Characterization of the human immune cell network at the gingival barrier

Dutzan, Nicolás; Konkel, Joanne E.; Greenwell-Wild, Teresa; Moutsopoulos, Niki M.

doi:10.1038/mi.2015.136

Cited by 239 publications

(311 citation statements)

References 49 publications

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“…For details on tape-striping experiments, see Supplemental Experimental Procedures. For humans, gingival biopsies were processed as previously described (Dutzan et al., 2016b). …”

Section: Methodsmentioning

confidence: 99%

On-going Mechanical Damage from Mastication Drives Homeostatic Th17 Cell Responses at the Oral Barrier

et al. 2017

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SummaryImmuno-surveillance networks operating at barrier sites are tuned by local tissue cues to ensure effective immunity. Site-specific commensal bacteria provide key signals ensuring host defense in the skin and gut. However, how the oral microbiome and tissue-specific signals balance immunity and regulation at the gingiva, a key oral barrier, remains minimally explored. In contrast to the skin and gut, we demonstrate that gingiva-resident T helper 17 (Th17) cells developed via a commensal colonization-independent mechanism. Accumulation of Th17 cells at the gingiva was driven in response to the physiological barrier damage that occurs during mastication. Physiological mechanical damage, via induction of interleukin 6 (IL-6) from epithelial cells, tailored effector T cell function, promoting increases in gingival Th17 cell numbers. These data highlight that diverse tissue-specific mechanisms govern education of Th17 cell responses and demonstrate that mechanical damage helps define the immune tone of this important oral barrier.

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“…For details on tape-striping experiments, see Supplemental Experimental Procedures. For humans, gingival biopsies were processed as previously described (Dutzan et al., 2016b). …”

Section: Methodsmentioning

confidence: 99%

On-going Mechanical Damage from Mastication Drives Homeostatic Th17 Cell Responses at the Oral Barrier

et al. 2017

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“…However, in the buccal tissues, CD4 + helper T cells are the dominant cell populations followed by CD8 + T cells and a small percentage of γδ T cells (121). We have already shown that γδ T cells are abundant in the oral cavity and play a protective role against oral candidiasis, which is one of the opportunistic fungal diseases associated with HIV infection (122).…”

Section: Immuno-phenotypes Of the Oral Cavitymentioning

confidence: 99%

“…Although they are found in abundance in the oral cavity of healthy individuals, periodontal disease results in a significant increase in CD15 + CD16 + neutrophils in the oral cavity (121). They are required to ensure homeostatic conditions in the oral cavity.…”

Section: Immuno-phenotypes Of the Oral Cavitymentioning

confidence: 99%

HIV Infection and Compromised Mucosal Immunity: Oral Manifestations and Systemic Inflammation

Heron

Elahi

2017

Front. Immunol.

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Mucosal surfaces account for the vast majority of HIV transmission. In adults, HIV transmission occurs mainly by vaginal and rectal routes but rarely via oral route. By contrast, pediatric HIV infections could be as the result of oral route by breastfeeding. As such mucosal surfaces play a crucial role in HIV acquisition, and spread of the virus depends on its ability to cross a mucosal barrier. HIV selectively infects, depletes, and/or dysregulates multiple arms of the human immune system particularly at the mucosal sites and causes substantial irreversible damage to the mucosal barriers. This leads to microbial products translocation and subsequently hyper-immune activation. Although introduction of antiretroviral therapy (ART) has led to significant reduction in morbidity and mortality of HIV-infected patients, viral replication persists. As a result, antigen presence and immune activation are linked to “inflammaging” that attributes to a pro-inflammatory environment and the accelerated aging process in HIV patients. HIV infection is also associated with the prevalence of oral mucosal infections and dysregulation of oral microbiota, both of which may compromise the oral mucosal immunity of HIV-infected individuals. In addition, impaired oral immunity in HIV infection may predispose the patients to periodontal diseases that are associated with systemic inflammation and increased risk of cardiovascular diseases. The purpose of this review is to examine existing evidence regarding the role of innate and cellular components of the oral cavity in HIV infection and how HIV infection may drive systemic hyper-immune activation in these patients. We will also discuss current knowledge on HIV oral transmission, HIV immunosenescence in relation to the oral mucosal alterations during the course of HIV infection and periodontal disease. Finally, we discuss oral manifestations associated with HIV infection and how HIV infection and ART influence the oral microbiome. Therefore, unraveling how HIV compromises the integrity of the oral mucosal tissues and innate immune components of the oral cavity and its association with induction of chronic inflammation are critical for the development of effective preventive interventions and therapeutic strategies.

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“…Regardless of the exact mechanisms, ample clinical evidence indicates that neutrophils mediate a substantial part of periodontal tissue destruction [125,130]. Moreover, the local neutrophil numbers correlate positively with the severity of chronic periodontitis [131,132]. This section focuses on the regulation of neutrophil recruitment to the periodontium and conditions that can result in supernumerary neutrophils leading to inflammatory bone loss in periodontitis.…”

Section: Endogenous Regulators Of Neutrophil Recruitment To the Pementioning

confidence: 99%

Immune and regulatory functions of neutrophils in inflammatory bone loss

Hajishengallis

Moutsopoulos

Hajishengallis

et al. 2016

Seminars in Immunology

114

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Although historically viewed as merely anti-microbial effectors in acute infection or injury, neutrophils are now appreciated to be functionally versatile with critical roles also in chronic inflammation. Periodontitis, a chronic inflammatory disease that destroys the tooth-supporting gums and bone, is particularly affected by alterations in neutrophil numbers or function, as revealed by observations in monogenic disorders and relevant mouse models. Besides being a significant debilitating disease and health burden in its own right, periodontitis is thus an attractive model to dissect uncharted neutrophil-associated (patho)physiological pathways. Here, we summarize recent evidence that neutrophils can contribute to inflammatory bone loss not only through the typical bystander injury dogma but intriguingly also through their absence from the affected tissue, where they normally perform important immunomodulatory functions. Moreover, we discuss recent advances in the interactions of neutrophils with the vascular endothelium and – upon extravasation – with bacteria, and how the dysregulation of these interactions leads to inflammatory tissue damage. Overall, neutrophils have both protective and destructive roles in periodontitis, as they are involved in both the maintenance of periodontal tissue homeostasis and the induction of inflammatory bone loss. This highlights the importance of developing approaches that promote or sustain a fine balance between homeostatic immunity and inflammatory pathology.

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Characterization of the human immune cell network at the gingival barrier

Cited by 239 publications

References 49 publications

On-going Mechanical Damage from Mastication Drives Homeostatic Th17 Cell Responses at the Oral Barrier

On-going Mechanical Damage from Mastication Drives Homeostatic Th17 Cell Responses at the Oral Barrier

HIV Infection and Compromised Mucosal Immunity: Oral Manifestations and Systemic Inflammation

Immune and regulatory functions of neutrophils in inflammatory bone loss

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