Pathogenic Microbes and Community Service Through Manipulation of Innate Immunity

Hajishengallis, George; Krauss, Jennifer L.; Liang, Shuang; McIntosh, Megan L.; Lambris, John D.

doi:10.1007/978-1-4614-0106-3_5

Cited by 42 publications

(40 citation statements)

References 88 publications

(144 reference statements)

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“…The net outcome of periodontal disease extent and severity appears dependent upon the characteristics of the oral microbial ecology. These include colonization/emergence of some opportunistic pathogens that appear to alter the local environment affecting the overall microbiome attributes and burden, and act in concert with host responses that are regulated by genetics and modified by the environment in humans [Kinane and Bartold, 2007; Hajishengallis et al, 2012; Armitage, 2013; Ebersole et al, 2013; Wade, 2013; Kornman and Polverini, 2014; Duran-Pinedo et al, 2014]. Since descendants of each of these matrilines still exist within the population and preliminary data suggests an increased risk of demonstrating periodontitis in living animals within the 065 matriline.…”

Section: Discussionmentioning

confidence: 99%

Familial periodontal disease in the cayo santiago rhesus macaques

González

Orraca

Kensler

et al. 2015

American J Primatol

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Substantial ongoing research continues to explore the contribution of genetics and environment to the onset, extent and severity of periodontal disease(s). Existing evidence supports that periodontal disease appears to have an increased prevalence in family units with a member having aggressive periodontitis. We have been using the nonhuman primate as a model of periodontal disease for over 25 years with these species demonstrating naturally-occurring periodontal disease that increases with age. This report details our findings from evaluation of periodontal disease in skulls from 97 animals (5–31 years of age) derived from the skeletons of the rhesus monkeys (Macaca mulatta) on Cayo Santiago. Periodontal disease was evaluated by determining the distance from the base of the alveolar bone defect to the cemento-enamel junction on 1st/2nd premolars and 1st/2nd molars from all 4 quadrants. The results demonstrated an increasing extent and severity of periodontitis with aging across the population of animals beyond only compensatory eruption. Importantly, irrespective of age, extensive heterogeneity in disease expression was observed among the animals. Linking these variations to multi-generational matriarchal family units supported familial susceptibility of periodontitis. As the current generations of animals that are descendants from these matrilines are alive, studies can be conducted to explore an array of underlying factors that could account for susceptibility or resistance to periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Familial periodontal disease in the cayo santiago rhesus macaques

González

Orraca

Kensler

et al. 2015

American J Primatol

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“…A recent example of these types of interbacterial processes that appear to occur in pathogenic oral biofilms are based upon the capacity of P. gingivalis to undermines critical components of innate immunity, including altering functional levels of effector molecules, as well as receptors and subsequent intracellular signaling pathways required for effective host responses. These authors suggested that these “subversive activities” of the periodontal pathogen could promote the adaptive fitness of the pathogenic biofilm communities and enable the chronicity of the inflammatory response resulting in the tissue destruction of periodontitis [108]. …”

Section: Models Of Multispecies Biofilm Functionmentioning

confidence: 99%

Multispecies biofilms and host responses: “Discriminating the Trees from the Forest”

Peyyala

Ebersole

2013

Cytokine

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Periodontal diseases reflect a tissue destructive process of the hard and soft tissues of the periodontium that are initiated by the accumulation of multispecies bacterial biofilms in the subgingival sulcus. This accumulation, in both quantity and quality of bacteria, results in a chronic immunoinflammatory response of the host to control this noxious challenge, leading to collateral damage of the tissues. As knowledge of the characteristics of the host-bacterial interactions in the oral cavity has expanded, new knowledge has become available on the complexity of the microbial challenge and the repertoire of host responses to this challenge. Recent results from the Human Microbiome Project continue to extend the array of taxa, genera, and species of bacteria that inhabit the multiple niches in the oral cavity; however, there is rather sparse information regarding variations in how host cells discriminate commensal from pathogenic species, as well as how the host response is affected by the 3-dimensional architecture and interbacterial interactions that occur in the oral biofilms. This review provides some insights into thes- processes by including existing literature on the biology of nonoral bacterial biofilms, and the more recent literature just beginning to document how the oral cavity responds to multispecies biofilms.

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“…Numerous studies have intended to characterize the host response to infection in periodontal/periapical diseases; providing valuable information on the interactions between the bacterial biofilm and the responding host cells [9][10][11]. With the progress of our knowledge from purely descriptive observations towards more mechanistic findings, we are beginning to get a reasonable glimpse of the whole picture.…”

Section: Introductionmentioning

confidence: 99%

Cytokine Networks Regulating Inflammation and Immune Defense in the Oral Cavity

Cavalla

Araujo-Pires

Biguetti

et al. 2014

Curr Oral Health Rep

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The host/pathogen interaction in infectious oral diseases is characterized by complex and precisely orchestrated host response mechanisms aimed to protect the host against the microbial challenge with minimal collateral damage to host cells and tissues. Central to the host response in this battlefront is the expression of cytokines. The resulting cytokine networks, which ultimately regulate the host response at multiple levels, thereby determine the clinical outcome of the disease and explain most of its defining features from a mechanistic viewpoint. This review intends to present a structured view of the intricate cytokine networks that regulate inflammation and immune defense in the oral cavity, guiding the reader throughout the evolving paradigms that describe how the simultaneous action of multiple cytokines shapes the nature of the immune response to oral infection.

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Pathogenic Microbes and Community Service Through Manipulation of Innate Immunity

Cited by 42 publications

References 88 publications

Familial periodontal disease in the cayo santiago rhesus macaques

Familial periodontal disease in the cayo santiago rhesus macaques

Multispecies biofilms and host responses: “Discriminating the Trees from the Forest”

Cytokine Networks Regulating Inflammation and Immune Defense in the Oral Cavity

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