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脂多糖和聚肌苷酸-聚胞苷酸在鼻息肉小鼠模型中的作用。

Effect of lipopolysaccharide and polyinosinic:polycytidylic acid in a murine model of nasal polyp.

机构信息

Department of Otorhinolaryngology-Head and Neck Surgery, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.

Graduate School of Medicine, Seoul National University College of Medicine, Seoul, Korea.

出版信息

Sci Rep. 2021 Jan 13;11(1):1021. doi: 10.1038/s41598-020-80483-y.

DOI:10.1038/s41598-020-80483-y
PMID:33441902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7806732/
Abstract

Several factors, including bacterial and viral infections, have been associated with rhinosinusitis and nasal tissue remodelling that may result in nasal polyp formation. However, the potential role of bacterial or viral stimuli triggering polyp development is unclear. Here, we used lipopolysaccharide (LPS) and polyinosinic:polycytidylic acid [poly(I:C)] in a murine model of allergic rhinosinusitis to compare different effects of bacterial- and virus-derived stimuli in the pathogenesis of nasal polyp formation. Briefly, BALB/c mice were sensitised and challenged with ovalbumin and staphylococcal enterotoxin, with or without LPS or poly(I:C), and the consequent histopathological profiles, cytokines, and systemic humoral responses were studied. While no significant differences in polyp formations and epithelial disruptions were observed among the experimental groups, the local cell recruitment patterns slightly differed in animals that received either LPS or poly(I:C). Additionally, the local immune environments generated by LPS or poly(I:C) stimulation varied. LPS stimulation induced a marked Th1/Th17 response and predominantly neutrophilic nasal polyp formations, whereas poly(I:C) induced a Th2-skewed environment in neutrophilic nasal polyp development. Overall, our findings show that both cell recruitment patterns and local immune environments induced by these two stimuli differ, which may have implications in the physiopathology of rhinosinusitis with nasal polyp.

摘要

多种因素,包括细菌和病毒感染,与鼻窦炎和鼻组织重塑有关,这可能导致鼻息肉形成。然而,细菌或病毒刺激引发息肉发展的潜在作用尚不清楚。在这里,我们使用脂多糖(LPS)和聚肌苷酸:聚胞苷酸[poly(I:C)]在过敏性鼻窦炎的小鼠模型中比较了细菌和病毒来源刺激物在鼻息肉形成发病机制中的不同作用。简而言之,BALB/c 小鼠用卵清蛋白和葡萄球菌肠毒素致敏和攻毒,有或没有 LPS 或 poly(I:C),并研究了随后的组织病理学特征、细胞因子和系统体液反应。虽然实验组之间在息肉形成和上皮破坏方面没有观察到明显差异,但接受 LPS 或 poly(I:C)刺激的动物的局部细胞募集模式略有不同。此外,LPS 或 poly(I:C)刺激产生的局部免疫环境也不同。LPS 刺激诱导明显的 Th1/Th17 反应和主要是嗜中性粒细胞性鼻息肉形成,而 poly(I:C)诱导嗜中性粒细胞性鼻息肉发展中的 Th2 偏倚环境。总的来说,我们的研究结果表明,这两种刺激物诱导的细胞募集模式和局部免疫环境存在差异,这可能对伴有鼻息肉的鼻窦炎的病理生理学有影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/d0b13096229c/41598_2020_80483_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/b235778f6332/41598_2020_80483_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/ba5896408150/41598_2020_80483_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/00ca043b2cf2/41598_2020_80483_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/66cd34360850/41598_2020_80483_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/d0b13096229c/41598_2020_80483_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/b235778f6332/41598_2020_80483_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/ba5896408150/41598_2020_80483_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/00ca043b2cf2/41598_2020_80483_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/66cd34360850/41598_2020_80483_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7c7/7806732/d0b13096229c/41598_2020_80483_Fig5_HTML.jpg

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