Anti-inflammatory effects of zinc and alterations in zinc transporter mRNA in mouse models of allergic inflammation

2007 ◽  
Vol 292 (2) ◽  
pp. L577-L584 ◽  
Author(s):  
Carol Lang ◽  
Chiara Murgia ◽  
Mary Leong ◽  
Lor-Wai Tan ◽  
Giuditta Perozzi ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Gene Array ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Mrna Levels ◽  
Solute Carrier Family ◽  
Zn Uptake ◽  
Solute Carrier

There is clinical evidence linking asthma with the trace element, zinc (Zn). Using a mouse model of allergic inflammation, we have previously shown that labile Zn decreases in inflamed airway epithelium (Truong-Tran AQ, Ruffin RE, Foster PS, Koskinen AM, Coyle P, Philcox JC, Rofe AM, Zalewski PD. Am J Respir Cell Mol Biol 27: 286–296, 2002). Moreover, mild nutritional Zn deficiency worsens lung function. Recently, a number of proteins belonging to the Solute Carrier Family 39 (ZIP) and Solute Carrier Family 30 (ZnT) have been identified that bind Zn and regulate Zn homeostasis. Mice were sensitized, and subsequently aerochallenged, with ovalbumin to induce acute and chronic airway inflammation. Mice received 0, 54, or 100 μg of Zn intraperitoneally. Tissues were analyzed for Zn content and histopathology. Inflammatory cells were counted in bronchoalveolar lavage fluid. Cytokine and Zn transporter mRNA levels were determined by cDNA gene array and/or real-time PCR. Zn supplementation decreased bronchoalveolar lavage fluid eosinophils by 40 and 80%, and lymphocytes by 55 and 66%, in the acute and chronic models, respectively. Alterations in Zn transporter expression were observed during acute inflammation, including increases in ZIP1 and ZIP14 and decreases in ZIP4 and ZnT4. Zn supplementation normalized ZIP1 and ZIP14, but it did not affect mRNA levels of cytokines or their receptors. Our results indicate that inflammation-induced alterations in Zn transporter gene expression are directed toward increasing Zn uptake. Increases in Zn uptake may be needed to counteract the local loss of Zn in the airway and to meet an increased demand for Zn-dependent proteins. The reduction of inflammatory cells by Zn in the airways provides support for Zn supplementation trials in human asthmatic individuals.

scholarly journals Allergic Inflammation Caused by Dimerized Translationally Controlled Tumor Protein is Attenuated by Cardamonin

2021 ◽  
Vol 12 ◽  
Author(s):  
Haejun Pyun ◽  
Joo-Won Nam ◽  
Hyunsoo Cho ◽  
Jiyoung Park ◽  
Eun Kyoung Seo ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage Fluid ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Allergic Diseases ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Translationally Controlled Tumor Protein ◽  
Dimeric Form ◽  
Allergic Mouse ◽  
Inflammatory Effect

We demonstrated in our previous reports that dimeric form of translationally controlled tumor protein (dTCTP) initiates a variety of allergic phenomena. In the present study, we examined whether and how dTCTP’s role in allergic inflammation can be modulated or negated. The possible potential of cardamonin as an anti-allergic agent was assessed by ELISA using BEAS-2B cells and OVA-challenged allergic mouse model. The interaction between cardamonin and dTCTP was confirmed by SPR assay. Cardamonin was found to reduce the secretion of IL-8 caused by dTCTP in BEAS-2B cells by interacting with dTCTP. This interaction between dTCTP and cardamonin was confirmed through kinetic analysis (KD = 4.72 ± 0.07 μM). Also, cardamonin reduced the migration of various inflammatory cells in the bronchoalveolar lavage fluid (BALF), inhibited OVA specific IgE secretion and bronchial remodeling. In addition, cardamonin was observed to have an anti-allergic response by inhibiting the activity of NF-κB. Cardamonin exerts anti-allergic anti-inflammatory effect by inhibiting dTCTP, suggesting that it may be useful in the therapy of allergic diseases.

scholarly journals Effects of prenatal ethanol exposure on the lungs of postnatal lambs

2011 ◽  
Vol 300 (1) ◽  
pp. L139-L147 ◽  
Author(s):  
Foula Sozo ◽  
Melissa Vela ◽  
Victoria Stokes ◽  
Kelly Kenna ◽  
Peter J. Meikle ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Phospholipid Composition ◽  
Lavage Fluid ◽  
Ethanol Exposure ◽  
Cytokine Gene Expression ◽  
Ethanol Administration ◽  
Mrna Levels ◽  
Prenatal Ethanol Exposure ◽  
Treatment Groups

