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