MATERNAL STRESS DURING PREGNANCY ENHANCES ALLERGIC AIRWAY INFLAMMATION RISK IN THE OFFSPRING IN AN AIRWAYSENSITIZATION ASTHMA MODEL

E MORALES; GUIDO RATTAY; M PERRONE SIBILIA; VANESA SÁNCHEZ; ALEJANDRA GOLDMAN; FENOY I

Mar del Plata

Congreso; Reunion Anual Biociencias 2022- reunion SAI FAIC; 2022

RATIONALE: Allergic asthma is increasing worldwide. The presence of atopic diseases in the mother propagates the onset of allergic diseases in the offspring considerably stronger than atopic diseases of the father. Such observation challenges genetic predispositions as the sole cause for allergic diseases. Epidemiological studies suggest that caregiver stress in the perinatal period may predispose offspring to asthma. Using an OVA/alum intraperitoneal asthma model we have previously shown that maternal stress during pregnancy results in an increase of litter susceptibility to develop allergic lung inflammation. In this work we aim to study whether this phenomenon is still observed using an asthma model that involves airway allergen sensitization in the absence of adjuvant. METHODS: Pregnant BALB/c mice (day 15 and 17) were subjected to 2 restraint stress exposure. On week 6 after birth, offspring were treated intranasally with papain (30 μg) during 5 consecutive days. After 3 days allergic airway inflammation was evaluated (S group). Negative controls included offspring of non-stress dams subjected to the same protocol (C group) or treated with PBS (N group). RESULTS: Offspring of stress, but not control dams, showed increased eosinophils infiltrate in bronchoalveolar lavage (p＜0.05). Perinatal stress resulted in pathological changes of pulmonary allergic inflammation. These changes included eosinophils and mononuclear cell infiltration around airway and vessels with no goblet cell hyperplasia. This increase was accompanied by high levels of IL-5 in bronchoalveolar lavage fluid (p＜0.05). CONCLUSIONS: Maternal stress during pregnancy resulted in an increase of litter susceptibility to develop allergic lung inflammation in a natural exposure asthma model.