PMID- 8977628
OWN - NLM
STAT- MEDLINE
DCOM- 19970121
LR  - 20191101
IS  - 0098-4108 (Print)
IS  - 0098-4108 (Linking)
VI  - 49
IP  - 6
DP  - 1996 Dec 27
TI  - Effect of influenza virus infection on ovalbumin-specific IgE responses to 
      inhaled antigen in the rat.
PG  - 619-30
AB  - Upper respiratory tract viral infections have been reported in clinical studies 
      to serve as risk factors for allergic sensitization. In order to study the 
      relationship linking influenza virus illnesses to development of allergy, murine 
      models of allergen sensitization were previously employed. These models showed 
      that lethal influenza viruses were able to trigger allergen-specific 
      immunoglobulin E (IgE) production and to inhibit tolerance to repeated exposure 
      to aerosolized allergen in the mouse. The disadvantage of these murine models 
      consists in the utilization of virulant and lethal strains of influenza virus. A 
      nonlethal rat-adapted influenza virus (RAIV) host resistance model has been 
      developed in our laboratory. It was used to evaluate the effect of influenza 
      virus infection on IgE responses to inhaled ovalbumin (OA) in the rat. The high 
      IgE-responder Brown-Norway (BN) rat was chosen for further study after comparing 
      the IgE response to OA in Fischer 344 (F344) and BN rats. On d 1, BN rats were 
      sensitized by administration of 1 mg OA subcutaneously alone or together with 
      aluminum hydroxide (200 mg) and Bordetella pertussis (15 x 10(9) killed bacilli 
      per rat in 1 ml), or only received saline. Rats were either infected with RAIV or 
      sham-infected on d 0 (24 h prior to sensitization) or on d 15, 17, or 57. Rats 
      were exposed for 3 min to aerosolized OA (OA 3% in phosphate-buffered saline) 
      every week, starting on d 18. Serum OA-specific IgE was evaluated by reverse 
      enzyme-linked immunosorbent assay (ELISA) 3 d after each OA challenge. BN rats 
      elicited a detectable OA-specific IgE response that decreased after repeated 
      aerosol exposures. Influenza virus infection transiently increased the 
      OA-specific IgE response when rats were immunized with OA alone and were infected 
      1 d prior to the first challenge and also when rats received only saline on d 1, 
      were exposed each week to aerosolized OA, and were infected prior to the seventh 
      challenge. These results, with data previously reported in mice, emphasize the 
      importance of upper respiratory tract viral infection in increasing IgE responses 
      to allergens and may be of importance in human disease.
FAU - Lebrec, H
AU  - Lebrec H
AD  - U.S. Environmental Protection Agency, Health Effects Research Laboratory, 
      Research Triangle Park, North Carolina, USA.
FAU - Sarlo, K
AU  - Sarlo K
FAU - Burleson, G R
AU  - Burleson GR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Toxicol Environ Health
JT  - Journal of toxicology and environmental health
JID - 7513622
RN  - 0 (Aerosols)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Administration, Inhalation
MH  - Aerosols
MH  - Animals
MH  - Disease Models, Animal
MH  - Female
MH  - Hypersensitivity/immunology
MH  - Immunoglobulin E/*biosynthesis
MH  - Injections, Subcutaneous
MH  - Orthomyxoviridae/*pathogenicity
MH  - Orthomyxoviridae Infections/physiopathology
MH  - Ovalbumin/administration & dosage/*toxicity
MH  - Rats
MH  - Rats, Inbred BN
MH  - Rats, Inbred F344
MH  - Risk Factors
MH  - Viral Plaque Assay
MH  - Virus Replication
EDAT- 1996/12/27 00:00
MHDA- 1996/12/27 00:01
CRDT- 1996/12/27 00:00
PHST- 1996/12/27 00:00 [pubmed]
PHST- 1996/12/27 00:01 [medline]
PHST- 1996/12/27 00:00 [entrez]
AID - 10.1080/009841096160664 [doi]
PST - ppublish
SO  - J Toxicol Environ Health. 1996 Dec 27;49(6):619-30. doi: 10.1080/009841096160664.