Association Between Gut and Nasal Microbiota and Allergic Rhinitis: A Systematic Review

Abstract

Allergic rhinitis is a chronic non-infectious inflammation of the nasal mucosa mediated by specific IgE. Recently, the human microbiome has drawn broad interest as a potential new target for treating this condition. This paper succinctly summarizes the main findings of 17 eligible studies published by February 2024, involving 1044 allergic rhinitis patients and 954 healthy controls from 5 countries. These studies examine differences in the human microbiome across important mucosal interfaces, including the nasal and intestinal areas, between patients and controls. Overall, findings suggest variations in the gut microbiota between allergic rhinitis patients and healthy individuals, although the specific bacterial taxa that significantly changed were not always consistent across studies. Due to the limited scope of existing research and patient coverage, the relationship between the nasal microbiome and allergic rhinitis remains inconclusive. The article discusses the potential immune-regulating role of the gut microbiome in allergic rhinitis. Further well-designed clinical trials with large-scale recruitment of allergic rhinitis patients are encouraged.

Keywords: allergic rhinitis; immunomodulation; microbiota dysbiosis; nasal microbiome; short-chain fatty acids.

Figure 1

Impact of gut and nasal microbial dysbiosis on AR. Disturbance of the gut microbiota and a decrease in intestinal metabolites (eg, short-chain fatty acids and tryptophan,) induces the production of TSLP, IL-25, and IL-33, which contributes to Th2 cytokine production and promotes localized inflammatory responses. It also creates an environment rich in transforming growth factor-β, which promotes cellular differentiation toward pro-inflammatory Th17 by increasing the amount of RORγ-t. Vibrio traumaticus in the nasal cavity induces cytokines such as IL-1β, IL-6, and TNF-α, participates in NF-κβ signaling, and elicits allergic reactions by releasing IFN-β, IL-27, and IL-1β. A. baumannii activates the Nod-like receptor NLRP3 via caspase-1, which promotes the release of IL-1β and TNF-α from macrophages, thereby triggering AR. In addition, A. baumannii induces the production of reactive oxygen species from dendritic cells, which activates NLRP3 and promotes the differentiation of cells towards pro-inflammatory Th2, triggering the immune response typical of AR.