Activation of the neutrophil respiratory burst by plasma from periodontitis patients is mediated by pro-inflammatory cytokines

Dias, Irundika H.K.; Matthews, J. B.; Chapple, Iain; Wright, Helen J.; Dunston, Christopher R.; Griffiths, Helen R.

doi:10.1111/j.1600-051x.2010.01628.x

Cited by 69 publications

(74 citation statements)

References 36 publications

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“…IL-8 in immune-related cells, such as endothelial cells, macrophages, mast cells, and keratinocytes (K€ ohidai and Csaba, 1998), can also induce a series of physiological reactions required for phagocytosis and migration, such as increasing the intracellular concentration of Ca 21 (Mahali et al, 2011), exocytosis (Yasuda et al, 2012), and respiratory bursts (Dias et al, 2011). Previous studies indicated that nickel can trigger activation of intracellular reactive oxygen species (ROS) (Oller, 2002;Stejskal et al, 2006;Freitas et al, 2010).…”

Section: Introductionmentioning

confidence: 97%

Involvement of L‐type Ca²⁺ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Lin

Chung

Wong

et al. 2014

Environmental Toxicology

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The metal nickel (Ni(2+)) is found everywhere in our daily lives, including coins, costume jewelry, and even nuts and chocolates. Nickel poisoning can cause inflammatory reactions, respiratory diseases, and allergic contact dermatitis. To clarify the mechanism by which nickel induces mediators of inflammation, we used the human acute monocytic leukemia THP-1 cell line as a model. Interleukin (IL)-8 promoter activity as well as gene expression were tested by luciferase assay and real-time polymerase chain reaction. The underlying mechanisms of nickel-induced IL-8 were investigated. We found that nickel induced IL-8 gene expression via the L-type Ca(2+) channel, Toll-like receptor-4 (TRL-4) and nuclear factor NF-κB signal transduction pathways. Nickel activated NF-κB expression through extracellular signal-regulated kinase 1/2 phosphorylation and then increased IL-8 expression. Thus, the L-type Ca(2+) channel and TRL-4 play important roles in nickel-induced inflammatory gene expressions.

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Section: Introductionmentioning

confidence: 97%

Involvement of L‐type Ca²⁺ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Lin

Chung

Wong

et al. 2014

Environmental Toxicology

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“…Phagocytosis and respiratory burst activity of leukocytes can also be substantially augmented by various proinflammatory cytokines such as IL-8, IL-1β, TNF-α, IL-6 etc. (Reato et al 2004;Dias et al 2011;Hellberg et al 2011). No data are available on the effects of sulbactam on cytokine activity; however, studies indicated that amoxicillin treatment up-regulates the expression of IL-8, TNF-α, IL-1β, IL-6 and IL-10 in response to many bacterial infections (Reato et al 1999;Melhus and Ryan, 2004).…”

Section: Discussionmentioning

confidence: 99%

Dynamics of milk leukocytes in response to intramammary infusion of amoxicillin plus sulbactam during bovine subclinical mastitis

De¹,

Mukherjee²

2012

Vet. Med. - Czech

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ABSTRACT:The therapeutic potential of amoxicillin plus sulbactam and its effect on dynamics of milk leukocytes in bovine sub clinical mastitis were investigated in this study. Therapeutic efficacy was measured by somatic cell count and total bacterial count of the milk, whereas, the dynamics of milk leukocytes were assessed by measuring phagocytosis, hydrogen peroxide production, myeloperoxidase and lactoperoxidase enzyme levels in the milk leukocytes. Forty-five crossbred cows were randomly divided into three equal groups. Group I consisting of 15 cows served as healthy control, whereas 30 cows (sub clinical mastitis) were randomly divided into Groups II and III on the basis of positive reactions in the California Mastitis Test. Group II cows received 300mg of amoxicillin plus sulbactam twice daily for three days and Group III received sterile 5 ml phosphate buffer saline (pH 7.4) for three days. Both treatments were administered via the intramammary route. Observations were made up to 15 days after initiation of treatment. The results revealed a pronounced drop in somatic cell count and total bacterial count, whereas significant (P < 0.05) enhancement of phagocytic activity (42.20%), hydrogen peroxide production (29.46%), myeloperoxidase (49.27%) and lactoperoxidase (147.10%) enzyme levels in the milk leukocytes in Group II cows during post treatment periods were observed. Such changes were statistically non-significant in Group III cows. The results of the present study indicate that intramammary use of amoxicillin plus sulbactam augments the bactericidal function of milk leukocytes during bovine sub clinical mastitis and demonstrate the strong therapeutic potential against bovine subclinical mastitis.

