Reactive Nasal Inflammation: Current Pathophysiological and Therapeutic Approach.

Mapping Intimacies ◽

10.46940/scmcrj.02.1008 ◽

2020 ◽

pp. 1-3

Keyword(s):

Allergic Rhinitis ◽

Chronic Rhinosinusitis ◽

Seasonal Allergic Rhinitis ◽

Therapeutic Approach ◽

Heterogeneous Group ◽

Inflammatory Conditions ◽

Nasal Inflammation

The pathophysiology of processes that underlie the onset and progression of reactive nasal inflammatory conditions is very complex. These include a heterogeneous group of disorders, ranging from seasonal allergic rhinitis to nonallergic, persisting, refractory forms of chronic rhinosinusitis (CRS). About 400 million people worldwide are affected by allergic rhinitis and another 200 million are thought to be affected by nonallergic forms of nasal inflammation including CRS.

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Airway function and nasal inflammation in seasonal allergic rhinitis and asthma

Clinical & Experimental Allergy ◽

10.1111/j.1365-2222.2004.01970.x ◽

2004 ◽

Vol 34 (6) ◽

pp. 891-896 ◽

Cited By ~ 46

Author(s):

G. Ciprandi ◽

I. Cirillo ◽

A. Vizzaccaro ◽

M. Milanese ◽

M. A. Tosca

Keyword(s):

Allergic Rhinitis ◽

Seasonal Allergic Rhinitis ◽

Airway Function ◽

Nasal Inflammation

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Erythromycin reduces nasal inflammation by inhibiting immunoglobulin production, attenuating mucus secretion, and modulating cytokine expression

Scientific Reports ◽

10.1038/s41598-021-01192-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Ting-Ting Yen ◽

Rong-San Jiang ◽

Ching-Yun Chang ◽

Chih-Ying Wu ◽

Kai-Li Liang

Keyword(s):

Allergic Rhinitis ◽

Chronic Rhinosinusitis ◽

Lymphoid Tissue ◽

Cytokine Expression ◽

Mucus Secretion ◽

Immunoglobulin Production ◽

Nasal Inflammation ◽

The Impact ◽

Nasal Histology ◽

Th 1

AbstractAllergic rhinitis (AR) and chronic rhinosinusitis (CRS) share some similar pathological mechanisms. In current study, we intend to investigate the impact of AR on CRS. In addition, we explored the efficacy of erythromycin (EM) treatment on CRS mice with or without AR (CRSwoAR, CRSwAR). Study subjects were divided into control, CRSwoAR, and CRSwAR groups. Experimental mice were divided similarly into control, CRSwoAR, and CRSwAR groups. In addition, CRS mice were treated with EM at 0.75, 7.5, or 75 mg/kg or with dexamethasone (Dex) at 1 mg/kg. In our results, allergy exacerbates inflammation that was evident in nasal histology and cytokine expression both in patients and in mice with CRS. Dex 1 mg/kg, EM 7.5 or 75 mg/kg treatments significantly inhibited serum IgE and IgG2a in CRS mice. EM-treated CRS mice had significantly elevated IL-10 levels and had a reversal of Th-1/Th-2 cytokine expression in nasal-associated lymphoid tissue. MUC5AC expressions were significantly reduced in the 7.5 or 75 mg/kg EM-treated mice compared with untreated mice. EM showed inhibitions on immunoglobulin production and mucus secretion stronger than Dex. We concluded that comorbid AR enhanced inflammation of CRS. EM and Dex treatments showed similar anti-inflammatory effects on CRS but through partly different mechanisms.

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