Decreased phagocytic function in neutrophils and monocytes from peripheral blood in periodontal disease

Carneiro, Valéria M. A.; Bezerra, Ana Cristina Barreto; Guimarães, Maria do Carmo Machado; Muniz‐Junqueira, Maria Imaculada

doi:10.1590/s1678-77572012000500002

Cited by 29 publications

(18 citation statements)

References 29 publications

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“…Interestingly, no difference was observed in NET production between young or old periodontitis patients and their age-matched healthy controls. Whether reduced NET generation only impacts upon the ability to combat periodontal infections in older adults, in which other aspects of neutrophil function are also compromised (Carneiro et al, 2012), remains a possibility. Another plausible explanation for the lack of difference in NET production between periodontitis patients and age-matched controls may relate to the stimulus employed.…”

Section: Discussionmentioning

confidence: 99%

Impaired neutrophil extracellular trap formation: a novel defect in the innate immune system of aged individuals

et al. 2014

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Neutrophil extracellular traps (NETs) are a recently discovered addition to the defensive armamentarium of neutrophils, assisting in the immune response against rapidly dividing bacteria. Although older adults are more susceptible to such infections, no study has examined whether aging in humans influences NET formation. We report that TNF-α-primed neutrophils generate significantly more NETs than unprimed neutrophils and that lipopolysaccharide (LPS)- and interleukin-8 (IL-8)-induced NET formation exhibits a significant age-related decline. NET formation requires generation of reactive oxygen species (ROS), and this was also reduced in neutrophils from older donors identifying a mechanism for reduced NET formation. Expression of IL-8 receptors (CXCR1 and CXCR2) and the LPS receptor TLR4 was similar on neutrophils from young and old subjects, and neutrophils challenged with phorbol-12-myristate-13-acetate (PMA) showed no age-associated differences in ROS or NET production. Taken together, these data suggest a defect in proximal signalling underlies the age-related decline in NET and ROS generation. TNF-α priming involves signalling through p38 MAP kinase, but activation kinetics were comparable in neutrophils from young and old donors. In a clinical setting, we assessed the capacity of neutrophils from young and older patients with chronic periodontitis to generate NETs in response to PMA and hypochlorous acid (HOCL). Neutrophil extracellular trap generation to HOCL, but not PMA, was lower in older periodontitis patients but not in comparison with age-matched controls. Impaired NET formation is thus a novel defect of innate immunity in older adults but does not appear to contribute to the increased incidence of periodontitis in older adults.

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Section: Discussionmentioning

confidence: 99%

Impaired neutrophil extracellular trap formation: a novel defect in the innate immune system of aged individuals

et al. 2014

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“…A similar pattern of neutrophil migration has been described in COPD where cells displayed poor migratory accuracy but with random movement in all directions at increased speed. 72 Recent publications have also described compromised neutrophil bacterial phagocytosis in periodontitis 86 (studies in COPD are less clear); enhanced neutrophil-derived ROS 87 , 88 and increased NET formation in both COPD and periodontitis, 89 , 90 all of which could contribute to the sustained inflammation that characterizes both the conditions. 34 , 53 The cause for such injurious cell behavior is unclear, and it is unknown whether neutrophil dysfunction precedes or is a consequence of disease.…”

Section: Mechanismsmentioning

confidence: 99%

Is periodontitis a comorbidity of COPD or can associations be explained by shared risk factors/behaviors?

