Pulmonary glass particles may persist in the lung suppressing function of immune cells.
The health effects of silica may depend on the inherent properties of crystalline silica or on external factors affecting the biological activity or distribution of its polymorphs. Inhaled crystalline silica is classified as a Group I carcinogen, however, information on the health effects of amorphous silica is still insufficient. Considering that alveolar macrophages play a key role in both innate and adaptive immune responses for removal of foreign bodies that enter via the respiratory system, we treated sheet-like glass particles (SGPs), a type of noncrystalline amorphous silica, to MH-S cells, an alveolar macrophage cell line. SGPs reduced the generation of ROS and NO and induced cell death via multiple pathways. Although the expression of CD80, CD86, and CD40, increased by exposure to SGPs, the expression of MHC class II molecules had not notably changed. Additionally, expression of ICAM-1 tended to decrease. In mice, SGPs were distributed in the interstitial region of the lung without notable pathological lesion on day 14 after a single intratracheal instillation. Pulmonary total cell number increased significantly with the highest dose, but the levels of all measured inflammatory cytokines and chemokines, except IL-1, were lower in BAL fluid from SGP-treated mice compared to control. More interestingly, the expression of antigen presentation-related proteins was enhanced in the lungs of SGP-exposed mice concomitant with an increase in the number of mature dendritic cells, whereas the expression of ICAM-1, an important adhesion molecule for helper T cell recruitment, was suppressed. Taken together, we suggest that SGPs may induce adverse health effects by down-regulating function of immune cells in the lungs. Furthermore, ICAM-1 may play a key role in immune response to remove pulmonary SGPs.
Department of Brain Science, Ajou University School of Medicine, 164, World cup-ro, Youngtong-gu, Suwon, 16499, Korea.
Eun-Jung
EJ
Park
School of Civil, Environmental, and Architectural Engineering, Korea University, Seoul, 136-713, Korea.
Gwang-Hee
GH
Lee
School of Civil, Environmental, and Architectural Engineering, Korea University, Seoul, 136-713, Korea.
Jae-Chan
JC
Kim
National Center for Efficacy Evaluation for Respiratory Disease product, Jeonbuk Department of Research Inhalation Safety, Korea Institute of Toxicology, Jeongeup, 580-185, Republic of Korea.
Sang
S
Jin Lee
National Center for Efficacy Evaluation for Respiratory Disease product, Jeonbuk Department of Research Inhalation Safety, Korea Institute of Toxicology, Jeongeup, 580-185, Republic of Korea.
Kyuhong
K
Lee
Toxicologic Pathology Center, Korea Institute of Toxicology, Daejeon, 34114, Korea.
Byoung-Seok
BS
Lee
Department of Brain Science, Ajou University School of Medicine, 164, World cup-ro, Youngtong-gu, Suwon, 16499, Korea.
Jaerak
J
Chang
School of Civil, Environmental, and Architectural Engineering, Korea University, Seoul, 136-713, Korea.
Dong-Wan
DW
Kim
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D018929:Cell Culture Techniques; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005898:Glass; D008168:Lung / Q000187:drug effects* / Q000276:immunology; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000276:immunology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009504:Neutrophils / Q000166:cytology; D010316:Particle Size; D017382:Reactive Oxygen Species / Q000378:metabolism; D012822:Silicon Dioxide / Q000633:toxicity*; D013499:Surface Properties
D018925:Chemokines; D016207:Cytokines; D017382:Reactive Oxygen Species; D012822:Silicon Dioxide
adhesion molecules; amorphous silica; antigen presentation; glass particles; inflammation