diisononyl-phthalate and Encephalitis

Diisononyl phthalate (DINP) and formaldehyde both are associated with asthma and allergies. However, it is unclear about the adverse effect of DINP and formaldehyde exposure on the brain for asthma patients. Here, we determined the effect of DINP and/or formaldehyde exposure on neuroinflammation in brain by a murine asthma model and investigated the underlying mechanisms. Mice were exposed to formaldehyde and/or DINP and sensitization with ovalbumin. The results show that exposure to formaldehyde and/or DINP not only exacerbated allergic asthma-like symptoms, but also promoted neuroinflammation in brain. The incrassation of the airway wall and exacerbation of neuroinflammation were more obviously when mice were subjected to a combined exposure to DINP and formaldehyde. Exposure to DINP and/or formaldehyde enhances oxidative stress and the activation of NF-κB in the prefrontal cortex of mouse asthma model. Exposure to DINP and/or formaldehyde also induced an increase in IL-1β, IL-17, and NGF. Blocking oxidative stress by administering melatonin or inhibiting NF-κB activation by treatment with Dehydroxymethylepoxyquinomicin effectively prevented increasing the levels IL-1β, IL-17 and nerve growth factor. The data indicated that DINP and/or formaldehyde exposure promoted neuroinflammation in the brain through enhanced oxidative stress and activation of NF-κB in a mouse asthma model.

Topics: Animals; Asthma; Disease Models, Animal; Encephalitis; Formaldehyde; Gene Expression Regulation; Interleukin-17; Interleukin-1beta; Male; Mice; Mice, Inbred BALB C; Nerve Growth Factor; NF-kappa B; Ovalbumin; Oxidative Stress; Phthalic Acids; Prefrontal Cortex; Respiratory Hypersensitivity; Signal Transduction