INTRODUCTION
Allergic diseases such as asthma, atopic dermatitis (AD), allergic
rhinitis (AR) and food allergy affect ~20% of the
population worldwide (1). The most prominent cells involved in allergy
are the mast cells (MCs), considered the primum movens of the
reaction upon their activation by IgE-allergen, followed by the
eosinophils (Eos), that heavily contribute to the inflammatory outcome.
Moreover, their soluble and physical crosstalk that we identified and
named the Allergic Effector Unit (AEU), is a key factor increasing the
pro-inflammatory potential of the two cells and hence the allergic
inflammation (AI) (2, 3). In addition, several reports have shown the
nearly exclusive presence of S. aureus (SA) and its exotoxins,
such as SA enterotoxin B (SEB) and others in asthma, AR, food allergy
and AD (4–6). Interestingly, SA was found to directly bind and activate
MCs (7) and Eos (8).
Until recently, the most common protocol used in the investigation of AI
in mice involved the use of the antigen ovalbumin (OVA), together with
aluminum hydroxide (Alum). However, it was shown that Alum can activate
the innate immune response by activating the NLRP3 inflammasome through
increasing uric acid levels (9). Furthermore, Alum was found to induce
AI via activation of dendritic cells (DCs) independently of MCs (10).
Indeed, it was shown that 24h following intraperitoneal (i.p) injection,
DCs and neutrophils were detected and increased during the inflammation
in the peritoneal cavity, while MCs and macrophages, typical resident
cells, decreased (10). In addition, Alum co-administration with an
antigen was demonstrated not to be necessary for the induction of acute
allergic airway inflammation (11) and of AD (12).
Noteworthy, BALB/C mice are often used in AI studies since they are
prone to Th2 responses. Nevertheless, C57BL6 are employed more often
because of the availability of transgenic and knockout (KO) strains
based on their background (13, 14).
Therefore, our aim was to develop a mast cell-dependent, rapid and
reproducible model of AI with the closest features to human Th2 allergic
diseases in C57BL6 mice. Hence, we established an allergic peritonitis
(AP) model by employing sensitization and challenge with OVA and SEB.