A novel mast cell‐dependent allergic peritonitis model. (20th June 2021) - Pahima, Hadas
Abstract: Typical murine models of allergic inflammation are induced by the combination of ovalbumin and aluminum hydroxide. However, accumulating evidence indicates that, in models of asthma and atopic dermatitis, allergic inflammation can be generated in the absence of aluminum hydroxide. Moreover, co‐administration of Staphylococcus aureus enterotoxin B with ovalbumin can enhance inflammation. The objective of this study was to establish a rapid and mast cell‐dependent murine model of allergic inflammation by inducing allergic peritonitis using ovalbumin and S. aureus enterotoxin B. Allergic peritonitis was induced in C57BL/6 mice by subcutaneous sensitization and intraperitoneal challenge with ovalbumin and S. aureus enterotoxin B. Disease characteristics were assessed by flow cytometry, enzyme‐linked immunosorbent assay (ELISA), trypan blue exclusion and colorimetric assays. The time–course of the allergic peritonitis revealed a peak of peritoneal inflammation 48 h after challenge, as assessed by total cells and eosinophil counts. The decrease of cell numbers started 96 h post‐challenge, with complete clearance within 168 h. Moreover, significantly higher levels of tryptase and increased vascular permeability were found 30 min following challenge. Allergic inflammation induction by ovalbumin and S. aureus enterotoxin B was impaired in mast cell‐deficient mice and partially restored by mice reconstitution with bone marrow‐derived mast cells, indicating the mast cell role in this model. We present a novel model of allergic peritonitis that is mast cell‐dependent, simple and robust. Moreover, the use of S. aureus enterotoxin B better resembles human allergic inflammation, which is known to be characterized by the colonization of S. aureus . Abstract : Novel murine, mast cells‐dependent model of allergic peritonitis, induced by ovalbumin and Staphylococcus aureus enterotoxin B. This model displays rapid mast cell activation, as detected by the release of tryptase and TNFα 30min after challenge. Thereafter, the peak of inflammation occurs 48h later, as demonstrated by eosinophil recruitment and increase of cell numbers in the peritoneal cavity.