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“…Neutrophils in AgP are in a hyperactive, primed state. 16 This hyperactivity may be attributed to circulating factors 15 or genetic make-up of individual or environmental effects. 32 These hyper responsive neutrophils may explain the difference in ROS production between patients with AgP or CP, observed in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Neutrophils from patients with AgP are hyperactive and primed and appear to release enhanced levels of oxygen radicals, inflammatory mediators such as cytokines and matrix-degrading enzymes. 14,15 This hyperactivity and reactivity of neutrophils destroys the adjacent host tissues and contributes to the destructive changes observed in inflammatory periodontitis. 16 An excess of ROS can cause oxidative stress and damage to critical biomolecules resulting in deleterious biological effects.…”

Section: Introductionmentioning

confidence: 99%

Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis

et al. 2016

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Objectives: Free radicals play an important role in the onset and progression of many diseases. The aim of this study was to investigate the contribution of oxidative stress in the pathology of aggressive (AgP) and chronic (CP) periodontitis and its relation with the clinical periodontal status. Methods: Eighty subjects were divided into two groups: 20 patients with AgP and 20 patients with CP with their 20 corresponding matched controls, based on clinical attachment loss (CAL), probing pocket depth (PPD), and bleeding on probing (BOP). Saliva reactive oxygen species (ROS), lipid peroxidation, and nonenzymatic antioxidant defences were measured by luminol-dependent chemiluminescence assay, as thiobarbituric acid-reactive substances (TBARs) and total radical-trapping antioxidant potential (TRAP), respectively. Pearson's correlation and multivariate analysis were used to determine the relationship between ROS and TBARs and the clinical parameters. Results: ROS and TBARs were increased in AgP while TRAP was decreased, comparing with CP. In AgP, a strong and positive correlation was observed between ROS and TBARs and they were closely associated with CAL and PPD. Discussion: In AgP, but not in CP, oxidative stress is a high contributor to periodontal pathology and it is closely associated with the clinical periodontal status.

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Activation of the neutrophil respiratory burst by plasma from periodontitis patients is mediated by pro-inflammatory cytokines

Abstract: This study demonstrates that plasma cytokines may have a role in inducing the hyperactive (IL-8, GM-CSF, IFN-α) and hyper-reactive (IFN-α) neutrophil phenotype seen in periodontitis patients.

Cited by 69 publications

References 36 publications

Involvement of L‐type Ca²⁺ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Involvement of L‐type Ca²⁺ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Dynamics of milk leukocytes in response to intramammary infusion of amoxicillin plus sulbactam during bovine subclinical mastitis

Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis

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Activation of the neutrophil respiratory burst by plasma from periodontitis patients is mediated by pro-inflammatory cytokines

Abstract: This study demonstrates that plasma cytokines may have a role in inducing the hyperactive (IL-8, GM-CSF, IFN-α) and hyper-reactive (IFN-α) neutrophil phenotype seen in periodontitis patients.

Cited by 69 publications

References 36 publications

Involvement of L‐type Ca2+ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Involvement of L‐type Ca2+ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Dynamics of milk leukocytes in response to intramammary infusion of amoxicillin plus sulbactam during bovine subclinical mastitis

Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis

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Involvement of L‐type Ca²⁺ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression

Involvement of L‐type Ca²⁺ channel and toll‐like receptor‐4 in nickel‐induced interleukin‐8 gene expression