[Study of ambient PM2.5 on the influence of the inflammation injury and the immune function of subchronic exposure rats].
OBJECTIVE
To explore ambient PM2.5 the influence of the inflammation injury and the on immune function.


METHODS
The model rats were administered with PM2.5 by the intratracheal instillation. The pathological varieties of rat's lungs and other important organs were observed by light microscope. The protein and SA levels in bronchoalveolar lavage fluids (BALF) were detected by relevant kits. The TNF-alpha, and IL-6 levels in the BALF were detected by ELISA, and the mRNA expression levels in the lung tissue were observed by RT-PCR. The AM were collected to detect the phogacytic function. The ConA-stimulated T lymphocyte proliferation tests were performed to research the proliferation of spleen.


RESULTS
Foreign-body granulomas were observed in the lungs of exposed rats. Monocytes-macrophages assembling in blood sinus of liver and the trend to form the granulomas were observed. Alveolar macrophages containing PM2.5 and dissociative PM2.5 were obviously observed in lung visceral pleural lymphatics and the blood vessels in lung and kidney. The number of the granulomas in the lungs of the rats become more and more as times goes on. The concentrations of total protein and SA in BALF were increased with the dose and time of exposure. TNF-alpha levels in the BALF increased by the dose and exposure time during 3 months, but TNF-alpha levels in the BALF decreased significantly on the 6th month. The expression levels of IL-6 in the BALF increased by the dose. It showed the dose-response relationship. The highest expression level of IL-6 was detected on the 3rd month. The expression level of IL-6 decreased on the 6th month. Phagocytiosis functions of AM were impaired by PM2.5 , which may in turn impair the nonspecific defenses function of airway. But the splenic lymphocyte proliferation were not obviously changed.


CONCLUSIONS
The persistent inflammatory injury was induced by the subchronic exposure to PM2.5. The injury of immunological system were increased with the dose and the time of the exposure. The cytokine net was disordered by PM2.5, which worsen the injury. The phagocytiosis function of AM was impaired by PM2.5, which may be the mechanism of chronic pulmonary diseases.
Xu
Dongqun
D
Institute for Environmental Health and Related Product Safety, Chinese Center for Disease Control and Prevention, Beijing100021, China.
Huang
Ninghua
N
Wang
Qin
Q
Liu
Honggang
H
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004781:Environmental Exposure; D005260:Female; D005549:Foreign-Body Reaction / Q000209:etiology / Q000276:immunology*; D007249:Inflammation / Q000378:metabolism*; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000473:pathology; D008171:Lung Diseases / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D008262:Macrophage Activation / Q000276:immunology; D052638:Particulate Matter / Q000633:toxicity*; D010587:Phagocytosis / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D015850:Interleukin-6; D052638:Particulate Matter; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha