Host responses induced by co‐infection with <i>Porphyromonas gingivalis</i> and <i>Actinobacillus actinomycetemcomitans</i> in a murine model

Chen, P. B.; Davern, Lynda B.; Katz, Jannet; Eldridge, John H.; Michalek, Suzanne M.

doi:10.1111/j.1399-302x.1996.tb00181.x

Cited by 30 publications

(28 citation statements)

References 46 publications

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“…However, the results of the present study indicated that neither P. gingivalis nor F. nucleatum induced the production of cross-reactive antibodies to B. forsythus, P. intermedia or A. actinomycetemcomitans. Chen et al [18] also showed that a subcutaneous injection of viable P. gingivalis together with A. actinomycetemcomitans resulted in the production of anti-P. gingivalis antibodies in mice injected with P. gingivalis alone with no anti-A. actinomycetemcomitans activity.…”

Section: Discussionmentioning

confidence: 99%

“…While animal studies have demonstrated the pathogenicity of mono-infections of periodontopathogens such as P. gingivalis [13][14][15][16][17], in recent years, reports have been published on the effects of mixed microbial infections including P. gingivalis and A. actinomycetemcomitans [18], P. gingivalis and F. nucleatum [19] and P. gingivalis and B. forsythus [20] which resulted generally in increased levels of pathogenicity with a synergistic effect observed in the humoral and cellular host responses. In the human, F. nucleatum colonizes the plaque prior to P. gingivalis and high levels of F. nucleatum have been demonstrated in association with P. gingivalis as well as other bacteria associated with periodontal disease, such as B. forsythus, Prevotella intermedia and Eikenella corrodens [21].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Gemmell

Bird

Carter

et al. 2002

Clinical and Experimental Immunology

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Periodontal disease results from the inflammatory response to bacteria in dental plaque (reviewed in [1]). Although there are well over 300 different bacterial species in the plaque, progression to periodontitis depends not on bacterial load, but on the presence of specific periodontopathic bacteria. The major pathogens identified at the 1996 World Workshop in Periodontics as causative agents are Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Bacteroides forsythus [2]. P. gingivalis has been found in 15% of subjects in an Australian population, the prevalence increasing with increasing pocket depth [3]. In another study, Slots and Ting [4] found that 40-100% of adult periodontitis patients were positive for P. gingivalis. This high occurrence, together with the pathogenic potential of P. gingivalis, has made it a major pathogen of adult periodontitis [5].Immunohistological studies have established that a T cell/macrophage lesion identical to a delayed hypersensitivity 238 Effect of Fusobacterium nucleatum on the T and B cell responses toPorphyromonas gingivalis in a mouse model SUMMARYT cell cytokine profiles and specific serum antibody levels in five groups of BALB/c mice immunized with saline alone, viable Fusobacterium nucleatum ATCC 25586, viable Porphyromonas gingivalis ATCC 33277, F. nucleatum followed by P. gingivalis and P. gingivalis followed by F. nucleatum were determined. Splenic CD4 and CD8 cells were examined for intracytoplasmic interleukin (IL)-4, interferon (IFN)-gamma and IL-10 by dual colour flow cytometry and the levels of serum anti-F. nucleatum and anti-P. gingivalis antibodies determined by an ELISA. Both Th1 and Th2 responses were demonstrated by all groups, and while there were slightly lower percentages of cytokine positive T cells in mice injected with F. nucleatum alone compared with the other groups immunized with bacteria, F. nucleatum had no effect on the T cell production of cytokines induced by P. gingivalis in the two groups immunized with both organisms. However, the percentages of cytokine positive CD8 cells were generally significantly higher than those of the CD4 cells. Mice immunized with F. nucleatum alone had high levels of serum anti-F. nucleatum antibodies with very low levels of P. gingivalis antibodies, whereas mice injected with P. gingivalis alone produced anti-P. gingivalis antibodies predominantly. Although the levels of anti-F. nucleatum antibodies in mice injected with F. nucleatum followed by P. gingivalis were the same as in mice immunized with F. nucleatum alone, antibody levels to P. gingivalis were very low. In contrast, mice injected with P. gingivalis followed by F. nucleatum produced equal levels of both anti-P. gingivalis and anti-F. nucleatum antibodies, although at lower levels than the other three groups immunized with bacteria, respectively. Anti-Actinobacillus actinomycetemcomitans, Bacteroides forsythus and Prevotella intermedia serum antibody levels were also determined and found to be negligible. In conclusion, F. nucleatum ...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Gemmell

