Neutral Sugar Accumulation in Lung Lavage Fluid Following Ozone Exposure

Biological effects indicators in bronchoalveolar lavage fluid were studied in Fischer 344 rats of different ages after exposure to 0.4-0.8 ppm ozone for periods of 2-6 h on a single day or on 4 consecutive days. The magnitude of alveolar protein transudation induced by ozone was not different between age groups, but the interindividual variability of protein changes was higher in senescent (24-mo-old) rats. By comparison to juvenile (2-mo-old) and adult (9-mo-old) rats, senescent animals had higher increases of interleukin-6 (up to 10-fold higher) and N-acetyl-beta-D-glucosaminidase (NAGA; 2-fold higher) in lung lavage after ozone. Ascorbic acid was lower in lungs of senescent rats (one-half of juvenile values), and acute ozone exposure brought a further decrease in lung ascorbate. Whereas alveolar protein transudation was attenuated after ozone exposure on 4 days, persistent elevation of NAGA in senescent rats suggested only partial adaptation. Injection of endotoxin did not modify the patterns of effects. Incorporation of 18O-ozone into macrophages and surfactant was not different between age groups, indicating that the magnified biological responses in senescent rats were not dominated by differences in internal dose of ozone. The results indicate that senescent rats respond differently than juvenile and adult rats to lung injury.

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Increased Elastase Inhibitory Capacity of Lung Lavage Fluid Following Acute Ozone Exposure: Role of Serum Transudation

Inhalation Toxicology ◽

10.3109/08958379409029695 ◽

1994 ◽

Vol 6 (1) ◽

pp. 57-65 ◽

Cited By ~ 3

Author(s):

C. Nadziejko ◽

J. Chen

Keyword(s):

Lavage Fluid ◽

Lung Lavage ◽

Ozone Exposure ◽

Inhibitory Capacity

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Protein accumulation in lung lavage fluid following ozone exposure

Environmental Research ◽

10.1016/0013-9351(82)90039-1 ◽

1982 ◽

Vol 29 (2) ◽

pp. 377-388 ◽

Cited By ~ 68

Author(s):

Ping C. Hu ◽

Frederick J. Miller ◽

Mary J. Daniels ◽

Gary E. Hatch ◽

Judith A. Graham ◽

...

Keyword(s):

Lavage Fluid ◽

Lung Lavage ◽

Ozone Exposure ◽

Protein Accumulation

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The Clinical Clues of Pulmonary Alveolar Proteinosis: A Report of 11 Cases and Literature Review

Canadian Respiratory Journal ◽

10.1155/2016/4021928 ◽

2016 ◽

Vol 2016 ◽

pp. 1-5 ◽

Cited By ~ 1

Author(s):

Qiongya Mo ◽

Bingbin Wang ◽

Nian Dong ◽

Lianmin Bao ◽

Xiaoqiong Su ◽

...

Keyword(s):

Bronchoalveolar Lavage Fluid ◽

Clinical Symptoms ◽

Pulmonary Alveolar Proteinosis ◽

Relevant Literature ◽

Neuron Specific Enolase ◽

Lavage Fluid ◽

Lung Lavage ◽

Serum Markers ◽

Open Lung Biopsy ◽

Alveolar Proteinosis

Pulmonary alveolar proteinosis (PAP) is a rare interstitial lung disease characterized by the abnormal alveolar accumulation of surfactant components. The diagnosis of PAP can be easily missed since it is rare and lacks specific clinical symptoms. It is of great importance to have a better understanding of the crucial clue to clinically diagnose PAP and take PAP into consideration in the differential diagnosis of interstitial pulmonary diseases or other diseases with similar manifestations. Here, we analyze the clinical characteristics of 11 cases of PAP patients in local hospital and review the relevant literature in order to provide more information in diagnosis and management of PAP. In our observation, cyfra21-1 and neuron-specific enolase (NSE) known as tumor markers probably can be useful serum markers for diagnosis of PAP. As for the method of pathologic diagnosis, open-lung biopsy was the gold standard but now it is less required because findings on examination of bronchoalveolar lavage fluid (BALF) can help to make the diagnosis. We also have deep experience about when and how to carry out lung lavage.

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Platelet-activating factor contributes to acute lung leak in rats given interleukin-1 intratracheally

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2000.279.1.l75 ◽

2000 ◽

Vol 279 (1) ◽

pp. L75-L80 ◽

Cited By ~ 29

Author(s):

Young M. Lee ◽

Brooks M. Hybertson ◽

Hyun G. Cho ◽

Lance S. Terada ◽

Okyong Cho ◽

...

