9-3OAS Prenatal Exposure to Farm Bacteria Protects Against Offspring Asthma

Friday, 16 October 2015: 16:00 - 16:15
Room R2 ABC (Floor 3) (Coex Convention Center)

Melanie Lynn Conrad, PhD , Charité Medical University, Berlin, Germany

Gail Deutsch , Seattle Children's Hospital, Seattle, WA

Harald Renz , Philipps University, Marburg, Germany

Holger Garn , Philipps University, Marburg, Germany

Sandra M. Blois , Charité Medical University, Berlin, Germany

Background:  Environmental exposures during critical developmental time points can influence allergy susceptibility later in life. Demonstrating this, epidemiological studies associate prenatal exposure to a farming environment with protection against childhood asthma; however, the mechanisms that underlie this phenomenon are currently unknown. The aim of this study is to use a murine ‘proof of concept’ model to investigate prenatal influences on offspring allergy susceptibility.

Methods: To examine prenatal protection against allergy, pregnant mice were exposed throughout pregnancy to the non-pathogenic, farm-associated bacteria Acinetobacter lwoffii, and then experimental asthma was induced in the offspring. In a second experiment, we analyzed the lung histology of gestation day 17.5 fetuses from control and bacterially treated pregnant mice.

Results: Offspring prenatally exposed to A.lwoffiihad a less severe asthma phenotype compared to control asthmatic offspring. This was shown by significantly decreased airway reactivity, decreased eosinophil influx into the lungs and decreased lung inflammation. No difference was seen in allergen specific IgE and IgG1 antibody titers between prenatal control and prenatally exposed offspring [1]. Examination of gestation day 17.5 fetal lungs indicated no major structural differences in fetuses from control or bacterially exposed pregnant mice.

Conclusions: Though there is much evidence that prenatal farming exposures are associated with protection against asthma in the offspring, little is known about the mechanisms that contribute to this process. Our prenatal protection model demonstrates a reduced asthma phenotype in offspring prenatally exposed to farming bacteria, however, no differences were seen in gestation day 17.5 lung development.

1. Conrad ML, Ferstl R, Teich R, Brand S, Blumer N, Yildirim AO, Patrascan CC, Hanuszkiewicz A, Akira S, Wagner H, Holst O, von Mutius E, Pfefferle PI, Kirschning CJ, Garn H, Renz H. Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78. J Exp Med. 2009 Dec 21;206(13):2869-77.