title: Single early prenatal lipopolysaccharide exposure prevents subsequent airway inflammation response in an experimental model of asthma.
abstract: OBJECTIVE
  There has been emerging interest in the prenatal determinants of respiratory disease. In utero factors have been reported to play a role in airway development, inflammation, and remodeling. Specifically, prenatal exposure to endotoxins might regulate tolerance to allergens later in life. The present study investigated whether prenatal lipopolysaccharide (LPS) administration alters subsequent offspring allergen-induced inflammatory response in adult rats.
  
  
  METHODS
  Pregnant Wistar rats were treated with LPS (100 μg/kg, i.p.) on gestation day 9.5 and their ovariectomized female offspring were sensitized and challenged with OVA later in adulthood. The bronchoalveolar lavage (BAL) fluid, peripheral blood, bone marrow leukocytes and passive cutaneous anaphylaxis were evaluated in these 75-day-old pups.
  
  
  RESULTS
  OVA sensitized pups of NaCl treated rats showed an increase of leucocytes in BAL after OVA challenge. This increase was attenuated, when mothers were exposed to a single LPS injection early in pregnancy. Thus, LPS prenatal treatment resulted in (1) lower increased total and differential (macrophages, neutrophils, eosinophils and lymphocytes) BAL cellularity count; (2) increased number of total, mononuclear and polymorphonuclear cells in the peripheral blood; and (3) no differences in bone marrow cellularity or passive cutaneous anaphylaxis.
  
  
  CONCLUSIONS
  In conclusion, female pups treated prenatally with LPS presented an attenuated response to experimentally-induced asthma. We observed reduced immune cell migration from peripheral blood to the lungs, with no effect on the production of bone marrow cells or antibodies. It was suggested that inflammatory events such as exposure to LPS in early fetal life can attenuate allergic inflammation in the lung, which is a common symptom in asthma.
authors.affiliation: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil. thik@hotmail.com
authors.forename: Thiago Berti
authors.initials: TB
authors.lastname: Kirsten
authors.forename: Beatriz Petri Soares
authors.initials: BP
authors.lastname: de Oliveira
authors.forename: Ana Paula Ligeiro
authors.initials: AP
authors.lastname: de Oliveira
authors.forename: Karin
authors.initials: K
authors.lastname: Kieling
authors.forename: Wothan Tavares
authors.initials: WT
authors.lastname: de Lima
authors.forename: João
authors.initials: J
authors.lastname: Palermo-Neto
authors.forename: Maria Martha
authors.initials: MM
authors.lastname: Bernardi
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001249:Asthma / Q000276:immunology*; D001854:Bone Marrow Cells; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D005260:Female; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology / Q000517:prevention & control*; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000633:toxicity*; D010047:Ovalbumin; D010052:Ovariectomy; D010323:Passive Cutaneous Anaphylaxis / Q000276:immunology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000276:immunology*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D008070:Lipopolysaccharides; D010047:Ovalbumin