Bird

Carter

et al. 2002

Clinical and Experimental Immunology

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“…Cumulative evidence has indicated the significance of polymicrobial infections in which selected microorganisms interact in a synergistic or antagonistic manner, impacting on pathogenesis [7,14,15]. In the present study, we examined the ability of P.…”

Section: Discussionmentioning

confidence: 99%

Differential ability of periodontopathic bacteria to modulate invasion of human gingival epithelial cells by Porphyromonas gingivalis

Saitô

Inagaki

Ishihara

2009

Microbial Pathogenesis

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Periodontitis is a polymicrobial infection caused by selected gram-negative bacteria including Porphyromonas gingivalis. Host cell invasion by P. gingivalis has been proposed as a possible mechanism of pathogenesis in periodontitis. The aim of the present study was to assess the influence of periodontopathogens on P. gingivalis invasion of gingival epithelial cells in polymicrobial infection. P. gingivalis was tested for its ability to invade a human gingival epithelial cell line Ca9-22 in co-infection with periodontopathogens, using an antibiotic protection assay. Among the pathogens tested, only Fusobacterium nucleatum demonstrated the ability to significantly promote P. gingivalis invasion (p < 0.01). This increased invasion was confirmed by confocal scanning laser microscopy utilizing a dual labeling technique. In contrast, co-infection with Aggregatibacter actinomycetemcomitans or Tannerella forsythia attenuated P. gingivalis invasion. The fusobacterial enhancement of host cell invasion was not observed in co-incubation with other periodontopathogens tested.These results suggested that complex synergistic or antagonistic physiologic mechanisms are intimately involved in host cell invasion by P. gingivalis in polymicrobial infection.

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“…In biofilms and biofilm-related infections, these 'effects' include increased growth, antimicrobial tolerance, virulence and persistence, and enhanced production of exopolysaccharide (EPS) [17][18][19][20][21][22][23][24][25][26][27][28]. Another classic cooperative interaction is metabolic cross-feeding, or syntrophy, where one species makes a metabolic byproduct which enhances the growth of a neighbor [29].…”

Section: • Synergismmentioning

confidence: 99%

Biofilm Models of Polymicrobial Infection

2015

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Interactions between microbes are complex and play an important role in the pathogenesis of infections. These interactions can range from fierce competition for nutrients and niches to highly evolved cooperative mechanisms between different species that support their mutual growth. An increasing appreciation for these interactions, and desire to uncover the mechanisms that govern them, has resulted in a shift from monomicrobial to polymicrobial biofilm studies in different disease models. Here we provide an overview of biofilm models used to study select polymicrobial infections and highlight the impact that the interactions between microbes within these biofilms have on disease progression. Notable recent advances in the development of polymicrobial biofilm-associated infection models and challenges facing the study of polymicrobial biofilms are addressed. Polymicrobial interactions in biofilmsOver the past 2 decades there has been a revolutionary paradigm shift in the field of microbiology with the appreciation that bacteria present in most biological systems exist in biofilms, rather than in a free-living state. This understanding has dramatically changed the way we study bacteria in the laboratory and resulted in the development of many new experimental systems that replicate biofilm environments [1][2][3][4][5]. Studies utilizing these systems have demonstrated time and time again that bacteria behave very differently when in a biofilm than during planktonic growth. In many ways, we now have to relearn everything we thought we knew about bacterial behavior through the view of the biofilm lens.Similarly, the recent explosion of metagenomic studies has significantly increased our appreciation of the complexity of the microbial populations present in biofilms [6,7]. This is also true for infections, most of which are thought to be biofilm related and inherently polymicrobial, including various species of bacteria, fungi and viruses [8]. It is thought that microbes act in concert to establish biofilms, which in turn can increase tolerance to antimicrobials, exacerbate of the host's immune response and increase persistence at the infection site [7,[9][10][11].Genetic diversity of microbes within biofilm communities is thought to increase the fitness of the residing community, making them more equipped to survive environmental stresses. In large part, this is due to an expanded gene pool, which can be more easily shared within the confines of a biofilm community [12]. Community composition and interactions within the community can have huge influences on bacterial behavior. Thus, just as the behavior of planktonic versus biofilm-associated bacteria is dramatically different, so is that of bacteria in single species versus multispecies systems.Interactions between microbes are complex and highly dependent on context. They can range from fierce competition for nutrients and niches, manifested by antagonistic behavior, to highly evolved cooperative mechanisms between different species that support their mutual grow...

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Host responses induced by co‐infection with Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in a murine model

Cited by 30 publications

References 46 publications

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Differential ability of periodontopathic bacteria to modulate invasion of human gingival epithelial cells by Porphyromonas gingivalis

Biofilm Models of Polymicrobial Infection

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