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Heat maps for gene expression analysis in allergic rhinitis patients (AR) (reference: control group) (a) and atopic dermatitis (AD) patients (reference: control group) (b).
Source publication
Methods:
In the study, we included 86 children diagnosed with atopic asthma (n = 25), allergic rhinitis (n = 20), and atopic dermatitis (n = 20) and healthy control subjects (n = 21) of Caucasian origin from the Polish population. The blood leukocyte expression of 31 genes involved in neuroinflammatory response (neurotrophins, their receptors, neu...
Citations
... Previous evidence suggests that nGF is persistently and highly expressed in nasal epithelium and submucosal tissues of patients with ar and is mostly localized in inflammatory cells (11,12). The level of serum NGF has equally been shown to markedly increase in subjects with ar following allergen stimulation (13,14). in addition, nGF is allegedly involved in the pathophysiological processes of airway inflammation and hyperresponsiveness in patients with AR (15). NGF mediates inflammation not only in the upper airway but also in the lower airway (12,16). ...
The presence of allergic rhinitis (AR) is an increased risk factor for the occurrence of bronchial asthma (BA). Nerve growth factor (NGF), in addition to its key role in the development and differentiation of neurons, may also be an important inflammatory factor in AR and BA. However, the pathogenesis of the progression of AR to BA remains to be elucidated. The present study aimed to investigate the ability of NGF to mediate nasobronchial interactions and explore possible underlying molecular mechanisms. In the present study, an AR mouse model was established and histology of nasal mucosa tissue injury was determined. The level of phenylethanolamine N‑methyl transferase in adrenal medulla was determined by immunofluorescence. Primary adrenal medullary chromaffin cells (AMCCs) were isolated and cultured from the adrenal medulla of mice. The expression levels of synaptophysin (SYP), STAT1, JAK1, p38 and ERK in NGF‑treated and untreated AMCCs were detected by reverse‑transcription‑quantitative PCR and western blotting. The epinephrine (EPI) and norepinephrine (NE) concentrations were measured by ELISA. It was found that the expression of SYP in AMCCs was enhanced in the presence of NGF, whereas, the concentration of EPI decreased significantly under the same conditions. Furthermore, NGF mediated the phenotypic and functional changes of AMCCs, resulting in decreased EPI secretion via JAK1/STAT1, p38 and ERK signaling. In conclusion, these findings could provide novel evidence for the role of NGF in regulating neuroendocrine mechanisms.
... e pathogenesis of neuroinflammation in allergic diseases has long been reported. Patients with chronic allergic inflammation have similar patterns of neuroinflammatory gene expression, which may be associated with the outcome of neuroimmune interactions [44,45]. Fever is regulated by hypothalamic temperature-sensitive neurons. ...
Objective:
To explore the potential mechanisms of Yupingfeng Powder (YPFP) in the treatment of allergic diseases by using network pharmacology and molecular docking technology.
Methods:
The active components and targets of YPFP were screened by the TCMSP database. The targets associated with atopic dermatitis, asthma, allergic rhinitis, and food allergy were obtained from GeneCards and OMIM databases, respectively. The intersection of the above disease-related targets was identified as allergy-related targets. Then, allergy-related targets and YPFP-related targets were crossed to obtain the potential targets of YPFP for allergy treatment. A protein-protein-interaction (PPI) network and a drug-target-disease topology network were constructed to screen hub targets and key ingredients. Next, GO and KEGG pathway enrichment analyses were performed separately on the potential targets and hub targets to identify the biological processes and signaling pathways involved. Finally, molecular docking was conducted to verify the binding affinity between key ingredients and hub targets.
Results:
In this study, 45 active ingredients were identified from YPFP, and 48 allergy-related targets were predicted by network pharmacology. IL6, TNF, IL1B, PTGS2, CXCL8, JUN, CCL2, IL10, IFNG, and IL4 were screened as hub targets by the PPI network. However, quercetin, kaempferol, wogonin, formononetin, and 7-O-methylisomucronulatol were identified as key ingredients by the drug-target-disease topological network. GO and KEGG pathway enrichment analysis indicated that the therapeutic effect of YPFP on allergy involved multiple biological processes and signaling pathways, including positive regulation of fever generation, positive regulation of neuroinflammatory response, vascular endothelial growth factor production, negative regulation of cytokine production involved in immune response, positive regulation of mononuclear cell migration, type 2 immune response, and negative regulation of lipid storage. Molecular docking verified that all the key ingredients had good binding affinity with hub targets.
Conclusion:
This study revealed the key ingredients, hub targets, and potential mechanisms of YPFP antiallergy, and these data can provide some theoretical basis for subsequent allergy treatment and drug development.
The role of neuroimmunomodulation in allergic diseases is a research hotspot in recent years. Allergic rhinitis（AR） is caused by overactive immune response to a foreign antigen in nasal mucosa. Immune cells release inflammatory mediators（including histamine, cytokines and neurotrophins）, which directly activate peripheral neurons to mediate nasal congestion, itching, sneezing, and other hyperresponsive symptoms. Upon activation, these peripheral neurons release neurotransmitters （including acetylcholine and norepinephrine） and neuropeptides（including calcitonin gene-related peptide, substance P and vasoactive intestinal peptide） that directly act on immune cells to drive allergic inflammation. Neuro-immune signaling may play a significant role in the pathophysiology of AR. Therefore, a better understanding of these cellular and molecular neuro-immune interactions may inspire the discovery of new targets and novel therapies.
