Ligation of IgE receptors causes an anaphylactic response and neutrophil infiltration but does not induce eosinophilic inflammation in mice

Masayuki Kaneko, Andrew Schimming, Gerald J. Gleich, Hirohito Kita

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Eosinophils are selectively recruited into the tissues during chronic allergic inflammation. IgE is considered an initiator of the allergic reaction; however, the roles of IgE in allergic inflammation are not fully understood. Objective: We tested the hypothesis that antigen interaction with specific IgE antibody provokes eosinophilic inflammation. Methods: BALB/c mice were actively sensitized with ragweed extract and passively sensitized with anti-dinitrophenyl (anti-DNP) mouse IgE and challenged intraperitoneally by injecting either ragweed extract or DNP- ovalbumin (OVA). Immediate anaphylactic responses were examined by monitoring vascular permeability and by measuring histamine content in peritoneal lavage fluids. Late-phase allergic responses were examined by total cell counts and cell differentials. Results: Mice sensitized and challenged with ragweed showed immediate anaphylactic responses followed by temporal increases in neutrophils at 3 to 12 hours and sustained increases in eosinophils in their peritoneal cavities after 24 hours. Double-sensitized mice (ie, sensitized actively for ragweed and passively for DNP-OVA) challenged with ragweed showed immediate anaphylactic responses and peritoneal eosinophilia at 48 hours. Double-sensitized mice challenged with DNP-OVA showed comparable immediate anaphylactic responses but no peritoneal eosinophilia. Furthermore, at 8 hours, ragweed-challenged animals recruited both eosinophils and neutrophils, but DNP-OVA-challenged animals recruited only neutrophils. Finally, after active sensitization and challenge with ragweed, mast cell- deficient mice (WBB6F1-W/W(v)) lacked the immediate response but showed comparable eosinophil accumulation as their litter mate controls (WBB6F1- +/+). Conclusion: Interaction of antigen with IgE antibody is insufficient to provoke eosinophilic inflammation in mice.

Original languageEnglish (US)
Pages (from-to)1202-1210
Number of pages9
JournalJournal of Allergy and Clinical Immunology
Volume105
Issue number6 I
DOIs
StatePublished - 2000
Externally publishedYes

Fingerprint

Ambrosia
IgE Receptors
Neutrophil Infiltration
Ligation
Inflammation
Immunoglobulin E
Eosinophils
Neutrophils
Eosinophilia
Peritoneal Lavage
Antigens
Antibodies
Ascitic Fluid
Peritoneal Cavity
Capillary Permeability
Mast Cells
Histamine
Hypersensitivity
Cell Count
dinitrophenol-ovalbumin

Keywords

  • Allergen
  • Hypersensitivity
  • IgE
  • Inflammation
  • Mast cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Ligation of IgE receptors causes an anaphylactic response and neutrophil infiltration but does not induce eosinophilic inflammation in mice. / Kaneko, Masayuki; Schimming, Andrew; Gleich, Gerald J.; Kita, Hirohito.

In: Journal of Allergy and Clinical Immunology, Vol. 105, No. 6 I, 2000, p. 1202-1210.

