PMID- 14616121
OWN - NLM
STAT- MEDLINE
DCOM- 20040409
LR  - 20190823
IS  - 0105-4538 (Print)
IS  - 0105-4538 (Linking)
VI  - 58
IP  - 11
DP  - 2003 Nov
TI  - Immunoglobulin E is not required for but enhances airway inflammation and 
      hyperresponsiveness.
PG  - 1117-24
AB  - The aim of this study was to investigate the role of immunoglobulin E (IgE) in 
      the late phase reaction (LPR) of murine experimental asthma. Our model consisted 
      of an implant of DNP-conjugated, heat-coagulated hen's egg white (DNP-EWI), 
      followed 14 days later by an intratracheal challenge with aggregated 
      DNP-ovalbumin. Airway inflammation was analyzed 48 h after challenge and compared 
      with a similarly immunized group of mice with highly suppressed humoral response 
      due to anti-micro and anti-delta antibody treatment. Total number of cells in the 
      bronchoalveolar lavage (BAL) (with predominance of eosinophils) and EPO activity 
      in the lung homogenate were increased in the DNP-EWI-immunized group compared 
      with immunosuppressed or nonimmunized mice. However, the cellular infiltration 
      and EPO activity observed in the immunosuppressed group were still significantly 
      above those obtained in the nonimmunized group, indicating that inhibition of 
      antibody production did not completely prevent the inflammatory manifestations in 
      BAL and lung. Airway hyperresponsiveness to methacoline was obtained in 
      DNP-EWI-immunized mice, but the respiratory mechanical parameters returned to 
      normal levels in the immunosuppressed group. When these mice were reconstituted 
      with monoclonal anti-DNP antibodies, only IgE, but not IgG1, restored lung 
      inflammation and decreased the conductance of the respiratory system, therefore, 
      increasing hyperresponsiveness. These results indicate that antibodies are not 
      essential for induction of LPR in the lung. However, IgE enhances pulmonary 
      inflammation and hyperresponsiveness.
FAU - Itami, D M
AU  - Itami DM
AD  - Laboratory of Immunopathology, Butantan Institute, Sao Paulo, Brazil.
FAU - Latinne, D
AU  - Latinne D
FAU - Bazin, H
AU  - Bazin H
FAU - Garcia, M L B
AU  - Garcia ML
FAU - Perini, A
AU  - Perini A
FAU - Martins, M A
AU  - Martins MA
FAU - Macedo, M S
AU  - Macedo MS
FAU - Macedo-Soares, M F
AU  - Macedo-Soares MF
LA  - eng
PT  - Journal Article
PL  - Denmark
TA  - Allergy
JT  - Allergy
JID - 7804028
RN  - 0 (Dinitrophenols)
RN  - 0 (Immunoglobulins)
RN  - 0 (dinitrophenol-ovalbumin)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9006-59-1 (Ovalbumin)
RN  - EC 1.11.1.- (Eosinophil Peroxidase)
RN  - EC 1.11.1.- (Peroxidases)
SB  - IM
MH  - Animals
MH  - *Antibody Formation
MH  - Asthma/immunology/pathology/*physiopathology
MH  - Bronchial Hyperreactivity/*immunology/physiopathology
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Cell Count
MH  - Dinitrophenols/immunology
MH  - Egg White
MH  - Eosinophil Peroxidase
MH  - Eosinophils/enzymology/pathology
MH  - Immunoglobulin E/*immunology
MH  - Immunoglobulins/blood
MH  - Inflammation
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Ovalbumin/immunology
MH  - Peroxidases/metabolism
EDAT- 2003/11/18 05:00
MHDA- 2004/04/10 05:00
CRDT- 2003/11/18 05:00
PHST- 2003/11/18 05:00 [pubmed]
PHST- 2004/04/10 05:00 [medline]
PHST- 2003/11/18 05:00 [entrez]
AID - 206 [pii]
AID - 10.1034/j.1398-9995.2003.00206.x [doi]
PST - ppublish
SO  - Allergy. 2003 Nov;58(11):1117-24. doi: 10.1034/j.1398-9995.2003.00206.x.