Increased leukotriene concentration× in submandibular glands from rats with experimental periodontitis

Busch, Lucila; Miozza, Valeria; Sterin‐Borda, Leonor; Borda, Enri

doi:10.1007/s00011-009-0008-8

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…Salivary glands are key organs in the regulation of hydric, mineral, and immunologic balance of the oral environment [31]. Besides its mechanic cleansing effect, saliva also exerts a role in mucosal host defense thanks to the presence of secretory immunoglobulin and many antimicrobial proteins.…”

Section: Discussionmentioning

confidence: 99%

The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

Terrizzi

Conti

Martínez

et al. 2018

Mediators of Inflammation

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The exposition to hypoxia is a stressful stimulus, and the organism develops acclimation mechanisms to ensure homeostasis, but if this fails, it leads to the development of pathological processes. Considering the large number of people under hypoxic conditions, it is of utmost importance to study the mechanisms implicated in hypoxic acclimation in oral tissues and the possible alteration of some important inflammatory markers that regulate salivary and periodontal function. It is the aim of the present study to analyze submandibular (SMG) and periodontal status of animals chronically exposed to continuous (CCH) or intermittent (CIH) hypoxia in order to elucidate the underlying molecular mechanisms that may lead to hypoxic acclimation. Adult Wistar rats were exposed to CCH or CIH simulating 4200 meters of altitude during 90 days. Salivary secretion was decreased in animals exposed to hypoxia, being lower in CIH, together with increased prostaglandin E2 (PGE2) content, TBARS concentration, and the presence of apoptotic nuclei and irregular secretion granules in SMG. AQP-5 mRNA levels decreased in both hypoxic groups. Only the CCH group showed higher HIF-1α staining, while CIH alone exhibited interradicular bone loss and increased concentration of the bone resorption marker CTX-I. In summary, animals exposed to CIH show a worse salivary secretion rate, which related with higher levels of PGE2, suggesting a negative role of this inflammatory mediator during hypoxia acclimation. We link the weak immunorreactivity of HIF-1α in CIH with improper hypoxia acclimation, which is necessary to sustaining SMG physiology under this environmental condition. The alveolar bone loss observed in CIH rats could be due mainly to a direct effect of PGE2, as suggested by its higher content in gingival tissue, but also to the indirect effect of hyposalivation. This study may eventually contribute to finding therapeutics to treat the decreased salivary flow, improving in that way oral health.

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Section: Discussionmentioning

confidence: 99%

The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

Terrizzi

Conti

Martínez

et al. 2018

Mediators of Inflammation

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“…Obesity, a chronic inflammatory condition, is becoming a major health issue worldwide and is closely associated with metabolic disorders such as diabetes, coronary heart disease and fatty liver disease [1]. Non-alcoholic fatty liver disease (NAFLD) is one of the most common forms of chronic liver disease and ranges from pure fatty liver to the more severe nonalcoholic steatohepatitis and cirrhosis, with build-up in liver cells of excess neutral lipids, mainly triglycerides, not due to alcohol consumption.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Soluble Epoxide Hydrolase Attenuates High-Fat-Diet–Induced Hepatic Steatosis by Reduced Systemic Inflammatory Status in Mice

