Formaldehyde inhalation during pregnancy abolishes the development of acute innate inflammation in offspring

Author(s)

Ibrahim, Beatriz Silva ^[1] ; da Silva, Cristiane Miranda ^[2] ; Barioni, Eric Diego ^[1] ; Correa-Costa, Matheus ^[3] ; Drewes, Carine Cristiane ^[1] ; Saraiva Camara, Niels Olsen ^[3] ; Tavares-de-Lima, Wothan ^[4] ; Poliselli Farsky, Sandra Helena ^[1] ; Lino-dos-Santos-Franco, Adriana ^[2]

Affiliation

^[1] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Clin & Toxicol Anal, Sao Paulo - Brazil

^[2] Univ Nove Julho UNINOVE, Post Grad Program Biophoton Appl Hlth Sci, BR-01504000 Sao Paulo - Brazil

^[3] Univ Sao Paulo, Dept Immunol, Sao Paulo - Brazil

^[4] Univ Sao Paulo, Dept Pharmacol, Sao Paulo - Brazil

• Document type: Journal article
• Source: Toxicology Letters; v. 235, n. 2, p. 147-154, JUN 1 2015.
• Web of Science Citations: 11

Abstract

Formaldehyde (FA) is an environmental and occupational pollutant that induces programming mechanisms on the acquired immune host defense in offspring when exposed during the prenatal period. Hence, here we investigated whether the exposure of FA on pregnant rats could affect the development of an innate acute lung injury in offspring induced by lipopolissacaride (LPS) injection. Pregnant Wistar rats were exposed to FA (0.92 mg/m(3)) or vehicle (distillated water), both 1 h/day, 5 days/week, from 1 to 21 days of pregnancy. Non-manipulated rats were used as control. After 30 days of birth, the offspring was submitted to injection of LPS (Salmonella abortus equi, 5 mg/kg, i.p.). Systemic and lung inflammatory parameters were evaluated 24 h later. Exposure to FA during gestation abolished the development of acute lung injury in offspring, as observed by reduced number of leukocytes in the bronchoalveolar fluid (BAL), in the blood and in the bone marrow, and decreased myeloperoxidase activity in the lung. Moreover, phagocytes from BAL presented normal phagocytosis, but reduced oxidative burst. Alterations on the profile of inflammatory cytokines were evidenced by reduced mRNA levels of IL-6 and elevated levels of IL-10 and IFN gamma in the lung tissue. Indeed, mRNA levels of toll-likereceptor-4 and nuclear factor-kappa B translocation into the nucleus were also reduced. Additionally, hyperresponsiveness to methacholine was blunted in the trachea of offspring of FA exposed mothers. Together, our data clearly show that FA exposure in the prenatal period modifies the programming mechanisms of the innate defense in the offspring leading to impaired defense against infections. (C) 2015 Elsevier Ireland Ltd. All rights reserved. (AU)

• FAPESP's process: 13/19708-3 - Evaluation of the impact of intrauterine exposure to formaldehyde in the development of pulmonary infection in the offspring
• Grantee: Beatriz Silva Ibrahim
• Support Opportunities: Scholarships in Brazil - Scientific Initiation