The effect of lead exposure on some inflammatory biomarkers of lung lavage fluid in rats

Toxin Reviews ◽  
2016 ◽  
Vol 36 (2) ◽  
pp. 161-164 ◽  
Author(s):  
Tahereh Farkhondeh ◽  
Saeed Samarghandian ◽  
Mohsen Azimi-Nezhad
2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Qiongya Mo ◽  
Bingbin Wang ◽  
Nian Dong ◽  
Lianmin Bao ◽  
Xiaoqiong Su ◽  
...  

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.


2000 ◽  
Vol 279 (1) ◽  
pp. L75-L80 ◽  
Author(s):  
Young M. Lee ◽  
Brooks M. Hybertson ◽  
Hyun G. Cho ◽  
Lance S. Terada ◽  
Okyong Cho ◽  
...  

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.


1994 ◽  
Vol 266 (6) ◽  
pp. L593-L611 ◽  
Author(s):  
M. D. Evans ◽  
W. A. Pryor

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Lei ◽  
Jara Palomero ◽  
Iris de Rink ◽  
Tom de Wit ◽  
Martijn van Baalen ◽  
...  

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.


2000 ◽  
Vol 94 (6) ◽  
pp. 564-568 ◽  
Author(s):  
B. SCHMEKEL ◽  
L. SEVEUS ◽  
S.Y. XU ◽  
P. VENGE

1987 ◽  
Vol 73 (s17) ◽  
pp. 21P-21P
Author(s):  
S C Afford ◽  
D Burnett ◽  
P Davis Cory ◽  
E J Campbell ◽  
R A Stockley

1984 ◽  
Vol 130 (2) ◽  
pp. 305-306 ◽  
Author(s):  
Madeleine Mordelet-Dambrine ◽  
Annie Arnoux ◽  
Gisèle Stanislas-Leguern ◽  
Daniel Sandron ◽  
Jacques Chrétien ◽  
...  
Keyword(s):  

1999 ◽  
Vol 277 (4) ◽  
pp. L823-L830 ◽  
Author(s):  
Timothy S. Blackwell ◽  
Lisa H. Lancaster ◽  
Thomas R. Blackwell ◽  
Annapurna Venkatakrishnan ◽  
John W. Christman

We examined the relationship between nuclear factor (NF)-κB DNA binding activity, cytokine gene expression, and neutrophilic alveolitis in rats after intratracheal (IT) instillation of endotoxin [lipopolysaccharide (LPS)]. NF-κB activation in lung tissue mirrored neutrophilic alveolitis after IT LPS instillation, with NF-κB activation and neutrophilic influx beginning 2 h after IT LPS doses of 0.01 mg/kg or greater. In lung lavage fluid cells, however, transient NF-κB activation was present in alveolar macrophages by 15 min after IT LPS instillation, followed by a second peak of NF-κB activation corresponding to the onset on neutrophilic alveolitis. For cytokines thought to be NF-κB dependent, two different patterns of mRNA expression were found. Interleukin (IL)-1α, IL-1β, and tumor necrosis factor-α showed increased mRNA by 30 min after IT LPS instillation, but IL-6- and cytokine-induced neutrophil chemoattractant mRNAs were not substantially increased until 2 h after IT LPS instillation. Therefore, IT LPS causes differential NF-κB activation in air space cells and lung tissue, which likely determines production of key cytokines and directs the evolution of neutrophilic alveolitis.


Viruses ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1175
Author(s):  
Anirban Sinha ◽  
René Lutter ◽  
Tamara Dekker ◽  
Barbara Dierdorp ◽  
Peter J. Sterk ◽  
...  

Accurate detection of human respiratory viral infections is highly topical. We investigated how strongly inflammatory biomarkers (FeNO, eosinophils, neutrophils, and cytokines in nasal lavage fluid) and lung function parameters change upon rhinovirus 16 infection, in order to explore their potential use for infection detection. To this end, within a longitudinal cohort study, healthy and mildly asthmatic volunteers were experimentally inoculated with rhinovirus 16, and time series of these parameters/biomarkers were systematically recorded and compared between the pre- and post-infection phases of the study, which lasted two months and one month, respectively. We found that the parameters’/biomarkers’ ability to discriminate between the infected and the uninfected state varied over the observation time period. Consistently over time, the concentration of cytokines, in nasal lavage fluid, showed moderate to very good discrimination performance, thereby qualifying for disease progression monitoring, whereas lung function and FeNO, while quickly and non-invasively measurable using cheap portable devices (e.g., at airports), performed poorly.


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