Inflammation in lung after acute myocardial infarction is induced by dendritic cell-mediated immune response.
The present study was performed to describe the changes of lung tissues in mice with acute myocardial infarction (AMI) and also explain the cell mechanism involved in inflammation in lung. AMI was established by left coronary ligation in mice. Then mice were divided into three groups: control group, MW1 group (sampling after surgery for one week) and MW2 group (sampling after surgery for two weeks). Afterwards, measurement of lung weight and lung histology, cell sorting in bronchoalveolar lavage (BAL) fluid and detection of several adhesive molecules, inflammatory molecules as well as enzyme associated with inflammation were performed. Moreover, dendritic cells (DCs) were isolated from bone marrow of C57B/L6 mice. After incubating with necrotic myocardium, the expression of antigen presenting molecules, co-stimulatory molecules and inflammatory molecules were detected by flow cytometry or immunohistochemistry in DCs. We also detected T-cell proliferation after incubating with necrotic myocardium-treated DCs. AMI induced pathological changes of lung tissue and increased inflammatory cell amount in BAL fluid. AMI also increased the expression of several inflammatory factors, adhesive molecules and enzymes associated with inflammation. CD11c and TLR9, which are DC surface markers, showed a significantly increased expression in mice with AMI. Additionally, necrotic myocardium significantly increased the expression of co-stimulatory factors including CD83 and CD80, inflammatory cytokines including TNF-α, IFN-γ and NF-κB in DCs. Furthermore, DCs treated with necrotic myocardium also significantly promoted T-cell proliferation. AMI induced inflammation in lung and these pathological changes were mediated by DC-associated immune response.
Department of Pulmonary Medicine, Research Institute of Respiratory Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
L J
LJ
Hu
Department of Geriatrics, Zhongshan Hospital, Fudan University, Shanghai, China.
W Y
WY
Ren
Department of Pulmonary Medicine, Research Institute of Respiratory Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Q J
QJ
Shen
Department of Pulmonary Medicine, Research Institute of Respiratory Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
H Y
HY
Ji
Department of Pulmonary Medicine, Research Institute of Respiratory Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
L
L
Zhu
D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology; D018122:B7-1 Antigen / Q000235:genetics / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D039521:CD11c Antigen / Q000235:genetics / Q000276:immunology; D049109:Cell Proliferation; D018920:Coculture Techniques; D054059:Coronary Occlusion / Q000601:surgery; D003331:Coronary Vessels / Q000601:surgery; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology; D005786:Gene Expression Regulation / Q000276:immunology*; D007136:Immunoglobulins / Q000235:genetics / Q000276:immunology; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D008168:Lung / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D009206:Myocardium / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D011014:Pneumonia / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D051217:Toll-Like Receptor 9 / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology; D000097802:CD83 Antigen
D015703:Antigens, CD; D018122:B7-1 Antigen; D039521:CD11c Antigen; D007136:Immunoglobulins; D007371:Interferon-gamma; D008562:Membrane Glycoproteins; D051217:Toll-Like Receptor 9; D014409:Tumor Necrosis Factor-alpha; D000097802:CD83 Antigen; C495370:Tlr9 protein, mouse