Role of the inflammasomes in the development of polyposis nasi

Introduction:

Chronic rhinosinusitis is a heterogeneous group with a Th1 or Th2 immune response. The mechanism of polypoid tissue formation has not been fully understood. A key signaling platform in the inflammatory reaction is the inflammasome. Atopic diseases such as dermatitis and asthma have an inhibitory effect on the inflammasome signal cascade due to a Th2-dominant environment. We therefore examined how inflammasome components are expressed in the chronically altered tissue of the nose and paranasal sinus.

Methods:

Inflammatory CRS tissue of n = 12 with or without nasal polyps (CRSwNP: age 29 – 69, CRSsNP: age 18 – 57) and non-inflammatory tissue of nasal turbinates (n = 4, age 20 – 54) were analyzed by expression analysis of 88 inflammasome genes. Subsequently, the localization of the regulated inflammasomes were investigated by immunohistochemistry in a larger collective (CRSwNP n = 20: age 18 – 75, CRSsNP n = 6: age 26 – 65, control n = 4: age 18 – 42).

Results:

The expression of NFKBiA and Bcl-2 were highly significant reduced in nasal polyps compared to CRSsNP and control tissue. IL-1ß and IL-18 remained unchanged at mRNA level. It was shown that NFKBiA, NLRP3, NLRc4 and AIM2 were immunohistochemically detectable in all tissue types. The epithelium of polyposis nasi tissue showed NOD2, AIM2 and NLRP3 reduced expression compared to the uninfected nasal tissue. In contrast, NFkBiA is significantly increased in CRSwNP and CRSsNP compared to the control tissue. Additionally, NLRP3 is downregulated in the stroma of CRSwNP and NLRc4 is increased in CRSwNP and CRSsNP.

Conclusion:

Our investigations have shown that CRSwNP tissue has mainly a downregulation effect of inflammasomes compared to CRSsNP. This leads to reduced immunocompetence against pathogens in sinonasale tissue.

Publication History

Publication Date:
18 April 2018 (online)