Literature DB >> 32763436

Immunomodulation Mediated by Azithromycin in Experimental Periapical Inflammation.

Ana Cristina Andrada1, Mariane Maffei Azuma2, Hisako Furusho3, Kimito Hirai4, Shuang Xu5, Robert R White6, Hajime Sasaki7.   

Abstract

INTRODUCTION: The purpose of the present study was to compare the immunomodulatory effect of azithromycin (AZM), ampicillin (AMP), amoxicillin (AMX), and clindamycin (CLI) in vitro and AZM on preexisting periapical lesions compared with AMP.
METHODS: The susceptibility of 4 common human endodontic pathogens (Parvimonas micra, Streptococcus intermedius, Prevotella intermedia, and Fusobacterium nucleatum) to AZM, AMP, AMX, and CLI was confirmed by agar disk diffusion assay. Preexisting periapical lesions in C57BL/6J mice were treated with AZM, AMP, or phosphate-buffered saline (PBS). Periapical bone healing and the pattern of inflammatory cell infiltration were evaluated after a 10-day treatment by micro-computed tomographic and histology, respectively. Besides, the effect of antibiotics in pathogen-stimulated nuclear factor kappa B activation and the production of interleukin 1 alpha and tumor necrosis factor alpha was assessed in vitro by luciferase assay and enzyme-linked immunosorbent assay.
RESULTS: All examined endodontic pathogens were susceptible to AZM, AMP, AMX, and CLI. AZM significantly attenuated periapical bone loss versus PBS. PBS resulted in widely diffused infiltration of mixed inflammatory cells. By contrast, AZM brought about localized infiltration of neutrophils and M2 macrophages and advanced fibrosis. Although the effect of AMP on bone was uncertain, inflammatory cell infiltration was considerably milder than PBS. However, most macrophages observed seemed to be M1 macrophages. AZM suppressed pathogen-stimulated nuclear factor kappa B activation and cytokine production, whereas AMP, AMX, and CLI reduced only cytokine production moderately.
CONCLUSIONS: This study showed that AZM led to the resolution of preexisting experimental periapical inflammation. Our data provide a perspective on host response in antibiotic selection for endodontic treatment. However, well-designed clinical trials are necessary to better elucidate the benefits of AZM as an adjunctive therapy for endodontic treatment when antibiotic therapy is recommended. Although both AZM and AMP were effective on preexisting periapical lesions, AZM led to advanced wound healing, probably depending on its immunomodulatory effect.
Copyright © 2020 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Ampicillin; azithromycin; endodontic infection; immunomodulation; periapical periodontitis

Year:  2020        PMID: 32763436      PMCID: PMC7862415          DOI: 10.1016/j.joen.2020.07.028

Source DB:  PubMed          Journal:  J Endod        ISSN: 0099-2399            Impact factor:   4.171


  25 in total

1.  Kinetics of bone-resorbing activity in developing periapical lesions.

Authors:  C Y Wang; P Stashenko
Journal:  J Dent Res       Date:  1991-10       Impact factor: 6.116

Review 2.  Apical periodontitis: a dynamic encounter between root canal infection and host response.

Authors:  P N Nair
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3.  Azithromycin protects mice against ischemic stroke injury by promoting macrophage transition towards M2 phenotype.

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4.  Azithromycin analogue CSY0073 attenuates lung inflammation induced by LPS challenge.

Authors:  V Balloy; A Deveaux; D Lebeaux; O Tabary; P le Rouzic; J M Ghigo; P F Busson; P Y Boëlle; J Guez Guez; U Hahn; A Clement; M Chignard; H Corvol; M Burnet; L Guillot
Journal:  Br J Pharmacol       Date:  2014-04       Impact factor: 8.739

5.  Development of non-antibiotic macrolide that corrects inflammation-driven immune dysfunction in models of inflammatory bowel diseases and arthritis.

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6.  Distribution of systemically administered ampicillin, benzylpenicillin, and flucloxacillin in excisional wounds in diabetic and normal rats and effects of local topical vasodilator treatment.

Authors:  S E Cross; M J Thompson; M S Roberts
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7.  IL-10, but not IL-4, suppresses infection-stimulated bone resorption in vivo.

Authors:  H Sasaki; L Hou; A Belani; C Y Wang; T Uchiyama; R Müller; P Stashenko
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8.  In vitro and in vivo uptake of azithromycin (CP-62,993) by phagocytic cells: possible mechanism of delivery and release at sites of infection.

Authors:  R P Gladue; G M Bright; R E Isaacson; M F Newborg
Journal:  Antimicrob Agents Chemother       Date:  1989-03       Impact factor: 5.191

9.  Azithromycin alters macrophage phenotype.

Authors:  Brian S Murphy; Vidya Sundareshan; Theodore J Cory; Don Hayes; Michael I Anstead; David J Feola
Journal:  J Antimicrob Chemother       Date:  2008-01-29       Impact factor: 5.790

10.  Activation of hypoxia-inducible factor 1 attenuates periapical inflammation and bone loss.

Authors:  Kimito Hirai; Hisako Furusho; Kiichi Hirota; Hajime Sasaki
Journal:  Int J Oral Sci       Date:  2018-04-13       Impact factor: 6.344

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Review 1.  Macrophages in periapical lesions: Potential roles and future directions.

Authors:  Yao Song; Xinying Li; Dingming Huang; Hongjie Song
Journal:  Front Immunol       Date:  2022-09-05       Impact factor: 8.786

2.  Effect of Azithromycin on Mineralized Nodule Formation in MC3T3-E1 Cells.

Authors:  Kengo Kato; Manami Ozaki; Kumiko Nakai; Maki Nagasaki; Junya Nakajima; Ryosuke Koshi; Hideki Tanaka; Takayuki Kawato; Morio Tonogi
Journal:  Curr Issues Mol Biol       Date:  2021-10-06       Impact factor: 2.976

  2 in total

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