Dataset Information

Mechanism and role of nitric oxide signaling in periodontitis.

ABSTRACT: The present study investigated the role of the nitric oxide (NO) signaling pathway in the progression of periodontal disease, and explored the related genetic mechanisms. An experimental model of periodontitis was established in Sprague-Dawley rats, then they were divided into normal control, and 2, 4 and 6 weeks post-surgery groups. NO content was determined in the saliva of rats from each group by the Griess reagent method. Pathological changes of the periodontal tissue sections were evaluated with hematoxylin-eosin staining. The periodontal tissue sections were also evaluated by immunohistochemistry to detect the expression of inducible nitric oxide synthase 2 (iNOS2). Significant differences were detected in the iNOS2 expression of the periodontal tissue based on immunohistochemistry. There was a significant time-dependent increase in NO serum levels post-surgery. Two single nucleotide polymorphisms (SNP), rs2297518 in the iNOS gene and rs841 of the GTP cyclohydrolase I gene, were identified to be closely related to alveolar bone resorption, which is associated with the SNP rs1049255 of the cytochrome b-245 ? chain gene. The present findings demonstrated that iNOS2 values increased and NO levels increased with the progression of periodontitis. These results are in agreement with the previous literature. It was hypothesized that NO has a role in the occurrence and development of periodontal disease by regulating the action of certain cytokines.

SUBMITTER: Wang Y

PROVIDER: S-EPMC6796435 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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Mechanism and role of nitric oxide signaling in periodontitis.

Wang Yan Y Huang Xiangdao X He Fuming F

Experimental and therapeutic medicine 20190925 5

The present study investigated the role of the nitric oxide (NO) signaling pathway in the progression of periodontal disease, and explored the related genetic mechanisms. An experimental model of periodontitis was established in Sprague-Dawley rats, then they were divided into normal control, and 2, 4 and 6 weeks post-surgery groups. NO content was determined in the saliva of rats from each group by the Griess reagent method. Pathological changes of the periodontal tissue sections were evaluated ...[more]

PMID: 31641379

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Project description:Tuberculosis is a current major world-health problem, exacerbated by the causative pathogen, Mycobacterium tuberculosis (Mtb), becoming increasingly resistant to conventional antibiotic treatment. Mtb is able to counteract the bactericidal mechanisms of leukocytes to survive intracellularly and develop a niche permissive for proliferation and dissemination. Understanding of the pathogenesis of mycobacterial infections such as tuberculosis (TB) remains limited, especially for early infection and for reactivation of latent infection. Signaling via hypoxia inducible factor α (HIF-α) transcription factors has previously been implicated in leukocyte activation and host defence. We have previously shown that hypoxic signaling via stabilization of Hif-1α prolongs the functionality of leukocytes in the innate immune response to injury. We sought to manipulate Hif-α signaling in a well-established Mycobacterium marinum (Mm) zebrafish model of TB to investigate effects on the host's ability to combat mycobacterial infection. Stabilization of host Hif-1α, both pharmacologically and genetically, at early stages of Mm infection was able to reduce the bacterial burden of infected larvae. Increasing Hif-1α signaling enhanced levels of reactive nitrogen species (RNS) in neutrophils prior to infection and was able to reduce larval mycobacterial burden. Conversely, decreasing Hif-2α signaling enhanced RNS levels and reduced bacterial burden, demonstrating that Hif-1α and Hif-2α have opposing effects on host susceptibility to mycobacterial infection. The antimicrobial effect of Hif-1α stabilization, and Hif-2α reduction, were demonstrated to be dependent on inducible nitric oxide synthase (iNOS) signaling at early stages of infection. Our findings indicate that induction of leukocyte iNOS by stabilizing Hif-1α, or reducing Hif-2α, aids the host during early stages of Mm infection. Stabilization of Hif-1α therefore represents a potential target for therapeutic intervention against tuberculosis.

Dataset Information

Mechanism and role of nitric oxide signaling in periodontitis.

Publications

Mechanism and role of nitric oxide signaling in periodontitis.

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