Bronchoalveolar cells

Lem, V.M., Lipscomb, M.F., Weissler, J.C., Nunez, G., Ball, E.J., Stastny, P. and Toews, G.B. (1985). Bronchoalveolar cells from sarcoid patients demonstrate enhanced antigen presentation. J. Immunol. 135, 1766-1771. 

Lipscomb, M.F., Pollard, A.M. and Yates, J.L. (1994). A role for TGF-beta in the suppression by murine bronchoalveolar cells of lung dendritic cell initiated immune responses. Reg. Immunol. 5, 151-157. 

Long, N.C. and Shore, S.A. (1994). Effect of capsaicin pretreatment on bronchoalveolar cells recovered from rats during SO2 induction of chronic bronchitis. Am. J. Respir. Crit. Care Med. 149, A72 (Abstract). 

Law K, Weiden M, Harkin T, et al. Increased release of interleukin-1 p, mterleukin-6, and tumor necrosis factor-a by bronchoalveolar cells lavaged from involved sites in pulmonary tuberculosis. Am J Respir Crit Care Med 1996 153 799-804. 

Ruan, Q., Gelhaus, S.L., Penning, T.M., Harvey, R.G., and Blair, I.A. (2007) Aldo-keto reductase- and cytochrome P450-dependent formation of benzo[a] pyrene-derived DNA adducts in human bronchoalveolar cells. Chem. Res. 

It inhibits the in vitro activation of, and mediator release from, a variety of inflammatory cell types associated with asthma, including eosinophils, neutrophils, macrophages, mast cells, monocytes and platelets. In vitro, nedocromil inhibits the release of mediators including histamine, leukotriene C4 and prostaglandin D2. Similar studies with human bronchoalveolar cells showed inhibition of histamine release from mast cells and beta-glucuronidase release from macrophages. 

The reactivity of either blood or bronchoal-veolar lymphocytes to beryllium can be determined using the LPT. To test peripheral blood, a sample of heparinized blood should be centrifuged over Ficoll-Hypaque to obtain blood mononuclear cells (-70% lymphocytes and 30% monocytes). Cells obtained by bronchoalveolar lavage can be used after washing (Rossman et al. 1988). While the major published studies have utilized bronchoalveolar cells in this manner, occasionally other techniques are employed to enhance the proliferative response of... 

Steinberg KP, Milberg JA, Martin TR, Maunder RJ, CockriU BA, Hudson LD. Evolution of bronchoalveolar cell populations in the adult respiratory distress syndrome. Am J Respir Crit Care Med 1994 150 113-122. 

Human lung fibroblasts isolated postmortem from patients free of lung disease. Bronchoalveolar cell carcinoma cell line used to simulate type II pneumocytes. Primary mesothelial cells derived from human pleural effusions. 

An additional major problem for any laboratory desiring to set up this assay is the lack of easily available positive controls. The only positive controls that are currently available are the blood or bronchoalveolar cells from subjects known to be positive. Because there are very few such persons, the availability of this material is limited. Therefore it is recommended that samples for beryllium proliferation testing only be sent to a laboratory with experience in beryllium testing. Since it is important that the cells arrive alive and in good condition, direct contact with the laboratory should be made before a sample is sent. A list of laboratories that are currently performing a beryllium proliferation assay can be obtained from the Medical Department at Brush Wellman, Inc., 17876 St. Clair Avenue, Cleveland, Ohio 44110-2697, USA. 

Despite all the problems listed above concerning the detection of a cell-mediated immune response to beryllium, the lymphocyte proliferative response to beryllium by bronchoalveolar cells is part of the currently accepted gold standard diagnosis for chronic beryllium disease [40]. 

As more than 40 different cell types were described in the respiratory organs (Sorokin 1970), Emura et al. (1990) developed Syrian hamster (foetus on day 15 of gestation) and human (foetus of 18-22 weeks of gestation) cell systems consisting of a certain type of stem cell capable of differentiating into at least two bronchoalveolar cell types the Clara cell and the alveolar type 11 epitheUal cell. Aufderheide etal. (1994) used this M3E3/C3 hamster cell line for a new in vitro approach to study cytotoxicity and carcinogenic effects of mineral fibres (croddolite and silicon carbide). 

Lem VM, Lipscomb ME, Weissler JC, et al. Bronchoalveolar cells from sarcoid patients demonstrate enhanced antigen presentation. J Immunol 1985 135 1766-1771. 

Mrazek F, Sekerova V, Drabek J, et al. Expression of the chemokine PARC mRNA in bronchoalveolar cells of patients with sarcoidosis. Inununol Lett 2002 84(l) 17-22. 

Sharma S, Stolina M, Zhu L, et al. Secondary lymphoid organ chemokine reduces pulmonary tumor burden in spontaneous murine bronchoalveolar cell carcinoma. Cancer Res 2001 61 6406-6412. 

