[Implications of lung interstitial dendritic cells of mice in multiple organ dysfunction syndrome].
OBJECTIVE
To explore the role of lung interstitial dendritic cells in immunodissonance and organ injury in multiple organ dysfunction syndrome (MODS).


METHODS
Animal model of MODS was established by injecting zymosan into the peritoneal cavity of C57BL/6 mice. The mice were randomly divided into groups of normal, 3 - 6 hours, 12 - 48 hours, 5 - 7 days, 10 - 12 days post injection. Pathological changes of lung and interstitial dendritic cells were studied by light and transmission electron microscope. Immunohistochemistry, RT-PCR and flow cytometry analyses were used to document status of biomarkers, including specific surface markers (CD205 and CD11c), costimulatory molecules (CD80 and CD86), SLC and its receptor CCR7 in lung, CD4+ and CD8+ T lymphocyte subtypes in peripheral blood.


RESULTS
At early stage of injury, interstitial dendritic cells showed an increase in proliferation with expression of low level of CD80 and CD86. In contrast, the expression of SLC and its receptor CCR7 in lung were increased. The ratio of CD4+/CD8+ declined in peripheral blood. At the stage of SIRS, interstitial dendritic cells continued to proliferate with high expressions of CD80 and CD86. SLC and CCR7 in lung also increased. The ratio of CD4+/CD8+ declined markedly in peripheral blood. At the MODS stage, interstitial dendritic cells further proliferated, but the expression of CD80 and CD86 declined to a very low level. Although the level of SLC increased consistently, the level of CCR7 continued to decrease, along with a markedly decreased CD4+/CD8+ ratio in peripheral blood.


CONCLUSIONS
Alterations of lung interstitial dendritic cells are likely to influence the course of immunological dysfunction of MODS. The level of CCR7 may serve as an indicator of the migration activity of interstitial dendritic cells and systemic immune response.
Wang
Hong-wei
HW
Department of Pathology, 304 Clinic Department of General Hospital of PLA, Beijing 100037, China.
Lu
Jiang-yang
JY
Wang
Xiao-hong
XH
Tian
Guang
G
Li
Ling
L
Yang
Yi
Y
D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D018122:B7-1 Antigen / Q000378:metabolism; D051940:B7-2 Antigen / Q000378:metabolism; D039521:CD11c Antigen / Q000378:metabolism; D016516:CD4-CD8 Ratio; D049109:Cell Proliferation; D054421:Chemokine CCL21 / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D004195:Disease Models, Animal; D037181:Lectins, C-Type / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015778:Minor Histocompatibility Antigens; D009102:Multiple Organ Failure / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D054400:Receptors, CCR7 / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism; D015054:Zymosan
D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D039521:CD11c Antigen; C515371:Ccr7 protein, mouse; D054421:Chemokine CCL21; C093569:DEC-205 receptor; D037181:Lectins, C-Type; D015778:Minor Histocompatibility Antigens; D054400:Receptors, CCR7; D011956:Receptors, Cell Surface; D015054:Zymosan