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A novel mast cell-dependent allergic peritonitis model
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Background: 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 S. aureus enterotoxin
B with ovalbumin can enhance inflammation. Objective: 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. Methods: 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, ELISA, Trypan
Blue exclusion and colorimetric assays. Results: Time course of the
allergic peritonitis revealed a peak of peritoneal inflammation 48h
after challenge, as assessed by total cells and eosinophil counts.
Decrease of cell numbers started 96h post challenge with complete
clearance within 168h. 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 cells deficient mice and partially
restored by mice reconstitution with bone marrow derived mast cells,
indicating the mast cell role in this model. Conclusion: 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 Staphylococcus aureus.
Title: A novel mast cell-dependent allergic peritonitis model
Description:
Background: 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 S.
aureus enterotoxin
B with ovalbumin can enhance inflammation.
Objective: 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.
Methods: 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, ELISA, Trypan
Blue exclusion and colorimetric assays.
Results: Time course of the
allergic peritonitis revealed a peak of peritoneal inflammation 48h
after challenge, as assessed by total cells and eosinophil counts.
Decrease of cell numbers started 96h post challenge with complete
clearance within 168h.
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 cells deficient mice and partially
restored by mice reconstitution with bone marrow derived mast cells,
indicating the mast cell role in this model.
Conclusion: 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 Staphylococcus aureus.
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