Kirby JG, Hargreave FE, Gleich GJ, O Byme PM. Bronchoalveolar cell profiles of asthmatic and non-asthmatic subjects. Am Rev Respir Dis 1987 136 379-383. 

Morgan AJ, Symon FA, Berry MA, Pavord ID, Corrigan CJ, Wardlaw AJ. IL-4-expressing bronchoalveolar T cells from asthmatic and healthy subjects preferentially express CCR 3 and CCR 4. J Allergy Clin Immunol 2005 116(3) 594-600. 

Findings from studies of schistosomiasis-induced liver fibrosis, as well as other models of pulmonary, kidney, and liver fibrosis, strongly support the role of CD4+ Th2 cells in the progression of fibrosis (4). In this regard, analyses of gene and protein expression after stimulation by Thl (vs. Th2) cytokines indicates that IL-4 is found at increased concentrations in the bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis, as well as in the peripheral blood mononuclear cells of those afflicted with periportal fibrosis (10,53-56). 

Wattiez R et al. Human bronchoalveolar lavage fluid protein two-dimensional database study of interstitial lung diseases. Electrophoresis 2000 21 2703-2712. Yanagida M et al. Matrix assisted laser desorption/ionization-time of flight-mass spectrometry analysis of proteins detected by anti-phosphotyrosine antibody on two-dimensional-gels of fibrolast cell lysates after tumor necrosis factor-alpha stimulation. Electrophoresis 2000 21 1890-1898. 

In phase I clinical trials 47 patients, all of whom had previously failed standard treatments for solid tumors, received the drug in the UK, Italy, and Switzerland on three different schedules.123,124 Dose-limiting toxicities have been defined as bone marrow depression and diarrhea. The latter is treatable with loperamide. Signs of biological activity were seen. Notably one patient with metastatic pancreatic cancer showed a partial response (for 4 months) and two further patients, one with metastatic melanoma and one with bronchoalveolar carcinoma, also showed partial responses. In a phase I trial in combination with 5-FU, a partial response in breast cancer was observed.125 Furthermore, a reduction in tumor marker levels was observed in two patients, one with ovarian cancer, and one with colon cancer. Phase II studies have shown partial responses in cisplatin-resistant ovarian and nonsmall-cell lung cancer.126,127 The indications are that the profile of clinical activity is different and complementary to the mononuclear platinum agents. 

NiS04 and NiCl2 instilled into rat lungs also produced an inflammatory response (17). However, analysis of bronchoalveolar lavage fluid from rodents exposed to diesel exhaust containing 3.5 mg soot/m3, 7 h/day for 2, 12 or 17 days indicated no influx of inflammatory cells (20). Thus, the diesel soot, at lung burdens of 0.5 mg/g lung, does not produce an acute inflammatory response. 

Walker, C. et al., Allergic and nonallergic asthmatics have distinct patterns of T-cell activation and cytokine production in peripheral blood and bronchoalveolar lavage, Am. Rev. Respir. Dis., 146, 109, 1992. 

After intratracheal instillation of nickel chloride or nickel sulphate in rats, a modest inflammatory response with increased number of macrophages and polynuclear leucocytes was obtained, together with increased activities of lactate dehydrogenase and -glucuronidase in bronchoalveolar fluid [351]. More severe lesions were characterized by type II cell hyperplasia with epithelialization of alveoli, and in some animals, fibroplasia of the pulmonary interstitium. By inhalation in rats, the nickel salts produced chronic inflammation and degeneration of the bronchiolar epithelium [352, 353]. There was also atrophy of the olfactory epithelium and hyperplasia of the bronchial and mediastinal lymph nodes. Nickel sulphate also produced a low incidence of emphysema and fibrosis [353]. 

In rats, the administration of fullerene by inhalation, as nano- and microparticles generated by aerosol, does not lead to lesions and only a little increase of protein concentration in bronchoalveolar lavage fluid was obtained (Baker et al., 2007). Recently, Sayes et al. (2007) analyzed in vivo pulmonary toxicity of C60 and C60(OH)24, after intratracheal instillation in rats. They verified only transient inflammatory and cell injury effects, 1 day postexposure, without differences from water-instilled controls. No adverse lung tissue effects were measured, and the results demonstrated little or no differences in lung toxicity effects between the C60 and fiillerols, compared to controls. 

Juillerat-Jeanneret L, Aubert JD, Leuenberger P (1997) Peptidases in human bronchoalveolar lining fluid, macrophages, and epithelial cells Dipeptidyl (amino)peptidase IV, aminopeptidase N, and dipeptidyl (carboxy)peptidase (angiotensin-converting enzyme). J Lab Clin Med 130(6) 603—614. 

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