epidermal-growth-factor and Anaphylaxis

Topics: Anaphylaxis; Animals; Epidermal Growth Factor; Giardiasis; Humans; Intestines; Microvilli; Yersinia Infections

To investigate the effects of desmoglein 3 (DSG3) gene mediating epidermal growth factor/epidermal growth factor receptor (EGF/EGFR) signaling pathway on inflammatory response and immune function of anaphylactic rhinitis (AR).. Ten of the seventy male BALB/c mice were randomly selected as the normal control group, and the remaining 60 were used to construct the AR mice model. AR model mice were divided into 6 groups: model group (instilled with 5 μL saline), empty vector group (instilled with 5 μL of liposome and empty vector mixture), siRNA-DSG3 group (instilled with 5 μL of liposome and siRNA-DSG3 carrier mixture), AG1478 group (instilled with 5 μL of EGF/EGFR inhibitor AG1478), siRNA-DSG3+AG1478 group (instilled with 5 μL of liposome and siRNA-DSG3 carrier and EGF/EGFR inhibitor AG1478 mixture) and oe-DSG3 group, 10 in each group. After taking serum, each group of mice was sacrificed to get nasal mucosa tissues. HE staining was used to observe the pathological changes of nasal mucosa tissues in each group. The expression levels of DSG3, EGF and EGFR in nasal mucosa tissues of mice in each group were detected by qRT-PCR and western blot methods respectively. TUNEL staining was used to observe the apoptosis of nasal mucosa cells in mice. The expression of IgE, INF-γ, TNF-α, IL-2, IL-4 and IL-6 in serum of mice was determined by ELISA method. The immune adhesion function of red blood cells was detected by complement sensitization yeast hemagglutination method.. All the mice with AR showed different degrees of nasal mucosa injury and inflammatory cell infiltration, and silencing DSG3 or inhibiting the activity of EGF signaling pathway could alleviate the nasal mucosa injury. Compared with control group, the INF-γ and IL-2 levels of serum in AR model mice were significantly decreased; IgE, TNF-α, IL-4 and IL-6 levels were significantly increased (all P < 0.05); the mRNA expression levels and protein levels of DSG3, EGF and EGFR were significantly increased (all P < 0.05); C. Silencing DSG3 gene can inhibit the activation of EGF signaling pathway, alleviate the inflammation of AR nasal mucosa, and enhance red blood cells immune adherence function.

Topics: Anaphylaxis; Animals; Desmoglein 3; Disease Models, Animal; Epidermal Growth Factor; ErbB Receptors; Gene Expression Regulation; Inflammation; Mice, Inbred BALB C; Nasal Mucosa; Rhinitis, Allergic; Signal Transduction

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.

Topics: Anaphylaxis; Animals; Bronchoalveolar Lavage Fluid; Catecholamines; Epidermal Growth Factor; Ganglia, Sympathetic; Immunization; Inflammation; Lung; Male; Nerve Growth Factors; Nippostrongylus; Polymerase Chain Reaction; Rats; Rats, Inbred Strains; Submandibular Gland; Sympathectomy; Transforming Growth Factor beta