PMID- 10340953
OWN - NLM
STAT- MEDLINE
DCOM- 19990707
LR  - 20131121
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 20
IP  - 6
DP  - 1999 Jun
TI  - Dissociation of airway hyperresponsiveness from immunoglobulin E and airway 
      eosinophilia in a murine model of allergic asthma.
PG  - 1326-34
AB  - Nonspecific airway hyperresponsiveness (AHR) is a hallmark of human asthma. Both 
      airway eosinophilia and high serum levels of total and antigen-specific 
      immunoglobulin E (IgE) are associated with AHR. It is unclear, however, whether 
      either eosinophilia or increased IgE levels contribute directly to, or predict, 
      the development of AHR. Investigations conducted with various murine models of 
      asthma and different mouse strains have resulted in conflicting evidence about 
      the roles that IgE and airway eosinophilia play in the manifestation of AHR. We 
      show that systemic priming with ovalbumin (OVA) in alum, followed by a single day 
      of OVA aerosol challenge, is sufficient to induce AHR, as measured by increased 
      pulmonary resistance in response to intravenously delivered methacholine in 
      BALB/c, but not C57BL/6 or B6D2F1, mice. This was observed despite the fact that 
      OVA-challenged BALB/c mice had less airway eosinophilia and smaller increases in 
      total IgE than either C57BL/6 or B6D2F1 mice, and had less pulmonary inflammation 
      and OVA-specific IgE than B6D2F1 mice. We conclude that airway eosinophilia, 
      pulmonary inflammation, and high serum levels of total or OVA-specific IgE are 
      all insufficient to induce AHR in C57BL/6 and B6D2F1 mice, whereas BALB/c mice 
      demonstrate AHR in the absence of airway eosinophilia. These data confirm that 
      the development of AHR is genetically determined, not only in naive mice, but 
      also in actively immunized ones, and cannot be predicted by levels of airway 
      eosinophilia, pulmonary inflammation, total IgE, or antigen-specific IgE.
FAU - Wilder, J A
AU  - Wilder JA
AD  - Department of Pathology, University of New Mexico, Albuquerque, New Mexico 87131, 
      USA. jwilder@salud.unm.edu
FAU - Collie, D D
AU  - Collie DD
FAU - Wilson, B S
AU  - Wilson BS
FAU - Bice, D E
AU  - Bice DE
FAU - Lyons, C R
AU  - Lyons CR
FAU - Lipscomb, M F
AU  - Lipscomb MF
LA  - eng
GR  - 5 P50 HL56384/HL/NHLBI NIH HHS/United States
GR  - 5T32 8HL 07733/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Bronchoconstrictor Agents)
RN  - 0W5ETF9M2K (Methacholine Chloride)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Asthma/genetics/*immunology
MH  - Bronchoconstrictor Agents/pharmacology
MH  - Cell Movement
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Eosinophilia/*immunology
MH  - Humans
MH  - Immunoglobulin E/*immunology
MH  - Inflammation
MH  - Lung/immunology/pathology
MH  - Methacholine Chloride/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Ovalbumin/immunology
MH  - Respiratory Hypersensitivity/*immunology
EDAT- 1999/05/26 00:00
MHDA- 1999/05/26 00:01
CRDT- 1999/05/26 00:00
PHST- 1999/05/26 00:00 [pubmed]
PHST- 1999/05/26 00:01 [medline]
PHST- 1999/05/26 00:00 [entrez]
AID - 10.1165/ajrcmb.20.6.3561 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1999 Jun;20(6):1326-34. doi: 10.1165/ajrcmb.20.6.3561.