Immunohistochemical study on changes of mast cell populations during allergic airway inflammation in mice using HDM model

Backround: It is necessary to clarify wheather murine asthma models display key features found in human asthma.

Aims and Objectives: MCs play a role in allergic asthma by releasing numerous mediators. They are located in human lungs with changes in their distribution during allergic airway inflammation. TLR-2 and TLR-3 agonists interact with MCs, resulting in altered inflammatory processes. Here we studied numeral and phenotypical changes of MCs in lung compartments in mice under allergic conditions and treatment with TLR-agonists.

Methods: Using a HDM model of allergic airway inflammation BALB/c mice were exposed to HDM intranasally. The additional treatments followed either with Pam3CSK4 or with Poly (I: C). Double staining against tryptase and mMCP-4 was used to detect mast cell phenotypes and PGP9.5 assigned nerve fibres.

Results: HDM and TLR-agonists treatment caused increases in total MC numbers (bronchus: saline 4.78 ± 2,8 vs. HDM 24.48 ± 7.1 p < 0.001; alveoli: saline 0.41 ± 0.3 vs. HDM 5.21 ± 2.0 p < 0.001; vessels: saline 1.47 ± 1.2 vs. HDM 18.98 ± 8.4 p < 0.001; nerves: not significant). Phenotypical changes assigned by elevated mMCP-4 expression appeared in bronchi (saline 0.08 ± 0.1 vs. HDM 1.72 ± 0.4 p < 0.01) and alveolar region (saline 0.02 ± 0.03 vs. HDM 0.19 ± 0.1 p < 0.05). No phenotypical changes appeared in vessels and nerves. BAL shows strong eosinophil recruitment compared to control group, but diminished in Pam3CSK4 treated animals.

Conclusion: HDM mouse model shares some characteristic features found in humans in regard to mast cell morphology. Pam3CSK4 might have protective functions in this model.