Key points:
1 Neutrophil aggregation is associated with acquired CFTR.
2 The expression of CFTR mRNA in the mucosa of the ABRS group was lower than that of the CRS group.
3 IL-6 and IL-8 in the mucosa of the ABRS group was significantly higher than that of the CRS.
4 IL-6, IL-8 and MCP-1 were upregulated in polyps.
5 CFTR dysfunction and neutrophil chemokines IL-6 and IL-8 play more important roles in ABRS than in chronic inflammation of nasal mucosa.
Introduction
Rhinosinusitis is an inflammation of the nasal mucosa, which can be divided into Acute rhinosinusitis (ARS) and Chronic rhinosinusitis (CRS) according to the length of medical history 1. At present, it is considered that viral infection is one of the most important causes of acute rhinosinusitis. The nasal mucosa epithelium is the first line of defense of the respiratory tract and is also the main entrance and initial reaction site of respiratory virus invasion2. The viruses that cause acute rhinosinusitis in children are mainly respiratory viruses, such as Rhinovirus ,Respiratory Syncytial Virus and Influenza Virus 3. Viruses enter cells through receptor-mediated endocytosis, and then express and replicate the viral genome within hours of infection, causing damage to the nasal mucosa epithelium4, 5. Children’s immune systems are not yet mature and are therefore more susceptible to pathogens that can induce ARS. Acute Bacterial sinusitis (ABRS) is a complication of viral upper respiratory tract infection. Mucosal injury and mucociliary dysfunction caused by viral infection may be the main causes of secondary bacterial infection in the nasal mucosa. In sinusitis, the most common bacteria are Streptococcus pneumoniae , Haemophilus influenzae , andMoraxella catarrhalis 6. Recurrent ARS or prolonged ABRS can lead to CRS. In China, the prevalence of CRS is approximately 2.1% in children1. CRS significantly affects the child’s quality of life.
CFTR is a glycoprotein expressed at the tip of mucosal epithelial cells. It is an important Cl channel protein in the mucosal epithelium which composed of 1480 amino acids. The airway epithelial surface is covered with a thin layer of airway surface liquid (ASL)7. The volume and viscosity of ASL are mainly regulated by CFTR. The dysfunction of CFTR will lead to the decrease of Cl-and HCO3- to the extracellular transport, and the excessive absorption of Na+ and H2O into the cell. Thus, ASL is dehydrated, resulting in the decrease of Mucociliary Clearance (MCC)8. Increased mucus viscosity on the airway surface makes the mucosal surface more susceptible to bacterial colonization and induces or exacerbates chronic infection9. However, CFTR dysfunction can be either primary or acquired. Cystic fibrosis (CF) is an autosomal recessive genetic disease caused by CFTR mutation, which is the cause of primary CFTR dysfunction. Therefore, the role of CFTR protein in airway mucosa has been widely discussed. In this study, we investigate the role of acquired CFTR dysfunction in acute and chronic rhinosinusitis in children.
Method