Association Between Microbiota and Nasal Mucosal Diseases in terms of Immunity

Abstract

The pathogenesis of nasal inflammatory diseases is related to various factors such as anatomical structure, heredity, and environment. The nasal microbiota play a key role in coordinating immune system functions. Dysfunction of the microbiota has a significant impact on the occurrence and development of nasal inflammation. This review will introduce the positive and negative roles of microbiota involved in immunity surrounding nasal mucosal diseases such as chronic sinusitis and allergic rhinitis. In addition, we will also introduce recent developments in DNA sequencing, metabolomics, and proteomics combined with computation-based bioinformatics.

Keywords: allergic rhinitis; chronic rhinosinusitis; immunity; microbiota; nasal mucosa.

Figure 1

Types of microbiota in normal nasal mucosa and other parts of the upper airway. (Figure created with Biorender.com).

Figure 2

(A) Different kinds of microbiota colonize healthy nasal mucosa such as Staphylococcus, Streptococcus, Propionibacterium, and Corynebacterium. (B) With the loss of epithelial integrity, pattern recognition molecules decrease, which provides an environment for bacteria to enter through the mucosal barrier in type 2 CRS. Mucosal ulceration is associated with increased abundance of Bacteroides, while squamous metaplasia is associated with increased Streptococcus abundance; enterotoxins produced by S. aureus can act as superantigens and promote Th-2 inflammation, thereby leading to the production of cytokines, such as IL-13, IL-4, and IL-5, in Type 2 CRS. At the same time, Prevotella is related to the release of proinflammatory cytokines, and fungal proteases can induce the production of TSLP, which leads to the activation of ILC2s producing IL-5 and IL-13. (C) In non-type 2 CRS, an increase in the abundance of Haemophilus or Streptococcus may be related to elevated IL-8 levels and neutrophil counts. Rhinovirus may increase the levels of IL-1B1, IL-6, and TNF-α; induce dendritic cell differentiation; and boost IL-22. At the same time, increased abundance of Clostridiales also elevates IL-22 levels. (Figure created with Biorender.com).

Figure 3

(A) S. aureus, Propionibacterium, Prevotella, Corynebacterium, Bacteroidetes, and Streptococcus are common in normal nasal mucosa. (B) In patients with AR, S. aureus can produce IL-5 and IL-13 by binding to TLR2, and SEB can induce the release of IL-5 and IL-13 by affecting Th2 cells. Rhinovirus stimulates human respiratory epithelial cells to produce IL-25 and IL-33, which drive the production of IL-5 and IL-13 by binding to Th2 cells, ILC2s, and basophils (Figure created with Biorender.com).