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At least 1,117 records · Page 62Linked to original sources
PubMed1990

Cell proliferation during the process of bleomycin-induced pulmonary fibrosis in rats.

To elucidate the relationship between cell proliferation and structural remodeling in pulmonary fibrosis, light and electron microscopy with immunohistochemistry for bromodeoxyuridine (BrdU) and morphometry for BrdU-positive cells were performed following a single intratracheal instillation of bleomycin in rats. The results showed that terminal bronchiolar epithelial cells, Type II alveolar epithelial cells and interstitial cells began to proliferate 2 days after the injury. Then each cell type showed a different style of proliferation. Interstitial cells which were located in the interstitium and migrated into intraalveolar spaces proliferated, then produced intra-alveolar fibrosis. Terminal bronchiolar epithelial cells proliferated rapidly and formed alveolar bronchiolization with squamous metaplasia in areas where alveoli were severely damaged and intraalveolar fibrosis was formed, and thereafter the proliferation ceased within 2 weeks. The degree of proliferation of type II alveolar epithelial cells and interstitial cells was rather slight, but continued constantly until the later stage. In addition, intraalveolar macrophages were BrdU-positive from an early stage. Endothelial cell proliferation was observed in small vessels and alveolar capillaries at 1 week after bleomycin instillation. Rapidly proliferating bronchiolar epithelial cells which formed alveolar bronchiolization with squamous metaplasia were important in preventing the progress of intraalveolar fibrosis, because the proliferation of type II alveolar epithelial cells was limited.

Administration, Oral↗
PubMed1990

Platelet-derived growth factor in idiopathic pulmonary fibrosis.

Fibrosis is a complex process involving an inflammatory reaction, fibroblast proliferation, and abnormal accumulation of interstitial collagens. Mononuclear cells are usually present in lung fibrosis. Activated monocytes and macrophages in culture have been shown to produce several growth factors including platelet-derived growth factor (PDGF). PDGF is a potent mitogen and chemoattractant for fibroblasts and smooth muscle cells and a stimulator of collagen synthesis. We have studied the expression of c-sis/PDGF-2 mRNA in lung tissues derived from five patients with idiopathic pulmonary fibrosis (IPF) and from four control individuals without IPF. Northern blot analysis of specimens obtained from four patients with IPF revealed the expression of the c-sis/PDGF-2 protooncogene. A control lung tissue without IPF did not express the c-sis protooncogene. In situ hybridization extended these studies demonstrating the expression of the c-sis mRNA in the five specimens with IPF but not in the four control specimens without IPF. The expression of c-sis mRNA was localized primarily in the epithelial cells. Invading alveolar macrophages also expressed c-sis mRNA. The expression of c-sis mRNA was accompanied by the expression of PDGF-like proteins in lung specimens with IPF but not in control lung specimens. These findings demonstrate the in vivo expression of the c-sis/PDGF-2 protooncogene and the production of PDGF-like proteins in the epithelial cells and macrophages of the fibrotic tissue. This localized and sustained production of PDGF-like mitogen may constitute an important contributing factor in the abnormal fibroblast proliferation and collagen production, events associated with pulmonary fibrosis.

Collagen↗
PubMed1997

Exhaled nitric oxide during exercise in primary pulmonary hypertension and pulmonary fibrosis.

