MATERNAL STRESS DURING PREGNANCY ENHANCES ALLERGIC AIRWAY INFLAMMATION RISK IN THE OFFSPRING

MARÍA DE LOS ÁNGELES ALDIRICO, FLORENCIA MAGALÍ GIORGIO, ARIADNA SOLEDAD SOTO, MARIANO SERGIO PICCHIO, MATÍAS DAMIÁN PERRONE SIBILIA, VANESA ROXANA SANCHEZ, NADIA ARCON, VALENTINA MARTIN, ALEJANDRA GOLDMAN, IGNACIO MARTÍN FENOY

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

RATIONALE: Allergicasthma is increasing worldwide. The presence of atopic diseases in the motherpropagates the onset of allergic diseases in the offspring considerablystronger than atopic diseases of the father. Such observation challengesgenetic predispositions as the sole cause for allergic diseases.Epidemiological studies suggest that caregiver stress in the perinatal periodmay predispose offspring to asthma. At the moment only three groups havestudied the link between prenatal stress and asthma severity/susceptibility inmurine models. To further study this phenomenon we aim to establish a micemodel of maternal stress and neonatal asthma susceptibility. METHODS: Pregnant BALB/c mice (day 15)were subjected to a single restraint stress exposure. On day 4 after birth,pups were treated with a suboptimal sensitization protocol (single i.p.injection of ovalbumin (OVA) in alum) prior to antigen aerosol challenge (days12-14) and evaluation of allergic airway inflammation (day 16) (S group).Negative controls included pups of non-stress dams subjected to the samesuboptimal protocol (C group) or i.p. sensitized and aerosol challenged withPBS (N group). RESULTS: Offspring ofstress, but not control dams, showed increased eosinophils infiltrate inbronchoalveolar lavage (p<0.05). Perinatal stress resulted in pathologicalchanges of pulmonary allergic inflammation. These changes included eosinophilsand mononuclear cell infiltration around airway and vessels and goblet cellhyperplasia. An increase in serum anti-OVA IgE antibodies was detected in pups ofstress, but not of control dams (p<0.05). This increase was accompanied by highlevels of IL-4 and IL-5 in bronchoalveolar lavage fluid (p<0.05). CONCLUSIONS: Maternal stress duringpregnancy resulted in an increase of litter susceptibility to develop allergiclung inflammation