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Immunopathologic Role of Fungi in Chronic Rhinosinusitis
Seung-Heon Shin1, Mi-Kyung Ye1, Dong-Won Lee1
1Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea.
Abstract:
Airborne fungi are ubiquitous in the environment and are commonly associated with airway inflammatory diseases. The innate immune defense system eliminates most inhaled fungi. However, some influence the development of chronic rhinosinusitis. Fungal CRS is thought of as not a common disease, and its incidence increases over time. Fungi are present in CRS patients and in healthy sinonasal mucosa. Although the immunological mechanisms have not been entirely explained, CRS patients may exhibit different immune responses than healthy people against airborne fungi. Fungi can induce Th1 and Th2 immune responses. In CRS, Th2-related immune responses against fungi are associated with pattern recognition receptors in nasal epithelial cells, the production of inflammatory cytokines and chemokines from nasal epithelial cells, and interaction with innate type 2 cells, lymphocytes, and inflammatory cells. Fungi also interact with neutrophils and eosinophils and induce neutrophil extracellular traps (NETs) and eosinophil extracellular traps (EETs). NETs and EETs are associated with antifungal properties and aggravation of chronic inflammation in CRS by releasing intracellular granule proteins. Fungal and bacterial biofilms are commonly found in CRS and may support chronic and recalcitrant CRS infection. The fungal-bacterial interaction in the sinonasal mucosa could affect the survival and virulence of fungi and bacteria and host immune responses. The interaction between the mycobiome and microbiome may also influence the host immune response, impacting local inflammation and chronicity. Although the exact immunopathologic role of fungi in the pathogenesis of CRS is not completely understood, they contribute to the development of sinonasal inflammatory responses in CRS.
Insights
Airborne fungi contribute to chronic rhinosinusitis (CRS) by triggering immune responses. Fungal presence and interactions with bacteria in the sinonasal cavity worsen inflammation and disease persistence.
Area of Science:
- Immunology
- Microbiology
- Otolaryngology
Background:
- Airborne fungi are common environmental triggers for airway inflammatory diseases.
- While the innate immune system typically clears inhaled fungi, some species can contribute to chronic rhinosinusitis (CRS).
- Fungal presence in sinonasal mucosa is observed in both CRS patients and healthy individuals, suggesting complex immune interactions.
Purpose of the Study:
- To explore the role of airborne fungi in the pathogenesis of chronic rhinosinusitis.
- To elucidate the immunological mechanisms underlying fungal-induced inflammation in CRS.
- To investigate the impact of fungal and bacterial interactions on CRS development and persistence.
Main Methods:
- Review of immunological mechanisms of fungal exposure in CRS.
- Analysis of Th1 and Th2 immune responses to fungi in CRS patients.
- Examination of fungal interactions with sinonasal cells, including epithelial cells, innate type 2 cells, lymphocytes, neutrophils, and eosinophils.
- Investigation of fungal and bacterial biofilms and their role in CRS.
Main Results:
- Fungi can induce Th1 and Th2 immune responses, with Th2 responses implicated in CRS pathogenesis.
- Nasal epithelial cells, pattern recognition receptors, and innate type 2 cells play a role in fungal-induced inflammation.
- Fungi interact with neutrophils and eosinophils, leading to the formation of neutrophil extracellular traps (NETs) and eosinophil extracellular traps (EETs), which can aggravate inflammation.
- Fungal and bacterial biofilms are frequently found in CRS, potentially supporting chronic infections and influencing host immune responses.
Conclusions:
- Airborne fungi play a significant role in the development of sinonasal inflammatory responses in CRS.
- Fungal-induced immune responses, extracellular traps, and interactions with bacterial communities contribute to the chronicity and recalcitrance of CRS.
- Further research is needed to fully understand the immunopathologic role of fungi in CRS pathogenesis.
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