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下颌下腺在全身性过敏反应诱导后调节肺部炎症中的作用。

Role for the submandibular gland in modulating pulmonary inflammation following induction of systemic anaphylaxis.

作者信息

Mathison R, Hogan A, Helmer D, Bauce L, Woolner J, Davison J S, Schultz G, Befus D

机构信息

Department of Medical Physiology, Faculty of Medicine, University of Calgary, Alberta, Canada.

出版信息

Brain Behav Immun. 1992 Jun;6(2):117-29. doi: 10.1016/0889-1591(92)90012-d.

DOI:10.1016/0889-1591(92)90012-d
PMID:1504367
Abstract

Previous studies have shown that bilateral decentralization of the superior cervical ganglia (SCG; decentralization) attenuates allergen-induced pulmonary inflammatory responses in male rats sensitized to the nematode Nippostrongylus brasiliensis. The present report examines the neuronal and glandular mechanisms mediating the protection against pulmonary inflammation afforded by decentralization. Tissues and organs innervated by the SCG are responsible for this protection since, in a manner similar to decentralization, bilateral removal of the SCG (ganglionectomy) reduced anaphylaxis-induced accumulation of inflammatory cells in bronchoalveolar lavage fluid. Removal of the submandibular gland (sialadenectomy) did not modify the severity of the pulmonary inflammation, but concurrent sialadenectomy and decentralization abolished the protective effect of decentralization. Thus, we postulate that cervical sympathetic nerves tonically inhibit release of anti-inflammatory factors from submandibular glands. No relationship was found between noradrenaline and serotonin content of submandibular glands and the degree of protection against pulmonary inflammation offered by decentralization and ganglionectomy. Both decentralization and ganglionectomy appeared to increase the level of transcripts that encode immunomodulatory growth factors (nerve growth factor and epidermal growth factor) in submandibular glands, but these denervations evidently did not modify the transcripts for TGF beta 2. Systemic inflammatory events are regulated by the central nervous system at a level superior to the SCG probably through modulation of immunoregulatory factors in submandibular glands.

摘要

先前的研究表明,双侧颈上神经节去传入(去传入;即去除神经节后的神经支配)可减轻对线虫巴西日圆线虫致敏的雄性大鼠中变应原诱导的肺部炎症反应。本报告研究了介导去传入所提供的针对肺部炎症保护作用的神经元和腺体机制。颈上神经节所支配的组织和器官负责这种保护作用,因为与去传入类似,双侧切除颈上神经节(神经节切除术)可减少过敏反应诱导的支气管肺泡灌洗液中炎症细胞的积聚。切除下颌下腺(涎腺切除术)并未改变肺部炎症的严重程度,但同时进行涎腺切除术和去传入则消除了去传入的保护作用。因此,我们推测颈交感神经可紧张性抑制下颌下腺释放抗炎因子。未发现下颌下腺中去甲肾上腺素和5-羟色胺含量与去传入及神经节切除术所提供的针对肺部炎症的保护程度之间存在关联。去传入和神经节切除术似乎均增加了下颌下腺中编码免疫调节生长因子(神经生长因子和表皮生长因子)的转录本水平,但这些去神经支配显然并未改变转化生长因子β2的转录本。全身性炎症事件可能通过调节下颌下腺中的免疫调节因子,在高于颈上神经节的水平受到中枢神经系统的调控。

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Role for the submandibular gland in modulating pulmonary inflammation following induction of systemic anaphylaxis.下颌下腺在全身性过敏反应诱导后调节肺部炎症中的作用。
Brain Behav Immun. 1992 Jun;6(2):117-29. doi: 10.1016/0889-1591(92)90012-d.
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Marked antiinflammatory effects of decentralization of the superior cervical ganglia.颈上神经节去中枢化具有显著的抗炎作用。
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Temporal analysis of the anti-inflammatory effects of decentralization of the rat superior cervical ganglia.大鼠颈上神经节去传入后抗炎作用的时间分析
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Salivary gland derived peptides as a new class of anti-inflammatory agents: review of preclinical pharmacology of C-terminal peptides of SMR1 protein.唾液腺来源肽作为一类新型抗炎药物:SMR1 蛋白 C 末端肽的临床前药理学研究综述。
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Submandibular gland peptide-T (SGP-T) inhibits intestinal anaphylaxis.
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