PubMed Health⌕ Search

Biomedical subjects

A Suwabe

Publications and source records attributed to A Suwabe.

26 records · Page 2Linked to original sources

Hypertrophic alveolar type II cells from silica-treated rats are committed to DNA synthesis in vitro.

Alveolar type II cell hyperplasia and hypertrophy are common reparative responses of the alveolar epithelium after silica-induced lung injury. We studied in vitro DNA synthesis in type II cells isolated after silica instillation in the rat to determine the proliferative potential of silica type II cells in primary culture and to correlate alveolar type II cell size with the level of in vitro DNA synthesis. To determine if the alveolar lining fluid is a source of growth factors that stimulate alveolar type II cell proliferation, we also examined the mitogenic effect of bronchoalveolar lavage fluid (BALF) from silica-treated rats on type II cells in primary culture. Alveolar type II cells were isolated from rats 1, 2, 3, and 4 wk after intratracheal silica instillation, cultured in DME supplemented with 10% fetal bovine serum, and labeled with [3H]thymidine from day 1 to day 3 in culture. DNA synthesis was determined by [3H]thymidine incorporation and autoradiographic labeling index. The level of thymidine incorporation increased progressively from 22.3 +/- 5.4 x 10(3) dpm/well 7 d after silica instillation to 34.4 +/- 5.0 x 10(3) dpm/well at 28 d. Type II cells isolated 14 d after silica instillation were separated into groups of increasing cell size by centrifugal elutriation. The plating efficiency and alveolar type II cell purity (greater than 88%) were the same in all groups of elutriated cells. The hypertrophic type II cells had a higher level of thymidine incorporation (22.0 +/- 2.8 x 10(3) dpm/well) than the normotrophic type II cells (11.1 +/- 0.7 x 10(3) dpm/well) [P less than 0.01]).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[The effect of foamy alveolar macrophages presented in bleomycin-injured rat lungs in pulmonary fibrosis].

Foamy alveolar macrophages (FAM) are observed in lungs injured by Bleomycin (BLM), but their relation to pulmonary fibrosis is not clearly understood. We purified FAM from BLM-instilled rat lungs by density gradient centrifugation on Percoll, and studied the effect of FAM on pulmonary fibrosis. The cells lavaged from the rat lungs 14 days after the administration of BLM (B) or saline (S), were applied on Percoll. After centrifugation, the cells layered on each interface were collected and named as SI, SII, SIII, and BI, BII, BIII in order of gravity. The BI layer included 8.5% of unfractionated cells (U). These BI cells were viable (88%), significantly larger than the others, nonspecific esterase positive cells, and included much ferritin and lysozyme, and were morphologically identified as alveolar macrophages (AM). Therefore, we called the BI cells FAM. We estimated the capacity of FAM (2.5 X 10(5] to synthesize DNA (3H-thymidine uptake) and RNA (3H-uridine uptake), and the activities of silica-stimulated FAM to cause proliferation of mouse thymocytes (IL-1 activity) and rat lung fibroblasts (FP activity), and to produce PGE2. FAM has a lower mitogenic activity but did not have been protein synthetic activity as compared with the others. Silica-stimulated FAM released less IL-1 than BII or BIII, and induced less fibroblast growth than BII, but induced as much as BIII, possibly because of the increased capacity of BIII cells to produce PGE2, which is known to inhibit fibroblast growth. In this way, FAM were considered to be "already activated" rather than "highly activated" cells, but the presence of FAM suggested that smaller or denser AM might receive bleomycin stimulation and release fibrogenic mediators (IL-1 or MDGF) into the alveolar spaces during FAM formation, and that AM might participate in the fibrogenic responses.

Animals↗

The effect of cigarette smoke on bleomycin-induced pulmonary fibrosis in hamsters.

To investigate the effect of cigarette smoke on the development of bleomycin (BLM)-induced pulmonary fibrosis in hamsters, four experimental groups were studied: a control group (C), a cigarette smoke-inhaled group (T), a BLM-administered group (B), and a cigarette smoke-inhaled plus BLM-administered group (TB). Groups T and TB were exposed to sidestream smoke of cigarettes for 30 min/day, 5 days/wk. Groups B and TB were administered 0.5 mg BLM hydrochloride per 100 g body weight endotracheally once on day 30 (Day 0) after housing start. Quantitative morphometry of the lungs revealed that Group TB showed less lung fibrotic change compared with Group B, but based on qualitative observation, the fibrotic lesions of Group TB were intermingled with slight emphysematous changes. Neutrophils in bronchoalveolar lavage fluid were remarkably increased in both the groups, with a peak on Day 1, but the increase in Group TB lasted longer. Alveolar macrophages were increased in both smoking groups (T and TB) compared to the non-smoking groups (C and B). These results suggest that cigarette smoke reduces BLM-induced lung fibrotic changes; however, it simultaneously causes derangement of alveolar architecture. The persistence of increased neutrophils in the early phase after BLM accompanied by exposure to cigarette smoke may play an important role in the mechanism by which smoke ameliorates the effect of BLM.

Animals↗

Bleomycin-stimulated hamster alveolar macrophages release interleukin-1.

The capacity of alveolar macrophages (AM) of bleomycin-instilled hamsters to proliferate mouse thymocytes (interleukin-1 activity) and hamster fibroblasts (fibroblast proliferation (FP) activity was studied. Using bleomycin-instilled hamsters, the FP activity of AM culture supernatants was increased significantly on days 1, 5, and 10 after instillation of bleomycin. The interleukin-1 (IL-1) activity, however, was increased significantly on day 1 only as compared with saline-treated hamsters. Next, normal AM were stimulated in vitro by bleomycin. After being fractionated by chromatography, their culture supernatant showed IL-1 activity, which also indicated FP activity. These results suggest that bleomycin directly stimulates AM to release IL-1 in the fibrogenic responses.

Animals↗