[Variabilities of the impacts of cold pathogen and cold-dampness pathogen on fractalkine mRNA expression in lung tissues of rats].
OBJECTIVE
To study the variabilities of the effects of cold pathogen and cold-dampness pathogen on the fractalkine (FKN) mRNA expression in lung tissues of rats.


METHODS
Twenty-four Wistar rats of SPF grade were randomly divided into 3 groups: normal temperature group, cold pathogen group and cold-dampness pathogen group. There were 8 rats in each group. Rats in normal temperature group were bred at (20+/-2)degrees centigrade and under normal humidity (50%-55%) for 2 h. Rats in cold pathogen group were bred at -10 degrees centigrade and under normal humidity (50%-55%) for 2 h, and the rats in cold-dampness pathogen group were bred at -10 degrees centigrade and under high humidity (90%-100%) for 2 h. Rats in the three groups were bred in thermostats under the corresponding conditions on the first day of experiment, and then the rats in different groups were all bred at normal temperature. Lung specimens in 3 groups were gathered four days later. The behavior and the pathological changes in the lung tissues of rats in different groups were observed. The content of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in lung homogenate was detected by radioimmunoassay (RIA) method. Expression of FKN mRNA in lung homogenate was detected by reverse transcription-polymerase chain reaction (RT-PCR).


RESULTS
The lung tissues of rats in both cold pathogen group and cold-dampness pathogen group had various degrees of pathological changes. Compared with normal temperature group, the content of IL-6 and TNF-alpha was increased obviously in lung homogenate of rats in both cold pathogen group and cold-dampness pathogen group (P<0.01). The content of IL-6 and TNF-alpha in lung homogenate of rats in cold-dampness pathogen group was obviously higher than that in cold pathogen group (P<0.01). The RT-PCR results showed a low expression of FKN mRNA in lung tissues of rats in normal temperature group. If the injured lung tissues were aggravated, the expression of FKN mRNA in the lung tissues was elevated. Compared with normal temperature group, FKN mRNA expressions in both cold pathogen group and cold-dampness pathogen group were increased obviously (P<0.01). FKN mRNA expression in lung homogenate of rats in cold-dampness pathogen group was also obviously higher than that in cold pathogen group (P<0.01).


CONCLUSIONS
Cold pathogen can induce lung injury and up-regulate the FKN mRNA expression in lung tissue. Dampness pathogen can up-regulate the FKN mRNA expression through aggravating the injury of lung tissues caused by cold pathogen. FKN has a close relationship with the lung injury.
Zhang
Wei
W
Department of Respiratory Medicine, Affiliated Hospital, Shandong University of Traditional Chinese Medicine, Jinan, Shandong Province, China. 05320835zh@sina.com
Liu
Hai-Yu
HY
D000818:Animals; D054428:Chemokine CX3CL1 / Q000235:genetics / Q000378:metabolism*; D003080:Cold Temperature; D005260:Female; D006813:Humidity; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008516:Medicine, Chinese Traditional; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
D054428:Chemokine CX3CL1; D012333:RNA, Messenger