Hobbins¹,

Chapple

Sapey³

et al. 2017

COPD

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COPD is recognized as having a series of comorbidities potentially related to common inflammatory processes. Periodontitis is one of the most common human inflammatory diseases and has previously been associated with COPD in numerous observational studies. As periodontitis and COPD are both chronic, progressive conditions characterized by neutrophilic inflammation with subsequent proteolytic destruction of connective tissue, it has been proposed that they share common pathophysiological processes. The mechanisms proposed to link COPD and periodontitis include mechanical aspiration of oral contents into the respiratory tree, overspill of locally produced inflammatory mediators into the systemic circulation or oral or lung-derived bacteremia activating an acute-phase response and also reactive oxygen species (ROS) and cytokine release by systemic neutrophils at distant sites. Studies of systemic neutrophils in COPD and chronic periodontitis describe altered cellular functions that would predispose to inflammation and tissue destruction both in the lung and in the mouth, again potentially connecting these conditions. However, COPD and periodontitis also share risk factors such as age, chronic tobacco smoke exposure, and social deprivation that are not always considered in observational and interventional studies. Furthermore, studies reporting associations have often utilized differing definitions of both COPD and periodontitis. This article reviews the current available evidence supporting the hypothesis that COPD and inflammatory periodontal disease (periodontitis) could be pathologically associated, including a review of shared inflammatory mechanisms. It highlights the potential limitations of previous studies, in particular, the lack of uniformly applied case definitions for both COPD and periodontitis and poor recognition of shared risk factors. Understanding associations between these conditions may inform why patients with COPD suffer such a burden of comorbid illness and new therapeutic strategies for both the diseases. However, further research is needed to clarify factors that may be directly causal as opposed to confounding relationships.

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“…‒ Similarly, failure to downregulate neutrophil transit resulting in increased neutrophil numbers or prolonged neutrophil exposure has been shown to increase alveolar bone loss . Furthermore, abnormalities in neutrophil activation and function, such as with decreased phagocytosis or increased superoxide production, was also found to be associated with this disease. Therefore, in health, neutrophil homeostasis is finely tuned in the oral cavity to prevent commensal dental plaque bacteria overgrowth without over responding to elicit tissue damage.…”

Section: Introductionmentioning

confidence: 99%

Toll‐like receptor‐2 and ‐4 responses regulate neutrophil infiltration into the junctional epithelium and significantly contribute to the composition of the oral microbiota

Chang

Liu

Hajjar

et al. 2019

Journal of Periodontology

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Background Oral gingival tissue, especially the junctional epithelium (JE), is constantly exposed to sub‐gingival plaque. A key component of gingival health is the regulation of the number of neutrophils that migrate into the gingival crevice to counteract its harmful effects. This report investigates the contribution of innate defense receptors, Toll‐like receptor (TLR)2, TLR4, and both (TLR2/4) to the maintenance of neutrophil homeostasis in the JE. Methods Bacterial composition was analyzed from whole oral swabs collected from 12‐ to 14‐week‐old TLR2, TLR4, TLR2/4 double knock‐out (KO) mice using a MiSeq platform targeting the V3‐V4 region of the 16S ribosomal RNA gene. Mandibles were histologically examined for quantification of neutrophils in the JE and bone loss. Lastly, total bacterial load was quantitated using quantitative real‐time PCR. Results Compared with wild‐type, all TLR KO mice displayed significantly increased recruitment of neutrophils (P = 0.0079) into the JE. In addition, TLR4 and TLR2/4 KO mice demonstrated a significant increase in the number of bacteria (P = 0.0022 and P = 0.0152, respectively). Lastly, comparative compositional analyses of the oral microbiome revealed that each KO strain harbored unique microbial communities that are distinct from each other but maintained similar levels of alveolar bone. Conclusions Neutrophil migration into healthy mouse JE does not require TLR2 or TLR4. However, a significant increase in the number of neutrophils as well as a significant change in the oral microbial composition in both TLR2 and TLR4 KO mice demonstrate that these TLRs contribute to the homeostatic relationship between bacteria and the host in healthy mice periodontal tissue.

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Decreased phagocytic function in neutrophils and monocytes from peripheral blood in periodontal disease

Cited by 29 publications

References 29 publications

Impaired neutrophil extracellular trap formation: a novel defect in the innate immune system of aged individuals

Impaired neutrophil extracellular trap formation: a novel defect in the innate immune system of aged individuals

Is periodontitis a comorbidity of COPD or can associations be explained by shared risk factors/behaviors?

Toll‐like receptor‐2 and ‐4 responses regulate neutrophil infiltration into the junctional epithelium and significantly contribute to the composition of the oral microbiota

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