Expression of RANTES, eotaxin-2, ICAM-1, LFA-1 and CCR-3 in chronic rhinosinusitis patients with nasal polyposis

Abstract

PURPOSE: To compare gene expression of the chemokines RANTES and eotaxin-2, its receptor, CCR-3, adhesion molecule ICAM-1 and its receptor LFA-1 in eosinophilic polyps and in control normal nasal mucosa. METHODS: Gene expression was quantified by Real Time PCR in polyps (n=35) and in healthy nasal mucosa (n=15). RESULTS: Eosinophilic polyps showed a higher expression of eotaxin-2 and RANTES, but not of CCR-3, ICAM-1 or LFA-1 compared to control nasal mucosa. CONCLUSION: Eosinophilic polyps present greater expression of eotaxin-2 and RANTES, but not of CCR-3, ICAM-1 or LFA-1 compared to control nasal mucosa.

Immune Imbalance in Nasal Polyps of Caucasian Chronic Rhinosinusitis Patients Is Associated with a Downregulation of E-Selectin

“…Nonetheless, ICAM1 is not specific for the lymphocyte response mainly of the Th2 type. In line with our results, Cavallari et al and Jahnsen et al observed no difference in the expression of ICAM1 between nasal polyps and inferior turbinates, but its role in CRSwNP has not been clarified despite its high levels of expression [26, 30, 31]. Apart from VCAM1, P-selectin has been suggested primarily to promote the recruitment of eosinophils in nasal polyp tissues.…”

Nasal fluid release of eotaxin‐3 and eotaxin‐2 in persistent sinonasal eosinophilic inflammation

“…Several studies on cytokines and chemokines have rapidly expanded our understanding of inflammatory responses in the pathogenesis of chronic eosinophilic inflammation. Several authors have demonstrated that protein expression of CCL11, CCL24 and CCL26 is significantly higher in nasal polyp patients than in controls. The total protein concentrations of samples were measured in homogenized tissue of nasal polyps.…”

Surfactant proteins A and D are related to severity of the disease, pathogenic bacteria and comorbidity in patients with chronic rhinosinusitis with and without nasal polyps

“…Another explanation is the damage of SPs by local factors of eosinophillic inflammation such as interleukin 5, eotaxin, eosinophillic cationic protein, major basic protein present in nasal secretions participating in pathogenesis of nasal polyps. 19,20 Further, we demonstrated the correlation of the severity of the CRS assessed by preoperative CT scans of paranasal sinuses and the amount of surfactant proteins. SP-A and SP-D were significantly elevated in NALF as well as in submucosal glands in nasal mucosa in patients from CRSsNP group with more severe form (CT score ≥16 points) compare to less severe form (CT score <16 points) of the disease.…”

“…Low amount of surfactant proteins in nasal lavage fluid from patients with CRSwNP can be explained by strong damage of the mucosa with upregulated synthesis of SPs and impaired secretion. Another explanation is the damage of SPs by local factors of eosinophillic inflammation such as interleukin 5, eotaxin, eosinophillic cationic protein, major basic protein present in nasal secretions participating in pathogenesis of nasal polyps …”