Carbon nanoparticles (CNP) are generated by incomplete combustion of diesel engines. Several epidemiological studies associated higher susceptibility to particulate matter related adverse respiratory outcomes with preexisting conditions like chronic bronchitis (CB). Therefore, we compared the effect of CNP exposure on primary bronchial epithelial cells (PBEC) developed in air-liquid interface (ALI) models of normal versus CB-like-mucosa.PBEC cultured at ALI represented normal mucosa (PBEC-ALI). To develop CB-like-mucosa (PBEC-ALI/CB), 1 ng/ml interleukin-13 was added to the basal media of PBEC-ALI culturing. PBEC-ALI and PBEC-ALI/CB were exposed to sham or to aerosolized CNP using XposeALI® system. Protein levels of CXCL-8 and MMP-9 were measured in the basal media using ELISA. Transcript expression of pro-inflammatory (CXCL8, IL6, TNF, NFKB), oxidative stress (HMOX1, SOD3, GSTA1, GPx), tissue injury/repair (MMP9/TIMP1) and bronchial cell type markers (MUC5AC, CC10) were assessed using qRT-PCR.Increased secretion of CXCL-8 and MMP-9 markers was detected 24 h post-exposure in both PBEC-ALI and PBEC-ALI/CB with more pronounced effect in the later. Pro-inflammatory and tissue injury markers were increased at both 6 h and 24 h post-exposure in PBEC-ALI/CB. Oxidative stress markers exhibited similar responses at 6 h and 24 h post-exposure in PBEC-ALI/CB. The club cell specific marker CC10 was increased by 300 fold in PBEC-ALI/CB and 20 fold in PBEC-ALI following CNP exposure.Our data indicates an earlier and stronger reaction of pro-inflammatory, oxidative stress and tissue injury markers in PBEC-ALI/CB models compared to PBEC-ALI models following CNP exposure. The findings may provide insight into the plausible mechanisms of higher susceptibility among predisposed individuals to nanoparticle exposure.
Keywords: Carbon nanoparticles; air-liquid interface model; chronic bronchitis–like model; inflammation; oxidative stress.