Prenatal ethanol exposure increases collagen deposition and alters surfactant protein (SP) expression and immune status in lungs of near-term fetal sheep. Our objectives were to determine 1) whether these prenatal effects of repeated gestational ethanol exposure persist after birth and 2) whether surfactant phospholipid composition is altered following prenatal ethanol exposure. Pregnant ewes were chronically catheterized at 90 days of gestational age (DGA) and given a 1-h daily infusion of ethanol (0.75 g/kg, n = 9) or saline ( n = 7) from 95 to 135 DGA; ethanol administration ceased after 135 DGA. Lambs were born naturally at full term (146 ± 0.5 DGA). Lung tissue was examined at 9 wk postnatal age for alterations in structure, SP expression, and inflammation; bronchoalveolar lavage fluid was examined for alterations in surfactant phospholipid composition. At 134 DGA, surfactant phospholipid concentration in amniotic fluid was significantly reduced ( P < 0.05) by ethanol exposure, and the composition was altered. In postnatal lambs, there were no significant differences between treatment groups in birth weight, postnatal growth, blood gas parameters, and lung weight, volume, tissue fraction, mean linear intercept, collagen content, proinflammatory cytokine gene expression, and bronchoalveolar lavage fluid surfactant phospholipid composition. Although SP-A, SP-B, and SP-C mRNA levels were not significantly different between treatment groups, SP-D mRNA levels were significantly greater ( P < 0.05) in ethanol-treated animals; as SP-D has immunomodulatory roles, innate immunity may be altered. The adverse effects of daily ethanol exposure during late gestation on the fetal lung do not persist to 2 mo after birth, indicating that the developing lung is capable of repair.

scholarly journals COMPARISON OF TWO TECHNIQUES FOR ASSESSING INFLAMMATORY CELLS IN BRONCHOALVEOLAR LAVAGE FLUID. 2021

1996 ◽  
Vol 39 ◽  
pp. 339-339
Author(s):  
Jan R McColm ◽  
Andrew J Lyon ◽  
Linda Middlemist ◽  
Neil Mclntosh
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Inflammatory Cells ◽  
Lavage Fluid

Relationship between Inflammatory Cells in Bronchoalveolar Lavage Fluid and Pathologic Changes in the Lung Interstitium

Respiration ◽  
1998 ◽  
Vol 65 (5) ◽  
pp. 386-392 ◽  
Author(s):  
Chiharu Yoshii ◽  
Nobuhiko Nagata ◽  
Yoshiaki Tao ◽  
Rika Suematsu ◽  
Yoshihiko Nikaido ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Inflammatory Cells ◽  
Lavage Fluid

scholarly journals Effects of Roflumilast, Selective PDE4 Inhibitor, on Airway Reactivity in Ovalbumin-Sensitized Guinea Pigs

2015 ◽  
Vol 5 (1) ◽  
pp. 12-19
Author(s):  
Nirmathan Tharmalingam ◽  
I. Medvedova ◽  
A. Eichlerova ◽  
M. Prso ◽  
D. Mokra ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Guinea Pigs ◽  
Bronchoalveolar Lavage Fluid ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Whole Body ◽  
Pde4 Inhibitor ◽  
Airway Reactivity

Abstract Background: Roflumilast as a phosphodiesterase 4 inhibitor has shown to increase lung functions and decrease the number of exacerbations in chronic obstructive lung disease. In this study, its ability to decrease the airway hyperresponsiveness in a model of eosinophil inflammation was evaluated. Methods: Healthy adult male guinea pigs were divided into groups as follows: the first group was considered as a healthy control group (without sensitization and therapy), animals in the second group were sensitized with ovalbumin, but left without further treatment, and the animals in the third group were sensitized with ovalbumin and treated with roflumilast perorally for 7 consecutive days. In vivo airway reactivity was evaluated using double-chamber whole body plethysmograph and measuring the specific airway resistance after nebulization of histamine aerosol. In vitro experiments were performed with tissue strips of trachea and lungs in organ bath, where their contractile responses to cumulative doses of acetylcholine and histamine were registered. The numbers of inflammatory cells in blood and bronchoalveolar lavage fluid were measured using standard staining. Results: Guinea pigs with roflumilast treatment showed decreased in vivo and in vitro airway reactivity associated with suppressed recruitment of inflammatory cells (especially eosinophils) in blood and bronchoalveolar lavage fluid. Conclusion: Roflumilast has demonstrated the therapeutic potential in the model of ovalbumin induced eosinophil inflammation typically present in patients with bronchial asthma.

