Bronchoalveolar fluid

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]. 

AGE — agarose gel electrophoresis, BAL = bronchoalveolar fluid, FAM = 6-carboxyfluorescein label, MGB = minor groove binder, n.s. - not specified, RAPD = randomly amplified polymorphic DNA, RT-PCR = reverse transcription PCR, TAMRA = 6-carboxytetramethylrhodamine label. 

Bronchoalveolar fluid Mix with sodium hypochlorite membrane filter dry PCM 1 AB/mL No data Spumy 1994... 

Hydrogen Peroxide and Superoxide Radical Generation in Bronchoalveolar Fluids... 

Information on the directed recruitment by chemokines of immune cells to and within secondary lymph tissue has increased significantly over the past several years. Most of this work has focused on the identification of novel chemokines, their structure, their receptors, and their chemoattractant function. Furthermore, most of this work has involved the most easily accessible specimens—blood, peripheral lymph nodes, and bronchoalveolar fluid. 

The rat is also a common model for human asthma and has a size advantage over the mouse, resulting in enhanced ability for collection of blood and bronchoalveolar fluid. The BN rat is the most commonly utihzed strain due to its pronounced IgE and inflammatory response to challenge following sensitization (Hylkema et al., 2002). As is the case with the mouse, rats are not considered a perfect model due to differences in the release of serotonin from mast cells between rats and humans. 

Hydrogen peroxide is also an oxidant with the potential to cause severe cell damage. It must therefore be rapidly removed by other antioxidants which occur intra-cellularly in the lung as well as in the bronchoalveolar fluid (Hefner and Repine, 1989), because ascorbic acid cannot react with hydrogen peroxide (Anderson and Lukey, 1987). 

The two predominant antioxidants in bronchoalveolar fluid and in alveolar cells are catalase (CAT) and glutathione (GSH). Both are able to render H2O2 inactive as illustrated by the following reactions ... 

Since ascorbic acid apparently suppresses catalase activity (Anderson and Lukey, 1987) and the ascorbic acid content of the bronchoalveolar fluid and of the type II epithelial cells as well as alveolar macrophages is high and since GSH peroxidase has a lower for H2O2 than catalase, glutathione (GSH) is seemingly more effective in removing H2O2. 

Upon activation, eosinophils release cytotoxic enzymes, e.g., eosinophil cationic protein (ECP), major basic protein (MBP), eosinophil-derived neurotoxin (EDN), and eosinophil peroxidase (EPO). Extravascular ECP (8) and MBP (9) deposits have been observed, and high levels of eosinophil cytotoxic enzymes are found in CSS patient s sera, urine, and bronchoalveolar fluids (9-11). In addition, the results of a recent study suggested that EPO released by activated eosinophils could cause oxidative tissue damage (12). Taken together, these elements incriminate eosinophil cytotoxicity in CSS development. 

Takahashi T, Munakata M, Suzuki I, et al. Serum and bronchoalveolar fluid KL-6 levels in patients with pulmonary alveolar proteinosis. Am J Respir Crit Care Med 1998 158(4) 1294-1298. 

Neutrophils play a key role in the development of human ALI and ARDS since they liberate the inflammatory mediators which cause the primary cellular damage. A large number of such mediators have been identified in experimental studies and detected in bronchoalveolar fluid washout smdies. These are considered to be four main groups of substances which cause damage. These are shown in Box 6.5. 

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