Monocyte Activation by <i>Porphyromonas gingivalis</i> LPS in Aggressive Periodontitis with the Use of Whole-blood Cultures

Mahanonda, Rangsini; Sa‐Ard‐Iam, Noppadol; Charatkulangkun, Orawan; Promsudthi, Ananya; Schifferle, Robert E.; Yongvanichit, Kosol; Pichyangkul, Sathit

doi:10.1177/154405910408300706

Cited by 18 publications

(15 citation statements)

References 32 publications

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“…The latter has been shown in several studies (Fredriksson et al 1998). Some authors have reported a reduced, and others a similar or even no release of IL‐1 β from mononuclear cells after LPS stimulation in periodontitis (Garrison & Nichols 1989, Shapira et al 1994, Fokkema et al 2002, Mahanonda et al 2004). An increase in the release of IL‐1 β from mononuclear cells after LPS stimulation is reported in patients with chronic periodontal disease (McFarlane et al 1990).…”

Section: Discussionmentioning

confidence: 99%

Hyper‐reactive mononuclear cells and neutrophils in chronic periodontitis

Gustafsson

Ito

Åsman

et al. 2006

J Clinic Periodontology

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Section: Discussionmentioning

confidence: 99%

Hyper‐reactive mononuclear cells and neutrophils in chronic periodontitis

Gustafsson

Ito

Åsman

et al. 2006

J Clinic Periodontology

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“…The activation of APCs after stimulation with periodontal pathogens has been reported both in terms of up-regulated expression of activation markers such as HLA-DR, CD40 and CD54 (Jotwani et al 2001, Kanaya et al 2004, Mahanonda et al 2004, 2006 as well as the production of inflammatory cytokines, e.g. IL-1b, IL-6 and TNF-a (Diya et al 2008, Nares et al 2009).…”

Section: Potential Drivers Of Th17 Cells/il-17 Responses In Gingival mentioning

confidence: 99%

The presence, function and regulation of IL‐17 and Th17 cells in periodontitis

Cheng

Hughes

Taams

2014

J Clinic Periodontology

144

113

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Periodontitis (PD) is a chronic inflammatory disease characterised by tissue inflammation and destruction of the associated alveolar bone. It is caused by the colonisation of the bacterial plaque biofilm and the resultant host immune responses in the surrounding periodontal tissues. The pro-inflammatory cytokine IL-17, and IL-17 producing CD4+ T cells (also called Th17 cells) have been shown to play an important role in many inflammatory diseases. There is increasing evidence of the presence of IL-17 and Th17 cells in human PD lesions and this may be associated with disease severity. Moreover, several animal studies indicate the potential role of IL-17 and Th17 cells in gingival inflammation and the resultant bone destruction in PD. Here we review recent findings regarding the presence, function and regulation of IL-17 and Th17 cells in PD, and we highlight potential areas of future research interest.

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“…To ascertain responder cell activation, co-cultured cells were surface immunostained and analyzed by flow cytometry gating on a CD3 − and a non-apoptotic monocyte size/density profile [42]. CD40 expression was measured as a sensitive indicator of monocyte activation [43]. We observed significant CD40 upregulation on monocytes co-cultured with DR3 activated CD161 + T cells, but only marginal change in CD40 levels on monocytes co-cultured with similarly activated CD161 − T cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

CD161 defines effector T cells that express light and respond to TL1A-DR3 signaling

Cohavy¹,

Shih²,

Doherty³

et al. 2011

European Journal of Microbiology and Immunology

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Expression of NK cell markers identifies pro-inflammatory T cell subsets in the liver and intestinal immune compartments. Specifically, CD161 is expressed on Th17 cells which play an important role in the regulation of mucosal inflammation. In this study, we characterized human peripheral blood CD161+ T cells as an effector population partially resembling a gut T cell phenotype. CD161+ CD4+ T cells express the gut-associated TNF family member, LIGHT, and respond to crosslinking of DR3, a receptor to another gut-associated cytokine, TL1A. Robust IFN-γ production in response to DR3 signaling correlated with enhanced expression of surface DR3 on CD161+ T cells and co-stimulation with IL12 and IL18. CD161+ T cell effector function was directly demonstrated by activation of responder monocytes in co-culture leading to CD40 upregulation and CD14 downregulation. CD161+ T cells reciprocally responded to activated monocytes, inducing expression of activation marker, CD69, and production of IL2 and IFN-γ, further demonstrating effective CD161+ T cell cross-talk with monocytes. Finally, CD161 defined a subset of T cells that co-express CD56, a second NK marker. Our findings implicate human CD161+ T cells in gut-associated signaling mechanisms, and suggest a monocyte mediated effector function in mucosal inflammation.

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Monocyte Activation by Porphyromonas gingivalis LPS in Aggressive Periodontitis with the Use of Whole-blood Cultures

Cited by 18 publications

References 32 publications

Hyper‐reactive mononuclear cells and neutrophils in chronic periodontitis

Hyper‐reactive mononuclear cells and neutrophils in chronic periodontitis

The presence, function and regulation of IL‐17 and Th17 cells in periodontitis

CD161 defines effector T cells that express light and respond to TL1A-DR3 signaling

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