Fipronil induces lung inflammation in a mouse model (LB508)

• Published in: The FASEB journal 2014-04, Vol.28 (S1), p.n/a
• Main Authors: Merkowsky, Kaitlin, Singh, Baljit, Gill, J.P.S., Sethi, R.S.
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.28.1_supplement.lb508

Fipronil is an insecticide present in anti‐flea and tick products used on household pets and on crops. Fipronil kills organisms by blocking the GABA‐gated chloride channels. Presently, very little data exists on the pulmonary impact of fipronil on mammals who may be exposed through inhalation, especially in situations where workers do not wear masks during sprays. We used a mouse model to investigate the pulmonary effects of oral or intranasal fipronil (8 mg/kg/bw for 7 days; n=15). Control mice (n=9) were given either ethanol (intranasal) or groundnut oil (oral) for 7 days. Hemotoxylin and eosin stained lung sections showed accumulation of inflammatory cells and changes in lung architecture in both the oral and intranasal groups compared to the controls. To determine whether exposure to fipronil may change susceptibility to bacterial infections through alterations of Toll‐like receptors (TLRs), TLR4 and 9 immunohistochemistry was performed. TLR4 was present in the nucleus of epithelium cells in the oral group and a robust staining observed in the alveolar septum, blood vessel and bronchial epithelium of the intranasal group. Increased TLR9 staining in the alveolar macrophages and septa was observed in the fipronil exposed groups compared to the control groups. We have also tested the effects of fipronil (5.72 um/1 ml) on U937 macrophage cell line, which reduced the viability of these cells. These data suggest that fipronil induces lung inflammation in vivo and cell death in vitro. Furthermore, the increased expression of TLR4 and TLR9 may increase susceptibility for bacterial lung inflammation.