[IL-17A promotes pulmonary inflammation in rats with pulmonary fibrosis induced by bleomycin].
OBJECTIVE
To investigate the role of IL-17A in the development of pulmonary fibrosis in rats.


METHODS
Twenty female Wistar rats were randomly divided into normal saline (NS) group and bleomycin (BLM) group. The BLM group was intratracheally instilled with BLM, while the NS group was treated with saline instead. Half of the rats in each group were sacrificed respectively on day 7 and 28 after intratracheal instillation. HE and Masson stainings were performed to show the pathological changes of lung tissues. The expression of IL-17A in lung tissues was detected by the immunohistochemistry. The bronchoalveolar lavage fluid (BALF) was harvested; one part of it was used for cell counting and classification, and for the detection of the concentration of IL-17A in BALF using ELISA; the other part of it was used for determining the concentration of IL-17A in the culture supernatant of the purified alveolar macrophage (AM) using ELISA and reverse transcription PCR (RT-PCR).


RESULTS
Compared with the NS group, the BLM group presented a great deal of inflammatory cells in the alveoli, the increased total number of cells, decreased AM level and increased neutrophil number in BALF on day 7; on day 28, the BLM group had milder alveolitis and more serious fibrosis. The expression of IL-17A protein in lung tissues was obviously higher on day 7 and 28 in the BLM group than in the NS group (P<0.05), and it was higher on day 7 than on day 28. The increased total number of BALF cells in BLM group returned to the normal level on day 28. The level of IL-17A in BALF increased significantly on day 7 and 28 in BLM group, however, compared with that on day 7, it decreased on day 28. Compared to the NS group, the expression of IL-17A protein in the culture supernatant of the BLM group was remarkably higher at 12th, 24th and 48th hours (P<0.05). RT-PCR showed that compared with the NS group, the expression of IL-17A mRNA increased significantly in BLM group on day 7 and 28 (P<0.05).


CONCLUSIONS
IL-17A promotes the development of pulmonary inflammation, indicating that it may be involved in the progress of pulmonary fibrosis.
Department of Respiratory Diseases, Outpatient Department, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China.
Chengliang
C
Huang
Outpatient Department, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China.
Yanyan
Y
Li
Department of Respiratory Diseases, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China.
Xianming
X
Fan
Department of Respiratory Diseases, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China.
Yanmei
Y
Ma
Department of Respiratory Diseases, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China.
Ming
M
Zhang
Department of Respiratory Diseases, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China.
Wenjun
W
Wang
D000818:Animals; D001761:Bleomycin / Q000009:adverse effects*; D001992:Bronchoalveolar Lavage Fluid; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism*; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016676:Macrophages, Alveolar / Q000378:metabolism; D011014:Pneumonia / Q000150:complications* / Q000276:immunology / Q000378:metabolism*; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000150:complications*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D020381:Interleukin-17; D012333:RNA, Messenger; D001761:Bleomycin