IL-23-producing CD68+ macrophage-like cells predominate within an IL-17-polarized infiltrate in chronic periodontitis lesions

Allam, Jean‐Pierre; Duan, Yong‐Gang; Heinemann, Friedhelm; Winter, Jochen; Götz, Werner; Deschner, James; Wenghoefer, Matthias; Bieber, Thomas; Jepsen, Søren; Novak, Natalija

doi:10.1111/j.1600-051x.2011.01752.x

Cited by 77 publications

(77 citation statements)

References 35 publications

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“…Similarly, the TLR4 agonist, LPS, induced IL-23 expression in peritoneal macrophages via TLR4 activation [286]. Finally, HMGB1-TLR4 signaling also increased myeloid IL-23 expression and subsequent T H 17 production/mobilization after myocardial ischemia-reperfusion [287], periodontitis [288], or neonatal hypoxia-ischemia [270], although this issues remains to be fully studied after TBI. Given the temporal delay between TBI and adaptive immune responses, blocking T H polarization, secondary to DAMP-induced macrophage activation, may provide a feasible approach to limit long-term progressive injury.…”

Section: Translational Implicationsmentioning

confidence: 99%

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Braun

Vaibhav

Saad

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.

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Section: Translational Implicationsmentioning

confidence: 99%

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Braun

Vaibhav

Saad

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…3C). Therefore, periodontitis is a manifestation of LAD-I due, in part, to its particular mucosal environment, where the presence of IL-23–inducing bacteria [44, 46] can act as the initial stimulus to unleash the dysregulated IL-23–IL-17 axis (Fig. 2).…”

Section: Bacteria Are Required To Unleash the Disinhibited Il-23–imentioning

confidence: 99%

Role of bacteria in leukocyte adhesion deficiency-associated periodontitis

Hajishengallis

Moutsopoulos

2016

Microbial Pathogenesis

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Leukocyte adhesion deficiency Type I (LAD-I)–associated periodontitis is an aggressive form of inflammatory bone loss that has been historically attributed to lack of neutrophil surveillance of the periodontal infection. However, this form of periodontitis has proven unresponsive to antibiotics and/or mechanical removal of the tooth-associated biofilm. Recent studies in LAD-I patients and relevant animal models have shown that the fundamental cause of LAD-I periodontitis involves dysregulation of a granulopoietic cytokine cascade. This cascade includes interleukin IL-23 (IL-23) and IL-17 that drive inflammatory bone loss in LAD-I patients and animal models and, moreover, foster a nutritionally favorable environment for bacterial growth and development of a compositionally unique microbiome. Although the lack of neutrophil surveillance in the periodontal pockets might be expected to lead to uncontrolled bacterial invasion of the underlying connective tissue, microbiological analyses of gingival biopsies from LAD-I patients did not reveal tissue-invasive infection. However, bacterial lipopolysaccharide was shown to translocate into the lesions of LAD-I periodontitis. It is concluded that the bacteria serve as initial triggers for local immunopathology through translocation of bacterial products into the underlying tissues where they unleash the dysregulated IL-23–IL-17 axis. Subsequently, the IL-23/IL-17 inflammatory response sustains and shapes a unique local microbiome which, in turn, can further exacerbate inflammation and bone loss in the susceptible host.

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“…DCs in the immature stage are capable of capturing microbes and their antigens, which induces phenotypic and functional changes and culminates in the transition to mature DCs (Banchereau et al, 2000;Cutler and Jotwani, 2004). Mature DCs are involved in the production of pro-inflammatory cytokines and a polarized pattern of Th1/Th2/Th17 response in periodontal disease (Cutler and Jotwani, 2004;Allam et al, 2011). It could be observed that a differentiation of LPS-stimulated DCs in the presence of nicotine induced lower levels of pro-inflammatory cytokines (Yanagita et al, 2012a,b) and altered Th1 immunity (Yanagita et al, 2012a,b).…”

Section: Discussionmentioning

confidence: 99%

“…Mature DCs are involved in the production of inflammatory cytokines and in the polarized pattern of Th1/Th2/Th17 responses in periodontal disease (Cutler and Jotwani, 2004;Allam et al, 2011). Moreover, DCs stimulate naive T cells to differentiate to effector T-cell subsets that may be actively involved in the immunopathogenesis of periodontal diseases (Cutler and Jotwani, 2004;Yanagita et al, 2012a,b).…”

Section: Introductionmentioning

confidence: 91%

Effect of smoking on immunity in human chronic periodontitis

et al. 2014

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IL-23-producing CD68+ macrophage-like cells predominate within an IL-17-polarized infiltrate in chronic periodontitis lesions

Abstract: In view of these data, a picture emerges that IL-17-producing cells in CP could be in part directed by CD68(+) Mo-like cells, which produce IL-23p19 upon TLR4 activation by Pg.

Cited by 77 publications

References 35 publications

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Role of bacteria in leukocyte adhesion deficiency-associated periodontitis

Effect of smoking on immunity in human chronic periodontitis

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