Immunopathologic Role of Eosinophils in Eosinophilic Chronic Rhinosinusitis

Abstract

Chronic rhinosinusitis (CRS) is a diverse chronic inflammatory disease of the sinonasal mucosa. CRS manifests itself in a variety of clinical and immunologic patterns. The histological hallmark of eosinophilic CRS (ECRS) is eosinophil infiltration. ECRS is associated with severe disease severity, increased comorbidity, and a higher recurrence rate, as well as thick mucus production. Eosinophils play an important role in these ECRS clinical characteristics. Eosinophils are multipotential effector cells that contribute to host defense against nonphagocytable pathogens, as well as allergic and nonallergic inflammatory diseases. Eosinophils interact with Staphylococcus aureus, Staphylococcal enterotoxin B, and fungi, all of which were found in the tissue of CRS patients. These interactions activate Th2 immune responses in the sinonasal mucosa and exacerbate local inflammation. Activated eosinophils were discovered not only in the tissue but also in the sinonasal cavity secretion. Eosinophil extracellular traps (EETs) are extracellular microbes trapping and killing structures found in the secretions of CRS patients with intact granule protein and filamentous chromatic structures. At the same time, EET has a negative effect by causing an epithelial barrier defect. Eosinophils also influence the local tissue microenvironment by exchanging signals with other immune cells and structural cells. As a result, eosinophils are multifaceted leukocytes that contribute to various physiologic and pathologic processes of the upper respiratory mucosal immune system. The goal of this review is to summarize recent research on the immunopathologic properties and immunologic role of eosinophils in CRS.

Exploring the immunopathology of type 2 inflammatory airway diseases

“…Various mechanisms have been identified by researchers to explain the occurrence of eosinophilic infiltration in CRSwNP (57,58). It is evident that in CRSwNP, there is an accumulation of Charcot-Leyden Crystals (CLCs) within the tissues, as indicated by previous research (42).…”

“…This effect is mirrored in the lungs of asthmatic patients who exhibit increased levels of TSLP compared to healthy individuals (110). After exposure to allergens, IL-25 is markedly upregulated in the bronchial mucosa and nasal polyps of CRSwNP patients (57,111). Elevated levels of IL-25 in nasal polyps are also indicative of a positive response to corticosteroid treatment (112).…”

IL‐4/IL‐13 pathway in nasal type 2 inflammation: The central role and targeted therapy

“…The activated Th2 cells and ILC2s recruit and activate basophils, mast cells and eosinophils by secreting IL-4, IL-5, and IL-13 [21,22]. IL-5 induces the maturation of eosinophils and the release of toxic granules to cause tissue damage and inflammation, leading to tissue remodeling and exacerbating nasal pathology [23,24]. Several studies have demonstrated that intravenous administration of a humanized anti-human IL-5 monoclonal antibody reduced the size of nasal polyps [25,26].…”

Diagnosis and Management of Allergic Rhinitis in Asthmatic Children

“…The clinical suspect of AR firstly relies on symptoms, including one or more of the following symptoms, such as pruritus, sneezing, rhinorrhoea, nasal congestion, and hyposmia that arise within minutes after the exposition to allergen until 1-2 hours; late symptoms are nasal obstruction, hyposmia, nasal hyper reactivity and post nasal mucous discharge. [46][47][48] Allergic rhinitis can be perennial or seasonal, according to the relevant allergen, but this classification is not applicable globally, so the Allergic Rhinitis and its Impact on Asthma (ARIA) group has classified AR into intermittent or persistent on the duration of symptoms. 22 The clinical history is essential for diagnosing and profiling rhinitis in children in order to provide the most appropriate treatment and to establish the best management for the patient.…”