“…Due to the similarity between human and primate microbiota and anatomy, we began investigating a primate model of disease. In these studies, we learned that inoculation of a labeled A. actinomycetemcomitans strain of human origin could not colonize and sustain itself in a Rhesus (Rh) monkey model [54]. In contrast, a strain derived from Rh monkeys could colonize and survive over a 4-5-week period [54].…”

Section: Interventional Studiesmentioning

confidence: 99%

“…In these studies, we learned that inoculation of a labeled A. actinomycetemcomitans strain of human origin could not colonize and sustain itself in a Rhesus (Rh) monkey model [54]. In contrast, a strain derived from Rh monkeys could colonize and survive over a 4-5-week period [54]. Using that same parental Rh A. actinomycetemcomitans strain, we also found to our surprise that deletion of ltxA resulted in a failure of the ltx knock-out strain to colonize.…”

Section: Interventional Studiesmentioning

confidence: 99%

Aggregatibacter, a Low Abundance Pathobiont That Influences Biogeography, Microbial Dysbiosis, and Host Defense Capabilities in Periodontitis: The History of a Bug, and Localization of Disease

2020

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Aggregatibacter actinomycetemcomitans, the focus of this review, was initially proposed as a microbe directly related to a phenotypically distinct form of periodontitis called localized juvenile periodontitis. At the time, it seemed as if specific microbes were implicated as the cause of distinct forms of disease. Over the years, much has changed. The sense that specific microbes relate to distinct forms of disease has been challenged, as has the sense that distinct forms of periodontitis exist. This review consists of two components. The first part is presented as a detective story where we attempt to determine what role, if any, Aggregatibacter plays as a participant in disease. The second part describes landscape ecology in the context of how the host environment shapes the framework of local microbial dysbiosis. We then conjecture as to how the local host response may limit the damage caused by pathobionts. We propose that the host may overcome the constant barrage of a dysbiotic microbiota by confining it to a local tooth site. We conclude speculating that the host response can confine local damage by restricting bacteremic translocation of members of the oral microbiota to distant organs thus constraining morbidity and mortality of the host.

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Colonization and Persistence of Labeled and “Foreign” Strains of Aggregatibacter actinomycetemcomitans Inoculated into the Mouths of Rhesus Monkeys

Cited by 10 publications

References 39 publications

Options and Limitations in Clinical Investigation of Bacterial Biofilms

Options and Limitations in Clinical Investigation of Bacterial Biofilms

Aggregatibacter actinomycetemcomitans (Aa) Under the Radar: Myths and Misunderstandings of Aa and Its Role in Aggressive Periodontitis

Aggregatibacter, a Low Abundance Pathobiont That Influences Biogeography, Microbial Dysbiosis, and Host Defense Capabilities in Periodontitis: The History of a Bug, and Localization of Disease

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