STUDY OBJECTIVES: Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of humans. We wished to quantify NO production in patients with abnormalities of the pulmonary circulation. PARTICIPANTS: Nine patients with primary pulmonary hypertension (PPH), six with pulmonary fibrosis (PF), and 20 normal volunteers were studied. INTERVENTIONS: All subjects were studied at rest and during continuous incremental (ramp) cycle ergometry exercise. All patients with PPH and nine matched normal volunteers also performed constant exercise at equal absolute work rates. MEASUREMENTS AND RESULTS: The concentration of NO was measured continuously in mixed expired air, and the rate of NO production (VNO) calculated. Peak exercise capacity was markedly impaired in both patient groups. VNO was similar at rest in the PPH patients (142 +/- 84 nL/min) and the normal subjects (117 +/- 45 nL/min), but lower in the PF patients (66 +/- 13 nL/min; p < 0.05; analysis of variance with Bonferonni correction). While VNO in normal subjects more than doubled by peak exercise to 268 +/- 85 nL/min, there was no significant rise with exercise in either patient group (PPH, 155 +/- 81 nL/min; PF, 91 +/- 67 nL/min). Constant work rate exercise induced a significant rise in VNO in the normal subjects (rest, 101 +/- 68 nL/min; exercise, 147 +/- 87 nL/min; p < 0.001) but no significant change in the PPH patients (rest, 127 +/- 111 nL/min; exercise, 68 +/- 65 nL/min). CONCLUSIONS: We conclude that the low resting VNO in PF may be due to loss of normal functional pulmonary capillary bed. The increase in VNO seen in normal subjects may be associated with dilatation and recruitment of the pulmonary capillary bed during exercise, and failure to increase VNO during exercise in disease states may reflect an inability to recruit the capillary bed.

Adult↗
PubMed1991

Pulmonary fibrosis associated with nabumetone.

A patient is described who developed a rapid onset of pulmonary fibrosis following treatment with a new non-steroidal anti-inflammatory drug, nabumetone. Resolution of symptoms, physical signs and radiographic changes followed drug withdrawal and steroid therapy.

Aged↗
PubMed2006

E- and P-selectins synergistically inhibit bleomycin-induced pulmonary fibrosis.

The development of bleomycin-induced lung injury, which is a model of pulmonary fibrosis, results from inflammatory cell infiltration, a process highly regulated by the expression of multiple adhesion molecules. Therefore, bleomycin-induced lung fibrosis was examined in E-selectin-/- mice, P-selectin-/- mice, and E-selectin-/- mice treated with anti-P-selectin monoclonal antibody (mAb) in comparison of wild-type mice. E-selectin-/- mice treated with anti-P-selectin mAb exhibited augmented lung fibrosis histologically, increased lung collagen deposition, and increased mortality compared to wild-type mice. Furthermore, lung interferon-gamma mRNA expression decreased in E-selectin-/- mice treated with anti-P-selectin mAb relative to wild-type mice, while tumor necrosis factor-alpha and interleukin-6 mRNA expression increased in these mice. Similar changes were observed in E-selectin-/- mice, albeit to a lesser extent than those treated with anti-P-selectin mAb. Remarkably, flow cytometric analysis revealed that the frequency of interferon-gamma-producing natural killer T (NKT) cells in the bronchoalveolar lavage was decreased in E-selectin-/- mice and E-selectin-/- mice treated with anti-P-selectin mAb compared with wild-type mice. Moreover, the majority of NKT cells expressed high levels of CXCR3, suggesting that NKT cell infiltration is also dependent on CXCR3 expression. These results suggest that E- and P-selectins synergistically inhibit lung fibrosis by promoting the recruitment of NKT cells.

Animals↗
PubMed2000

Serum levels of connective tissue growth factor are elevated in patients with systemic sclerosis: association with extent of skin sclerosis and severity of pulmonary fibrosis.

OBJECTIVE: To determine the serum levels and clinical correlation of connective tissue growth factors (CTGF) in patients with systemic sclerosis (SSc). METHODS: Serum samples from patients with limited cutaneous SSc (lSSc, n = 32), diffuse cutaneous SSc (dSSc, n = 28), systemic lupus erythematosus (SLE, n = 30), polymyositis/dermatomyositis (PM/DM, n = 20), and healthy control subjects (n = 30) were examined by ELISA for detection of CTGF. RESULTS: Serum CTGF levels in patients with SSc were significantly higher than those in patients with SLE or PM/DM, and in controls. CTGF levels in patients with dSSc were significantly higher than those in patients with lSSc. As for clinical correlation of CTGF, SSc patients with elevated CTGF had pulmonary fibrosis, decreased DLCO, and decreased vital capacity more frequently than those with normal CTGF levels. Further, DLCO and vital capacity were inversely and directly correlated with serum CTGF levels in patients with SSc. The dSSc patients with disease duration of 1-3 years had significantly elevated levels of CTGF compared with dSSc patients with duration < 1 year or more than 3 years. CONCLUSION: Serum CTGF levels were increased in patients with SSc, and correlated with the extent of skin sclerosis and the severity of pulmonary fibrosis. In addition, it appears that production of CTGF is involved in the development or maintenance of fibrosis rather than in initiation of fibrosis in SSc. These data suggest that CTGF plays a critical role in the development of fibrosis in SSc.

