LEAP-2, LL-37 and RNase7 in tonsillar tissue: downregulated expression in seasonal allergic rhinitis.

In the upper airway, the production of antimicrobial peptides (AMPs) protects against bacteria, viruses and fungi. Previous investigations have revealed downregulated expression of AMPs in different manifestations of allergic disease. In this study, we examined the expression of LL-37, Ribonuclease7 (RNase7) and Liver-expressed antimicrobial peptide 2 (LEAP-2) in tonsillar tissue and studied a possible relation to seasonal allergic rhinitis (SAR).

Upregulated levels of human β-defensins in patients with seasonal allergic rhinitis after allergen-specific immunotherapy treatment.

Background: Antimicrobial peptides (AMPs) are important actors in the innate immune system. One class of AMPs is the human β-defensins (HBDs), a group of small peptides with a broad spectrum of antimicrobial activities. Expression of HBDs is downregulated in different manifestations of allergic disease.

Reduced tonsillar expression of human β-defensin 1, 2 and 3 in allergic rhinitis.

Airway infections are known to cause exacerbations of allergy and asthma. Tonsils constitute a primary site for microbial recognition and triggering of the immune system in the airways. Human β-defensins (HBDs) are antimicrobial peptides with an important role in this defense.

Retinoic acid-inducible gene 1-like receptors in the upper respiratory tract.

Background: Retinoic acid-inducible gene 1-like receptors (RLRs) are a novel family of pattern recognition receptors that include retinoic acid-inducible gene 1 (RIG-1), melanoma differentiation-associated gene 5 (MDA-5), and laboratory of genomics and physiology 2 (LGP-2). The knowledge of RLRs and their function in the human airway is limited. This study explores the role of RLRs in the upper respiratory tract.

Topical steroids do not downregulate expression of growth-related oncogene-alpha in nasal polyps.

Conclusions: Topical steroids did not affect expression of growth-related oncogene-alpha (GRO-alpha) in nasal polyps. The results of this study suggest roles for steroid-resistant gene expression in the pathogenesis of nasal polyps and point to the need for additional pharmacological strategies.

Objective: Infiltration of inflammatory cells is believed to play a role in the development of nasal polyps.