et al. 2012

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Non-alcoholic fatty liver disease is associated with obesity and considered an inflammatory disease. Soluble epoxide hydrolase (sEH) is a major enzyme hydrolyzing epoxyeicosatrienoic acids and attenuates their cardiovascular protective and anti-inflammatory effects. We examined whether sEH inhibition can protect against high-fat (HF)-diet–induced fatty liver in mice and the underlying mechanism. Compared with wild-type littermates, sEH-null mice showed lower diet-induced lipid accumulation in liver, as seen by Oil-red O staining and triglycerides levels. We studied the effect of sEH inhibition on diet-induced fatty liver by feeding C57BL/6 mice an HF diet for 8 weeks (short-term) or 16 weeks (long-term) and administering t-AUCB, a selective sEH inhibitor. sEH inhibition had no effect on the HF-diet–increased body and adipose tissue weight or impaired glucose tolerance but alleviated the diet-induced hepatic steatosis. Adenovirus-mediated overexpression of sEH in liver increased the level of triglycerides in liver and the hepatic inflammatory response. Surprisingly, the induced expression of sEH in liver occurred only with the long-term but not short-term HF diet, which suggests a secondary effect of HF diet on regulating sEH expression. Furthermore, sEH inhibition attenuated the HF-diet–induced increase in plasma levels of proinflammatory cytokines and their mRNA upregulation in adipose tissue, which was accompanied by increased macrophage infiltration. Therefore, sEH inhibition could alleviate HF-diet–induced hepatic steatosis, which might involve its anti-inflammatory effect in adipose tissue and direct inhibition in liver. sEH may be a therapeutic target for HF-diet–induced hepatic steatosis in inhibiting systemic inflammation.

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“…Thus, fibroblasts are known to participate in the histopathology changes associated with periodontitis (Schroeder and Page, 1972), and the inflammatory reaction observed during the course of experimental periodontitis could be the result of the large amounts of PGE 2 produced by gingival fibroblasts in response to sympathetic stimulation. Moreover, increase in sympathetic activity in experimental periodontitis has been described (Busch et al, 2009). The fact that gingival fibroblasts functionally express the CD40 receptor, point to the role of CD40L‐expressing cells in playing an immunopathogenic function in periodontitis.…”

Section: Discussionmentioning

confidence: 99%

β‐Adrenergic‐induced CD40 overexpression on gingival fibroblasts: Role of PGE₂

Furlan

Sterin‐Borda

Borda

2010

Cell Biology International

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CD40, a member of the tumour necrosis factor-alpha receptor family, is constitutively expressed by cells of haematopoietic and non-haematopoietic origin, including fibroblasts. Signalling through this receptor molecule regulates inflammatory mediator secretion by many cell types. The work has been performed in healthy subjects and the authors studied, by cellular culture, flow cytometric analysis and ELISA assay, the expression of CD40 and PGE2 (prostaglandin E2) generation on gingival fibroblasts stimulated by beta-AR (beta-adrenoceptor) agonists. Herein, the authors demonstrate that beta-AR subtype activation via their own specific agonists markedly increased CD40 expression on human gingival fibroblasts. This effect was prevented by beta-AR subtype-specific antagonists. In addition, gingival fibroblast beta-AR stimulation resulted in an increase in PGE2 generation. The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Our work has revealed an endogenous beta-AR mediator network involving gingival fibroblasts.

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Increased leukotriene concentration× in submandibular glands from rats with experimental periodontitis

Abstract: In submandibular glands from rats with periodontitis, the increment in mucin release and cysteinyl-leukotrienes production are related events and both are associated with the sympathetic system.

Cited by 8 publications

References 33 publications

The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

Inhibition of Soluble Epoxide Hydrolase Attenuates High-Fat-Diet–Induced Hepatic Steatosis by Reduced Systemic Inflammatory Status in Mice

β‐Adrenergic‐induced CD40 overexpression on gingival fibroblasts: Role of PGE₂

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Increased leukotriene concentration× in submandibular glands from rats with experimental periodontitis

Abstract: In submandibular glands from rats with periodontitis, the increment in mucin release and cysteinyl-leukotrienes production are related events and both are associated with the sympathetic system.

Cited by 8 publications

References 33 publications

The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

Inhibition of Soluble Epoxide Hydrolase Attenuates High-Fat-Diet–Induced Hepatic Steatosis by Reduced Systemic Inflammatory Status in Mice

β‐Adrenergic‐induced CD40 overexpression on gingival fibroblasts: Role of PGE2

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β‐Adrenergic‐induced CD40 overexpression on gingival fibroblasts: Role of PGE₂