Binding of Pro-Matrix Metalloproteinase 9 by<i>Fusobacterium nucleatum</i>subsp.<i>nucleatum</i>as a Mechanism To Promote the Invasion of a Reconstituted Basement Membrane

Gendron, Renée; Plamondon, Pascale; Grenier, Daniel

doi:10.1128/iai.72.10.6160-6163.2004

Cited by 16 publications

(15 citation statements)

References 17 publications

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“…Given the reported capacity of F. nucleatum ssp. nucleatum to bind recombinant human MMP‐9 to its cell surface (9), fusobacterial cells were incubated in a culture supernatant of lipopolysaccharide‐stimulated macrophage‐like cells and then tested for cell‐associated MMP‐9 activity by zymography. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…We previously reported the capacity of F. nucleatum ssp. nucleatum whole cells to bind recombinant MMP‐9 (9). In this study, we showed that this bacterium was able to acquire MMP‐9 activity following incubation in a supernatant of PMA‐differentiated U937 cells stimulated by lipopolysaccharide.…”

Section: Discussionmentioning

confidence: 99%

“…The acquisition of MMP‐9 activity may facilitate bacterial dissemination to surrounding periodontal tissues as we demonstrated that MMP‐9‐coated F. nucleatum ssp. nucleatum cells penetrate a reconstituted basement membrane model significantly more efficiently than uncoated cells (9).…”

Section: Discussionmentioning

confidence: 99%

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Response of human macrophage‐like cells to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide

Grenier

Grignon

2006

Oral Microbiology and Immunology

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Monocytes/macrophages are key members of the innate immune system and are present in higher numbers in active periodontal lesions than in inactive sites. The aim of this study was to characterize the response of human monocyte U937 cells, differentiated into adherent macrophages by treatment with phorbol-12-myristate 13-acetate, to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide. Attachment of (3)H-lipopolysaccharide to macrophage-like cells was partially inhibited by anti-CD14 and anti-TLR4 polyclonal antibodies. Fusobacterial lipopolysaccharide did not cause cell apoptosis or block apoptosis induced by camptothecin. Lipopolysaccharide up-regulated the secretion of the pro-inflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha as well as the chemokine interleukin-8 by macrophage-like cells. In addition, it increased phospholipase C and D activities, which likely contributed to the high levels of prostaglandin E(2) detected in the cell culture supernatant. Lastly, the amount of matrix metalloproteinase-9 produced by macrophage-like cells was significantly increased by the lipopolysaccharide treatment. Interestingly, fusobacterial cells acquired matrix metalloproteinase-9 activity following incubation in the presence of the culture supernatant of lipopolysaccharide-stimulated macrophage-like cells. In summary, the lipopolysaccharide of F. nucleatum ssp. nucleatum has a large array of biological effects on macrophage-like cells. This monocytic responsiveness to lipopolysaccharide may be a key regulator of periodontitis.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Response of human macrophage‐like cells to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide

Grenier

Grignon

2006

Oral Microbiology and Immunology

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“…However, this may have been a result of the low concentrations of bacteria (5 × 10 6 per well) used in this assay. Notably, F. nucleatum has been reported to convert pro‐MMP‐9 into the proteolytically active form ; thus, it is possible that F. nucleatum may have similar effects on pro‐MMP‐2. Little is known about proteases expressed by F. nucleatum and their ability to degrade host tissues; therefore, future studies may be aimed at investigating these as a potential pathomechanism in periodontal tissue breakdown.…”

Section: Discussionmentioning

confidence: 99%

Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis

Hirschfeld

Howait

Movila³

et al. 2017

European J Oral Sciences

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Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and counter-regulator of endogenous glucocorticoids. It is implicated in acute and chronic inflammatory diseases. This study investigated the role of the MIF-glucocorticoid (GC) regulatory dyad in MMP2 expression and release during periodontitis in vivo and in vitro. In a MIF knockout (KO) mouse model of ligature-induced periodontitis, gingival tissues and blood were collected and analyzed for levels of IL6, MIF, MMP2 and corticosterone. In addition, human gingival fibroblasts (HGF) were tested for production of IL6 and MMP2 after stimulation with hydrocortisone (HC), MIF, TNF-α or Fusobacterium nucleatum, a pathogen known to elicit immune responses during periodontitis. Wild type (WT) mice showed a local and systemic increase of MIF levels during inflammation, which was confirmed by increased local IL6 concentrations. Systemic GC were reduced in WT and MIF KO mice during inflammation with overall lower concentrations in MIF KO mice. In vivo and in vitro, MMP2 production was not dependent on MIF or inflammatory stimuli, but was inhibited by HC. Therefore, MIF does not appear to stimulate MMP2 expression in the gingival tissues, whereas GC upregulate MIF and downregulate MMP2. Our findings further suggest that MIF may regulate systemic GC levels.

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“…This interaction leads to increased invasion of the pathogens in a matrigel model (i.e. a reconstituted BM) (Gendron et al, 2004).…”

Section: Periodontal Pathogens Utilize Host Mmps For Degrading Host Ementioning

confidence: 99%

Human pathogens utilize host extracellular matrix proteins laminin and collagen for adhesion and invasion of the host

et al. 2012

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Laminin (Ln) and collagen are multifunctional glycoproteins that play an important role in cellular morphogenesis, cell signalling, tissue repair and cell migration. These proteins are ubiquitously present in tissues as a part of the basement membrane (BM), constitute a protective layer around blood capillaries and are included in the extracellular matrix (ECM). As a component of BMs, both Lns and collagen(s), thus function as major mechanical containment molecules that protect tissues from pathogens. Invasive pathogens breach the basal lamina and degrade ECM proteins of interstitial spaces and connective tissues using various ECM-degrading proteases or surface-bound plasminogen and matrix metalloproteinases recruited from the host. Most pathogens associated with the respiratory, gastrointestinal, or urogenital tracts, as well as with the central nervous system or the skin, have the capacity to bind and degrade Lns and collagen(s) in order to adhere to and invade host tissues. In this review, we focus on the adaptability of various pathogens to utilize these ECM proteins as enhancers for adhesion to host tissues or as a targets for degradation in order to breach the cellular barriers. The major pathogens discussed are Streptococcus, Staphylococcus, Pseudomonas, Salmonella, Yersinia, Treponema, Mycobacterium, Clostridium, Listeria, Porphyromonas and Haemophilus; Candida, Aspergillus, Pneumocystis, Cryptococcus and Coccidioides; Acanthamoeba, Trypanosoma and Trichomonas; retrovirus and papilloma virus.

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Binding of Pro-Matrix Metalloproteinase 9 byFusobacterium nucleatumsubsp.nucleatumas a Mechanism To Promote the Invasion of a Reconstituted Basement Membrane

Cited by 16 publications

References 17 publications

Response of human macrophage‐like cells to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide

Response of human macrophage‐like cells to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide

Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis

Human pathogens utilize host extracellular matrix proteins laminin and collagen for adhesion and invasion of the host

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