Multi-cellular human bronchial models exposed to diesel exhaust particles: assessment of inflammation, oxidative stress and macrophage polarization

• DOI: 10.1186/s12989-018-0256-2
• Publication Date: 2018-05-02T01:39:35Z
• Authors: Jie Ji; Swapna Upadhyay; Xiaomiao Xiong; Maria Malmlöf; Thomas Sandström; Per Gerde; Lena Palmberg
• Keywords: Interleukin 8; HMOX1; Macrophage polarization

Diesel exhaust particles (DEP) are a major component of outdoor air pollution. DEP mediated pulmonary effects plausibly linked to inflammatory and oxidative stress response in which macrophages (MQ), epithelial cells their cell-cell interaction plays crucial role. Therefore, this study we aimed at studying the cellular crosstalk between airway with MQ polarization following exposure aerosolized by assessing inflammation, stress, markers. Lung mucosa models including primary bronchial (PBEC) cultured air-liquid interface (ALI) were co-cultured without (PBEC-ALI) (PBEC-ALI/MQ). Cells exposed 12.7 μg/cm2 using XposeALI®. Control (sham) clean air. Cell viability was assessed. CXCL8 IL-6 measured basal medium ELISA. The mRNA expression markers (CXCL8, IL6, TNFα), (NFKB, HMOX1, GPx) (IL10, IL4, IL13, MRC1, MRC2 RETNLA, IL12 andIL23) qRT-PCR. surface/mRNA TLR2/TLR4 detected FACS In PBEC-ALI significantly increased secretion CXCL8, TNFα) GPx). However, expressions these NFKB, HMOX1) reduced PBEC-ALI/MQ after exposure. TLR2 TLR4 PBEC-ALI. surface on PBEC sham-exposed compared After PBEC-ALI/MQ, while decreased both models. resulted similar pattern as PBEC. anti-inflammatory M2 macrophage MRC2). pivotal role for phenotypic alteration towards M2-subtypes, thereby promoting an efficient resolution inflammation. Furthermore, highlighted fact that cell–cell multicellular ALI-models combined vivo-like inhalation system is critical better mimicking physiology traditional cell culture systems.