Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2003 Dec;110(4):493-500.
doi: 10.1111/j.1365-2567.2003.01757.x.

Parental allergic status influences the risk of developing allergic sensitization and an asthmatic-like phenotype in canine offspring

Edward G Barrett  1 , Karin Rudolph, Larry E Bowen, David E Bice
Affiliations

Parental allergic status influences the risk of developing allergic sensitization and an asthmatic-like phenotype in canine offspring

Edward G Barrett et al. Immunology. 2003 Dec.

Abstract

Increasing evidence suggests that parental allergic status, especially that of the mother, may play a unique and important role in influencing the development of fetal infant immune responses to inhaled allergens, independently of genetic predisposition. We have developed an experimental model in dogs where the offspring from allergic parents, when exposed to inhaled allergen, develop allergic sensitization and an asthmatic phenotype, whereas the offspring from non-allergic parents do not. Offspring from ragweed-sensitized (two litters, n = 10) or non-sensitized (two litters, n = 11) Beagle dogs were exposed repeatedly, by inhalation, to ragweed or filtered air (negative control) beginning within 1 week after birth. Serum levels of total immunoglobulin (Ig)E, and ragweed-specific IgE and IgG, were measured at specific time-points up to 40 weeks after birth. Cell differentials in the bronchoalveolar lavage were determined on days 1 and 4 following ragweed instillation into the offspring's lungs at 26 weeks of age. Changes in pulmonary resistance following challenge with histamine and ragweed (five breaths) were measured at 40 weeks after birth. Offspring from sensitized parents exposed to ragweed developed elevated serum total IgE and ragweed-specific IgE and IgG, and showed an increased pulmonary resistance to histamine and ragweed, and increased numbers of eosinophils in bronchoalveolar lavage. In contrast, offspring from non-sensitized parents did not exhibit this immune response. These results suggest that parental allergic sensitivity is important in the development of allergic sensitization and an asthmatic phenotype in the offspring.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Offspring were exposed to ragweed (RW) by inhalation, repeatedly after birth. Blood was collected periodically to measure serum antibody levels. At 24 weeks of age, a baseline bronchoalveolar lavage (BAL) was performed. Approximately 4 weeks later, RW was instilled into six different lung lobes (100 µg each), and BAL was performed 1 and 4 days afterwards. Pulmonary resistance (RL) to histamine, and RW challenge (five breaths), was measured in offspring when ≈26 and 40 weeks of age.
Figure 2
Figure 2
Serum total immunoglobulin E (IgE) (a, b), ragweed (RW)-specific IgE (c, d) and immunoglobulin G (IgG) (e, f) levels in offspring, exposed to either RW or air (control), from non-allergic (a, c, e) or allergic (b, d, f) parents. After the collection of blood at 28 weeks of age, dogs were challenged by instillation with RW, and further blood samples were collected on day 1 (d1) and day 4 (d4) after challenge. *P < 0·05 versus control. #P < 0·05 versus non-allergic [one-way analysis of variance (anova) with Tukey multiple comparison post-test]. Linear trend post-test analysis using 12–28 week samples (†P < 0·05). Linear trend analysis for RW-specific IgE did not reach statistical significance (P = 0·08). All error bars are expressed as mean + standard error of the mean (SEM).
Figure 3
Figure 3
Serum ragweed (RW)-specific immunoglobulin G1 (IgG1) (a) and immunoglobulin G4 (IgG4) (b) levels in offspring (from allergic parents) exposed to either RW or air (control). After the collection of blood at 28 weeks of age, dogs were challenged by instillation with RW, and further blood samples were collected on day 1 (d1) and day 4 (d4) after challenge. No statistically significant differences were determined by one-way one-way analysis of variance (anova) with Tukey multiple comparison post-test. Linear trend post-test analysis using 12–28 week samples (†P < 0·05).
Figure 4
Figure 4
Numbers of eosinophils (a) and neutrophils (b) in bronchoalveolar lavage (BAL) from offspring following ragweed (RW) instillation into the lung at 28 weeks of age. *P < 0·05 versus non-sensitized and baseline values. #P < 0·05 versus all treatment groups [one-way analysis of variance (anova) with Tukey multiple comparison post-test].
Figure 5
Figure 5
Changes in pulmonary resistance after histamine (a, b) and ragweed (RW) (c, d) challenge in offspring (26 weeks of age) from non-allergic (a, c) or allergic (b, d) parents. *P < 0·05 versus control group [one-way analysis of variance (anova) with Tukey multiple comparison post-test].
Figure 6
Figure 6
Changes in pulmonary resistance after histamine (a) and ragweed (RW) (b) challenge in offspring (40 weeks of age) from allergic parents. Numbers in parentheses above the bars indicate the number of offspring challenged at that dose. Some offspring were too reactive to safely challenge at the higher doses. Thus, these results probably underestimate the magnitude of the true average response at the higher doses. *P < 0·05 versus the control group [one-way analysis of variance (anova) with Tukey multiple comparison post-test].
See this image and copyright information in PMC

Comment in

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Ruiz RG, Richards D, Kemeny DM, Price JF. Neonatal IgE: a poor screen for atopic disease. Clin Exp Allergy. 1991;21:467. - PubMed
    1. Aberg N. Familial occurrence of atopic disease: genetic versus environmental factors. Clin Exp Allergy. 1993;23:829. - PubMed
    1. Omran M, Russell G. Continuing increase in respiratory symptoms and atopy in Aberdeen schoolchildren. Br Med J. 1996;312:34. - PMC - PubMed
    1. Martinez FD. Maternal risk factors in asthma. Ciba Found Symp. 1997;206:233. - PubMed
    1. Holberg CJ, Morgan WJ, Wright AL, Martinez FD. Differences in familial segregation of FEV1 between asthmatic and nonasthmatic families. Role of a maternal component. Am J Respir Crit Care Med. 1998;158:162. - PubMed

MeSH terms