Allergic rhinitis, asthma and laryngopharyngeal reflux disease: a cross-sectional study on their reciprocal relations.

Allergic rhinitis (AR) is a common medical condition worldwide. It is an inflammation in the nasal mucosa due to allergen exposure throughout the year. Laryngopharyngeal reflux (LPR) is another medical condition that can overlap with AR. LPR can be considered an extra oesophageal manifestation of gastro-oesophageal reflux disease (GORD) or a different entity. Its diagnosis imposes a real challenge as it has a wide range of unspecific symptoms. Although AR and LPR are not life-threatening, they can severely affect the quality of life for years and cause substantial distress. Moreover, having AR is associated with having asthma which is also in turn associated with GORD. This is a cross-sectional study which used surveys distributed online on Social Media and targeted people across Syria. All participants who responded to the key questions were included. Reflux symptom index (RSI) was used for LPR, and score for allergic rhinitis (SFAR) was used for AR. Demographic questions and whether the participant had asthma were also included in the survey. We found that there was an association between the symptoms of LPR and AR p < 0.0001 (OR, 2.592; 95% CI 1.846-3.639), and their scores were significantly correlated (r = 0.334). Having asthma was associated with LPR symptoms p = 0.0002 (OR 3.096; 95% CI 1.665-5.759) and AR p < 0.0001 (OR 6.772; 95% CI 2.823-16.248). We concluded that there was a significant association between having LPR, AR, and asthma. We need more studies to distinguish between their common symptoms and aetiologies.

Laryngeal T regulatory cells in the setting of smoking and reflux.

OBJECTIVES/HYPOTHESIS: The larynx is a mucosal organ rich in lymphatic tissue that is regularly exposed to a multitude of inhaled, ingested, and refluxed microorganisms and irritants. The first line of mucosal immune defense is the barrier, including resident immune cells. T regulatory (Treg) cells are a specialized subset of CD4+ T cells that suppress or dampen immune responses to prevent damaging immunopathology. As Treg cells have been shown to preferentially accumulate at sites of infection, and Treg responses may contribute to persistence of infection by impairing antibacterial immunity, we sought to quantify these cells in laryngeal tissue exposed to smoking and reflux. STUDY DESIGN: Cross-sectional study. METHODS: Using an epigenetic assay, we quantified Treg and T cells and calculated the ratio of Treg to T cells (i.e., cellular ratio of immune tolerance [ImmunoCRIT]) in disease-free laryngeal biopsies representing four inflammatory states: 1) tobacco-exposed tissue, 2) refluxate and tobacco-exposed tissue, 3) refluxate-exposed tissue, and 4) unexposed tissue. RESULTS: There was epigenetic evidence of Treg cells in all tissues, and we found no differences in Treg cell frequency relative to smoking and reflux in laryngeal tissue collected from 42 non-treatment-seeking participants. There was a decrease in total T cell frequency and an increase in ImmunoCRIT values in smokers regardless of reflux status. CONCLUSIONS: In this study, laryngeal tissue from smokers show decreased overall T cells and increased ImmunoCRIT values. Our findings indicate that laryngeal inflammation is not directly mediated by loss of Treg cells in response to smoking and reflux in local tissue and increased ImmunoCRIT values in smokers implicate a role for this environmental exposure in modulating laryngeal immune homeostasis. More studies are indicated to explore Treg cell dysfunction in the pathophysiology of laryngeal disease. LEVEL OF EVIDENCE: NA Laryngoscope, 127:882-887, 2017.