Research output: Contribution to journalArticle

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abstract = "Background: Eosinophils are selectively recruited into the tissues during chronic allergic inflammation. IgE is considered an initiator of the allergic reaction; however, the roles of IgE in allergic inflammation are not fully understood. Objective: We tested the hypothesis that antigen interaction with specific IgE antibody provokes eosinophilic inflammation. Methods: BALB/c mice were actively sensitized with ragweed extract and passively sensitized with anti-dinitrophenyl (anti-DNP) mouse IgE and challenged intraperitoneally by injecting either ragweed extract or DNP- ovalbumin (OVA). Immediate anaphylactic responses were examined by monitoring vascular permeability and by measuring histamine content in peritoneal lavage fluids. Late-phase allergic responses were examined by total cell counts and cell differentials. Results: Mice sensitized and challenged with ragweed showed immediate anaphylactic responses followed by temporal increases in neutrophils at 3 to 12 hours and sustained increases in eosinophils in their peritoneal cavities after 24 hours. Double-sensitized mice (ie, sensitized actively for ragweed and passively for DNP-OVA) challenged with ragweed showed immediate anaphylactic responses and peritoneal eosinophilia at 48 hours. Double-sensitized mice challenged with DNP-OVA showed comparable immediate anaphylactic responses but no peritoneal eosinophilia. Furthermore, at 8 hours, ragweed-challenged animals recruited both eosinophils and neutrophils, but DNP-OVA-challenged animals recruited only neutrophils. Finally, after active sensitization and challenge with ragweed, mast cell- deficient mice (WBB6F1-W/W(v)) lacked the immediate response but showed comparable eosinophil accumulation as their litter mate controls (WBB6F1- +/+). Conclusion: Interaction of antigen with IgE antibody is insufficient to provoke eosinophilic inflammation in mice.",
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N2 - Background: Eosinophils are selectively recruited into the tissues during chronic allergic inflammation. IgE is considered an initiator of the allergic reaction; however, the roles of IgE in allergic inflammation are not fully understood. Objective: We tested the hypothesis that antigen interaction with specific IgE antibody provokes eosinophilic inflammation. Methods: BALB/c mice were actively sensitized with ragweed extract and passively sensitized with anti-dinitrophenyl (anti-DNP) mouse IgE and challenged intraperitoneally by injecting either ragweed extract or DNP- ovalbumin (OVA). Immediate anaphylactic responses were examined by monitoring vascular permeability and by measuring histamine content in peritoneal lavage fluids. Late-phase allergic responses were examined by total cell counts and cell differentials. Results: Mice sensitized and challenged with ragweed showed immediate anaphylactic responses followed by temporal increases in neutrophils at 3 to 12 hours and sustained increases in eosinophils in their peritoneal cavities after 24 hours. Double-sensitized mice (ie, sensitized actively for ragweed and passively for DNP-OVA) challenged with ragweed showed immediate anaphylactic responses and peritoneal eosinophilia at 48 hours. Double-sensitized mice challenged with DNP-OVA showed comparable immediate anaphylactic responses but no peritoneal eosinophilia. Furthermore, at 8 hours, ragweed-challenged animals recruited both eosinophils and neutrophils, but DNP-OVA-challenged animals recruited only neutrophils. Finally, after active sensitization and challenge with ragweed, mast cell- deficient mice (WBB6F1-W/W(v)) lacked the immediate response but showed comparable eosinophil accumulation as their litter mate controls (WBB6F1- +/+). Conclusion: Interaction of antigen with IgE antibody is insufficient to provoke eosinophilic inflammation in mice.

AB - Background: Eosinophils are selectively recruited into the tissues during chronic allergic inflammation. IgE is considered an initiator of the allergic reaction; however, the roles of IgE in allergic inflammation are not fully understood. Objective: We tested the hypothesis that antigen interaction with specific IgE antibody provokes eosinophilic inflammation. Methods: BALB/c mice were actively sensitized with ragweed extract and passively sensitized with anti-dinitrophenyl (anti-DNP) mouse IgE and challenged intraperitoneally by injecting either ragweed extract or DNP- ovalbumin (OVA). Immediate anaphylactic responses were examined by monitoring vascular permeability and by measuring histamine content in peritoneal lavage fluids. Late-phase allergic responses were examined by total cell counts and cell differentials. Results: Mice sensitized and challenged with ragweed showed immediate anaphylactic responses followed by temporal increases in neutrophils at 3 to 12 hours and sustained increases in eosinophils in their peritoneal cavities after 24 hours. Double-sensitized mice (ie, sensitized actively for ragweed and passively for DNP-OVA) challenged with ragweed showed immediate anaphylactic responses and peritoneal eosinophilia at 48 hours. Double-sensitized mice challenged with DNP-OVA showed comparable immediate anaphylactic responses but no peritoneal eosinophilia. Furthermore, at 8 hours, ragweed-challenged animals recruited both eosinophils and neutrophils, but DNP-OVA-challenged animals recruited only neutrophils. Finally, after active sensitization and challenge with ragweed, mast cell- deficient mice (WBB6F1-W/W(v)) lacked the immediate response but showed comparable eosinophil accumulation as their litter mate controls (WBB6F1- +/+). Conclusion: Interaction of antigen with IgE antibody is insufficient to provoke eosinophilic inflammation in mice.

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