Keyword(s):

Interleukin 1 ◽

Platelet Activating Factor ◽

Lavage Fluid ◽

Lung Lavage ◽

Myeloperoxidase Activity ◽

Cerium Chloride ◽

Neutrophil Accumulation ◽

Web 2086

Lung lavage fluid of patients with acute lung injury (ALI) has increased levels of interleukin-1 (IL-1) and neutrophils, but their relationship to the lung leak that characterizes these patients is unclear. To address this concern, we investigated the role of the neutrophil agonist platelet-activating factor [1- O-alkyl-2-acetyl- sn-glycero-3-phosphocholine (PAF)] in the development of the acute neutrophil-dependent lung leak that is induced by giving IL-1 intratracheally to rats. We found that PAF acetyltransferase and PAF activities increased in lungs of rats given IL-1 intratracheally compared with lungs of sham-treated rats given saline intratracheally. The participation of PAF in the development of lung leak and lung neutrophil accumulation after IL-1 administration was suggested when treatment with WEB-2086, a commonly used PAF-receptor antagonist, decreased lung leak, lung myeloperoxidase activity, and lung lavage fluid neutrophil increases in rats given IL-1 intratracheally. Additionally, neutrophils recovered from the lung lavage fluid of rats given IL-1 intratracheally reduced more nitro blue tetrazolium (NBT) in vitro than neutrophils recovered from control rats or rats that had been given WEB-2086 and then IL-1. Histological examination indicated that the endothelial cell-neutrophil interfaces of cerium chloride-stained lung sections of rats given IL-1 contained increased cerium perhydroxide (the reaction product of cerium chloride with hydrogen peroxide) compared with lungs of control rats or rats treated with WEB-2086 and then given IL-1 intratracheally. These in vivo findings were supported by parallel findings showing that WEB-2086 treatment decreased neutrophil adhesion to IL-1-treated cultured endothelial cells in vitro. We concluded that PAF contributes to neutrophil recruitment and neutrophil activation in lungs of rats given IL-1 intratracheally.

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Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1994.266.6.l593 ◽

1994 ◽

Vol 266 (6) ◽

pp. L593-L611 ◽

Cited By ~ 13

Author(s):

M. D. Evans ◽

W. A. Pryor

Keyword(s):

Cigarette Smoke ◽

Proteinase Inhibitor ◽

Inflammatory Cells ◽

Lavage Fluid ◽

Lung Lavage ◽

Tissue Destruction ◽

Phagocytic Cells ◽

Lung Fluid

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.

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Flagellin/TLR5 Stimulate Myeloid Progenitors to Enter Lung Tissue and to Locally Differentiate Into Macrophages

Frontiers in Immunology ◽

10.3389/fimmu.2021.621665 ◽

2021 ◽

Vol 12 ◽

Author(s):

Xin Lei ◽

Jara Palomero ◽

Iris de Rink ◽

Tom de Wit ◽

Martijn van Baalen ◽

...

Keyword(s):

Epithelial Cells ◽

Low Frequency ◽

Lavage Fluid ◽

Lung Lavage ◽

Alveolar Epithelial Cells ◽

Mouse Bone Marrow ◽

Alveolar Epithelial ◽

Toll Like Receptor 5

Toll-like receptor 5 (TLR5) is the receptor of bacterial Flagellin. Reportedly, TLR5 engagement helps to combat infections, especially at mucosal sites, by evoking responses from epithelial cells and immune cells. Here we report that TLR5 is expressed on a previously defined bipotent progenitor of macrophages (MΦs) and osteoclasts (OCs) that resides in the mouse bone marrow (BM) and circulates at low frequency in the blood. In vitro, Flagellin promoted the generation of MΦs, but not OCs from this progenitor. In vivo, MΦ/OC progenitors were recruited from the blood into the lung upon intranasal inoculation of Flagellin, where they rapidly differentiated into MΦs. Recruitment of the MΦ/OC progenitors into the lung was likely promoted by the CCL2/CCR2 axis, since the progenitors expressed CCR2 and type 2 alveolar epithelial cells (AECs) produced CCL2 upon stimulation by Flagellin. Moreover, CCR2 blockade reduced migration of the MΦ/OC progenitors toward lung lavage fluid (LLF) from Flagellin-inoculated mice. Our study points to a novel role of the Flagellin/TLR5 axis in recruiting circulating MΦ/OC progenitors into infected tissue and stimulating these progenitors to locally differentiate into MΦs. The progenitor pathway to produce MΦs may act, next to monocyte recruitment, to fortify host protection against bacterial infection at mucosal sites.

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