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The mechanisms underlying the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) remain largely unknown. CRSwNP has garnered considerable public health concern owing to its high incidence and unsatisfactory treatment outcomes. Herbal remedies are promising candidates for the treatment of CRSwNP. We examined the utility of andrographolide, a diterpenoid lactone extracted from the Chinese herb Andrographis paniculata, an anti-inflammatory agent for CRSwNP treatment by evaluating interleukin (IL)-6 and IL-17 production and monitoring T helper 17 (Th17) differentiation of peripheral blood mononuclear cells (PBMCs) isolated from 20 Chinese CRSwNP patients and 11 control subjects. All CRSwNP patients exhibited clinical features of CRSwNP. Andrographolide significantly inhibited IL-6 and IL-17 production, suppressed p-Stat3 expression, and inhibited Th17 differentiation of PBMCs in vitro. These findings suggested that andrographolide has useful anti-inflammatory properties and could be used for the treatment of CRSwNP.

A predominant Th17 population is a marker of chronic rhinosinusitis with nasal polyps (CRSwNP) in Chinese patients. As a ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR) plays a vital role in promoting or inhibiting specific Th cell development. However, its role in CRSwNP remains to be defined. The aim of the present study was to investigate whether AhR, which regulates Th17 cell differentiation, played a role in the pathogenesis of CRSwNP by evaluating AhR expression in nasal polyps and peripheral blood mononuclear cells (PBMCs) obtained from CRSwNP patients. Forty-eight patients (atopic, 24; non-atopic, 24) and 13 controls were studied. To explore the role of AhR in CRSwNP, we analyzed the expression of AhR, retinoid-related orphan receptor C (RORC), interleukin (IL)-17, and IL-10 and the differentiation of Th17 using mRNA or protein detection methods. Notably, the expression of AhR was reduced in CRSwNP, and the expression of AhR was lower in the atopic group than in the non-atopic group. However, there was a very low level of Th17 and its associated factors (RORC, IL-17) in the control group compared to the two CRSwNP groups. In particular, the polarization of Th17 cells in atopic CRSwNP patients was increased compared with non-atopic individuals. In addition, ITE intervention in PBMCs promoted AhR expression and attenuated Th17 responses, demonstrating that AhR was more likely to suppress Th17 cells differentiation in Chinese CRSwNP patients. This information is valuable for obtaining a clear understanding of the pathogenesis of CRSwNP. Moreover, patients with atopic CRSwNP may exhibit reduced expression of AhR, leading to aggravation of the disproportionate distribution of Th17 cells in polyp tissues and PBMCs, thereby suggesting that atopic CRSwNP has a distinct pathogenesis from that of non-atopic CRSwNP.