Adolescent↗
PubMed2003

A case of polyarteritis nodosa limited to lower legs with a high titer of MPO-ANCA under precedence of idiopathic pulmonary fibrosis.

A 58-year-old man with a 15-year history of idiopathic pulmonary fibrosis was hospitalized for rapid progression of muscle weakness to bilateral foot drop. Although laboratory data revealed high titers of myeloperoxidase anti-neutrophil cytoplasmic antibody (489 EU), the patient was diagnosed as polyarteritis nodosa limited to the lower portions of the legs. Despite of the treatment with large doses of corticosteroids and cyclosporin A, his symptoms barely improved during the following two months.

Adrenal Cortex Hormones↗
PubMed1995

Surfactant protein A predicts survival in idiopathic pulmonary fibrosis.

The purpose of this study was to determine if the measurement of surfactant protein A (SP-A) in bronchoalveolar lavage (BAL) fluid predicts survival in patients with idiopathic pulmonary fibrosis (IPF). We performed BAL on 44 patients with IPF and 33 healthy volunteers. SP-A and total phospholipid (PL) were measured in the surfactant pelleted by centrifugation and expressed as a ratio to account for differences in the alveolar surface area sampled. The mean SP-A/PL was lower in patients with IPF than in healthy volunteers (31.8 +/- 2.8 versus 63.9 +/- 6.4 micrograms/mumol, p = 0.006) and in patients who died within 2 yr than in those who survived (23.4 +/- 2.6 versus 37.5 +/- 4.2 micrograms/mumol, p = 0.015). Using Cox's proportional hazard model, we found that SP-A/PL modeled continuously was associated with survival time (p = 0.002). The 5-yr survival of patients with SP-A/PL above the median level for all patients with IPF (29.7 micrograms/mumol) was more than twice that of patients below the median (68 versus 30%, p = 0.007). SP-A/PL improved upon prediction of survival modeled by most routine physiologic variables with the exception of percent predicted TLC or the multifarious clinical-radiographic-physiologic score (CRP). Cellular analysis of lavage did not predict survival in this cohort of patients. We conclude that SP-A/PL is a biochemical marker in lavage that predicts survival in patients with IPF.

Adult↗
PubMed1981

[Coincidence of pulmonary fibrosis and bronchial carcinoma (author's transl)].

Eight cases of endothoracal carcinoma associated with pulmonary fibrosis or with interstitial pneumonia are reported. The interstitial pneumonia and the fibrosis and carcinoma are confirmed in all cases. Statements on incidence cannot be made: they are more or less random observations in recent years. There are, however, grounds for supposing that this coincidence is by no means rare. Problems arise in differential diagnosis and the decision to operate, for irradiation therapy and for chemotherapy. The question of a possible causal connection, whether in the sense of a paraneoplasia or of cancer development due to previous damage to the lung is left open.

Adenocarcinoma↗
PubMed1990

Efficacy of cyclosporin A for idiopathic pulmonary fibrosis.

In an 11-year-old girl with severe dyspnoea and cyanosis, idiopathic pulmonary fibrosis (IPF) was diagnosed. The PaO2 of blood could be maintained between 50 mm Hg and 70 mm Hg with a high dose pulse corticosteroid therapy, although this dose could not be reduced. Azathioprine in addition to prednisolone provoked deterioration. Twelve weeks after admission, cyclosporin A (Cs A), a known immunosuppressant, was started together with prednisolone. The PaO2 reverted to normal within 1 month and prednisolone could be tapered off within 6 months. Two years after admission, the patient is free of symptoms on continuous Cs A therapy. This case seems to be the first case successfully treated with Cs A.

Administration, Oral↗