Smoking effect on chemokines of the human chronic periodontitis

Souto, Giovanna Ribeiro; Queiroz-Junior, Celso Martins; Costa, Fernando Oliveira; Mesquita, Ricardo Alves

doi:10.1016/j.imbio.2014.03.014

Cited by 21 publications

(27 citation statements)

References 30 publications

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“…It is therefore important to take smoking into account when analyzing inflammatory markers in periodontitis. Increased levels of MCP-1 in serum and GCF have previously been observed in smokers with periodontitis compared to non-smoking periodontitis patients and healthy subjects [ 39 , 40 ] and Souto et al reported an altered chemokine expression in gingival tissue samples from smokers with chronic periodontitis compared to non-smoking patients [ 41 ]. There are no reports about smoking and effects of eotaxin serum- or gingival levels in individuals with periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Increased Eotaxin and MCP-1 Levels in Serum from Individuals with Periodontitis and in Human Gingival Fibroblasts Exposed to Pro-Inflammatory Cytokines

et al. 2015

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Periodontitis is a chronic inflammatory disease of tooth supporting tissues resulting in periodontal tissue destruction, which may ultimately lead to tooth loss. The disease is characterized by continuous leukocyte infiltration, likely mediated by local chemokine production but the pathogenic mechanisms are not fully elucidated. There are no reliable serologic biomarkers for the diagnosis of periodontitis, which is today based solely on the degree of local tissue destruction, and there is no available biological treatment tool. Prompted by the increasing interest in periodontitis and systemic inflammatory mediators we mapped serum cytokine and chemokine levels from periodontitis subjects and healthy controls. We used multivariate partial least squares (PLS) modeling and identified monocyte chemoattractant protein-1 (MCP-1) and eotaxin as clearly associated with periodontitis along with C-reactive protein (CRP), years of smoking and age, whereas the number of remaining teeth was associated with being healthy. Moreover, body mass index correlated significantly with serum MCP-1 and CRP, but not with eotaxin. We detected higher MCP-1 protein levels in inflamed gingival connective tissue compared to healthy but the eotaxin levels were undetectable. Primary human gingival fibroblasts displayed strongly increased expression of MCP-1 and eotaxin mRNA and protein when challenged with tumor necrosis factor-α (TNF-α and interleukin-1β (IL-1β), key mediators of periodontal inflammation. We also demonstrated that the upregulated chemokine expression was dependent on the NF-κΒ pathway. In summary, we identify higher levels of CRP, eotaxin and MCP-1 in serum of periodontitis patients. This, together with our finding that both CRP and MCP-1 correlates with BMI points towards an increased systemic inflammatory load in patients with periodontitis and high BMI. Targeting eotaxin and MCP-1 in periodontitis may result in reduced leukocyte infiltration and inflammation in periodontitis and maybe prevent tooth loss.

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Section: Discussionmentioning

confidence: 99%

Increased Eotaxin and MCP-1 Levels in Serum from Individuals with Periodontitis and in Human Gingival Fibroblasts Exposed to Pro-Inflammatory Cytokines

et al. 2015

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“…Our analysis of the serum chemokine levels in the ALA, AC, and E. dispar groups revealed several interesting aspects. First, the three groups had equivalently high levels of CCL2, but high serum levels of CCL2 had also been shown in other healthy control groups [ 45 ],[ 46 ]. Second, sex analyses revealed that the male AC subjects had significantly higher CCL2 levels than female AC.…”

Section: Discussionmentioning

confidence: 78%

Immune markers characteristic for asymptomatically infected and diseased Entamoeba histolytica individuals and their relation to sex

et al. 2014

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BackgroundThe protozoan parasite Entamoeba histolytica (E. histolytica) usually asymptomatically colonizes the human intestine. In the minority of the cases, the parasite evades from the gut and can induce severe symptoms like colitis or amebic liver abscess (ALA). Interestingly, ALA predominates in adult men despite a higher prevalence of the parasite in women. The present study aimed to identify characteristic serum markers in a unique cohort of clearly defined asymptomatically infected E. histolytica individuals in comparison to patients with an E. histolytica liver manifestation of both sex.MethodsThe following study groups were investigated: ALA patients (n = 38), healthy asymptomatic E. histolytica carriers (AC) (n = 44), and healthy E. dispar-infected controls (n = 24) out of an amebiasis endemic area. E. histolytica-specific immunoglobulin G (IgG) and the IgG subclasses against proteinaceous and non-proteinaceous amebic antigens were measured by ELISA. Serum cytokine and chemokine levels were investigated using a flow cytometry bead-based multiplex immunoassay.ResultsThe IgG results revealed that not only ALA patients, but also AC, developed high E. histolytica-specific titers of IgG and all IgG subclasses as well as IgA. IgG and IgG2 titers against the glycolipid E. histolytica lipophosphoglycan were highest in ALA patients. As in ALA patients, high cytokine levels of interleukin (IL-) 4 were detected in AC compared to E. dispar infected individuals, while IL-6 was exclusively elevated in ALA patients. IL-10 was lower in AC compared to ALA patients. Equal serum levels of CCL2 were found in all study groups but ALA patients showed decreased levels of CCL3. Sex dependent analysis of the data indicated significantly higher IgG and IgG1 titers in female AC compared to male AC. CCL2, the chemokine involved in immunopathology in the mouse model for the disease, was higher in male AC compared to female AC.ConclusionIn this study we characterize for the first time an asymptomatic carrier stage in amebiasis that is associated with a significant immune reaction and provide immunological markers that might give first hints towards an understanding of immune mechanisms underlying the control or development of invasive amebiasis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-014-0621-1) contains supplementary material, which is available to authorized users.

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“…Likewise, in vitro studies also revealed that cigarette smoke constituents induced or attenuated the production of the TNF-␣, IL-6, INF-␥, IL-12, and IL-23 cytokines by DCs (Vassallo et al, 2005Kroening et al, 2008;Mortaz et al, 2009). In addition, it was demonstrated decrease of CCL3 and CXCL8, and increase of CCL5 in smokers diagnosed with CP (Souto et al, 2014). Therefore, the present study sought to evaluate whether or not smoking provoked alterations in the production of cytokines in gingival tissue samples of individuals with CP.…”

Section: Discussionmentioning

confidence: 93%

“…In a prior analysis, results demonstrated that smoking decreased both the inflammatory infiltrate and dendritic cells (DCs) in samples of chronic gingivitis (Souto et al, 2011). In addition, prior analysis also demonstrated that smoking decreased CC chemokine ligand (CCL)3 and CXC chemokine ligand (CXCL)8, while CC chemokine ligand (CCL)5 was increased in samples of CP (Souto et al, 2014). Srinivas et al (2012) also identified a delayed neutrophil chemotaxis in smokers as compared to non-smokers on CP.…”

Section: Introductionmentioning

confidence: 99%