Granulocyte-colony stimulating factor: Missing link for stratification of type 2–high and type 2–low chronic rhinosinusitis patients

Neutrophilic inflammation in chronic rhinosinusitis

“…In Asian patients, both numbers of neutrophils and rates of apoptosis correlated with G-CSF in nasal polyps and suppressed apoptosis could be reversed by anti-G-CSF treatment [25]. These observations were recently confirmed in Caucasian patients with low-type 2 CRSwNP [26 ▪ ]. It has been shown that co-stimulation of neutrophils with GM-CSF, TNF-α and IL-4 leads to the generation of long-living populations of neutrophils; and the concentration of all these mediators have been reported to be increased in CRS mucosa [27,28].…”

“…As the type 2 CRSsNP patients have worse clinical outcomes by means of recurrence, comorbid asthma and reduced smell/taste, neutrophils cannot be associated with a more severe clinical outcome in CRSsNP. Interestingly, more and more studies over the last decade report the existence of a mixed eosinophilic-neutrophilic inflammation, associated with high type 2 responses and a worse clinical outcome in about 26…”

Immunological mechanisms and treatable traits of chronic rhinosinusitis in Asia: A narrative review

“…Although upregulation of neutrophil infiltration was found in Chinese patients with both eosinophilic and noneosinophilic CRSwNP, noneosinophilic CRSwNP Chinese patients displayed even higher numbers of neutrophils than eosinophilic CRSwNP patients 61–63 . Recently, Nevel et al also found that T2‐low CRSwNP patients have elevated levels of neutrophils compared to T2‐high CRSwNP patients in Western countries 66 . Recently, Wang et al found that IL‐36γ produced by nasal epithelial cells could activate neutrophils and further exaggerate neutrophilic inflammation by promoting the production of neutrophil chemokines in CRS 63 .…”

“…63 By performing a comprehensive and integrated analysis of neutrophilic inflammation in a large cohort of CRSwNP patients in China, Ruan et al identified granulocyte-colony stimulating factor (G-CSF) as an important factor in suppressing neutrophil apoptosis and promoting tissue neutrophilia in Chinese CRSwNP patients, 67 which was confirmed in White CRSwNP patients. 66 Interestingly, although IL-17 has been demonstrated to promote neutrophilic inflammation in infectious and autoimmune diseases, there was a weak or no correlation between IL-17A and neutrophil levels in CRS in both Chinese and Western CRSwNP patients, disfavouring a role of IL-17A in the development of neutrophilic inflammation in CRSwNP. 6 Neutrophilic inflammation is also associated with poor treatment outcomes in CRS patients.…”

“…[61][62][63] Recently, Nevel et al also found that T2-low CRSwNP patients have elevated levels of neutrophils compared to T2-high CRSwNP patients in Western countries. 66 Recently, Wang et al found that IL-36γ produced by nasal epithelial cells could activate neutrophils and further exaggerate neutrophilic inflammation by promoting the production of neutrophil chemokines in CRS. 63 By performing a comprehensive and integrated analysis of neutrophilic inflammation in a large cohort of CRSwNP patients in China, Ruan et al identified granulocyte-colony stimulating factor (G-CSF) as an important factor in suppressing neutrophil apoptosis and promoting tissue neutrophilia in Chinese CRSwNP patients, 67 which was confirmed in White CRSwNP patients.…”