Altered pulmonary defense system in lung injury induced by didecyldimethylammonium chloride in mice

Abstract

Didecyldimethylammonium chloride (DDAC), a representative dialkyl-quaternary ammonium compound (QAC), could contaminate working atmospheres when used in disinfectant operation and adversely affect human health. Furthermore, the development of bacteria resistant to DDAC might become public health concern. We postulated that DDAC instillation in the lungs alters pulmonary antioxidant and antimicrobial responses and increases susceptibility to systemic administration of a bacterial component lipopolysaccharide (LPS). Mice were intratracheally instilled with DDAC and sacrificed 1, 3, or 7 days after treatment. Pulmonary cytotoxicity in recovered bronchoalveolar lavage was evident on Days 1 and 7, and inflammatory cell influx and interleukin-6 expression peaked on Day 7, in association with altered antioxidant and antimicrobial responses, as demonstrated by measuring heme oxygenase-1, glutathione peroxidase 2, lactoferrin, and mouse β-defensin-2 and -3 mRNA in the lung samples. The impaired defense system tended to enhance the inflammatory reaction caused by a systemic administration of LPS; the effect was in association with increased expression of toll-like receptor-4 mRNA. The results suggest that DDAC alters pulmonary defense system, which may contribute to susceptibility to an exogenous infectious agent.

Keywords::

• Heme oxygenase-1
• lactoferrin
• β-defensin
• toll-like receptor-4
• lipopolysaccharide
• dialkyl-quaternary ammonium

Acknowledgement

We would like to thank Yuko Chiba, Mutsumi Kumagai, Takako Kazami, Yukie Jibiki, Satoshi Akema, Chizuko Tomiyama, and Kayoko Iijima for their assistance in tissue preparation, and Yoshimi Kurosawa and Junya Sasaki for their assistance in cell count in the BAL fluid.

Declaration of interest

The authors declare no conflict of interest.