CYFRA 21-1, a Cytokeratin Subunit 19 Fragment, in Bronchoalveolar Lavage Fluid from Patients with Interstitial Lung Disease

1998 ◽  
Vol 94 (5) ◽  
pp. 531-535 ◽  
Author(s):  
Hiroshi Kanazawa ◽  
Takahiro Yoshikawa ◽  
Masashi Yamada ◽  
Seiichi Shoji ◽  
Tatsuo Fujii ◽  
...  
Keyword(s):  
Interstitial Lung Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Bronchoalveolar Lavage ◽  
Lung Disease ◽  
Bronchoalveolar Lavage Fluid ◽  
Inflammatory Cells ◽  
Normal Subjects ◽  
Lavage Fluid ◽  
Arterial Oxygen

1. It has been suggested that CYFRA21-1, a cytokeratin subunit 19 fragment, is potentially useful for diagnosis and monitoring of lung carcinoma. However, serum levels of CYFRA21-1 are also increased in a high proportion of patients with interstitial lung disease. In this study we measured CYFRA21-1 levels in bronchoalveolar lavage fluid from 10 normal subjects, 18 patients with idiopathic pulmonary fibrosis and 14 patients with sarcoidosis, and determined whether any relationship exists between CYFRA21-1 levels in bronchoalveolar lavage fluid and clinical parameters. 2. CYFRA21-1 levels in bronchoalveolar lavage fluid were significantly higher in patients with sarcoidosis (mean value 8.3 ng/ml, P < 0.01) and idiopathic pulmonary fibrosis (42.5 ng/ml, P < 0.005) than in normal controls (1.0 ng/ml). Moreover, higher CYFRA21-1 levels in bronchoalveolar lavage fluid were found in sarcoidosis patients in radiological stage 2 or 3 than in those in stage 1. In patients with idiopathic pulmonary fibrosis, there was a significant correlation between CYFRA21-1 levels, and percentage of inflammatory cells in bronchoalveolar lavage fluid (r = 0.56, P < 0.05) and the magnitude of the alveolar — arterial oxygen pressure difference [P(a — a)o2] gradient (r = 0.66, P < 0.01). 3. Serial bronchoalveolar lavage samples were obtained from six patients with clinically active pneumonitis after they had undergone systemic corticosteroid therapy. CYFRA21-1 levels were significantly lower after these patients exhibited clinical improvement (P < 0.05). 4. These findings suggest that the level of CYFRA21-1 in bronchoalveolar lavage fluid is a useful marker for the clinical diagnosis of pneumonitis, and is also adequate for the evaluation of disease activity, especially over the course of treatment.

scholarly journals Leukocytic cell sources of airway tissue kallikrein

2004 ◽  
Vol 286 (4) ◽  
pp. L734-L740 ◽  
Author(s):  
Isabel T. Lauredo ◽  
Rosanna M. Forteza ◽  
Yelena Botvinnikova ◽  
William M. Abraham
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Hyperresponsiveness ◽  
Bronchoalveolar Lavage Fluid ◽  
Allergen Challenge ◽  
Serine Proteinase ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Lavage Fluid ◽  
Initial Increase ◽  
Tissue Kallikrein

Lung tissue kallikrein (TK) is a serine proteinase that putatively plays a role in the pathophysiology of asthma by generating kallidin and bradykinin, mediators that contribute to airway hyperresponsiveness. In previous studies we observed biphasic increases in TK activity in bronchoalveolar lavage fluid following airway allergen challenge in allergic sheep. Although glandular TK is likely a major source of the initial increase in TK, the sources of the late increases in TK that are associated with the development of airway hyperresponsiveness may be dependent on activated resident and recruited inflammatory cells including alveolar macrophages (AMs) and neutrophils (PMNs). These cells increase concomitantly with the late increases in TK activity. To test this hypothesis, we obtained AMs from bronchoalveolar lavage fluid and PMNs and monocytes (precursors of AMs) from sheep blood and determined whether these cells contained TK and whether these same cells could release TK upon activation. Using confocal microscopy, immunocytochemical techniques, and enzyme activity assays, we found that all three cell types contained and secreted TK. All three cell types demonstrated basal release of TK, which could be increased after stimulation with zymosan. In addition, PMNs also released TK in the presence of phorbol ester, suggesting multiple secretory pathways in these cells. Furthermore, we showed that human monocytes also contain and secrete TK. We conclude that in the airways, monocytes, PMNs, and AMs may contribute to increased TK activity. Knowing the sources of TK in the airways could be important in understanding the mechanisms of inflammation that contribute to the pathophysiology of asthma and may help in the development of new therapies to control the disease.

scholarly journals Allergic inflammatory responses induced by traffic-related PM2.5  in BALB/c mice

2021 ◽  
Author(s):  
Hai Ying Wei ◽  
Huan Yu ◽  
Lifeng Zhang ◽  
Zhenyu Dong
Keyword(s):  
Lung Injury ◽  
Public Transportation ◽  
Bronchoalveolar Lavage Fluid ◽  
Inflammatory Responses ◽  
Heavy Traffic ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Rt Pcr ◽  
Soluble Extract

Abstract Previous studies have shown that PM2.5 is associated with airway inflammation and lung injury. However, the association between traffic-related PM2.5 (TR-PM) exposure and OVA-induced allergic inflammation is not fully elucidated. In this study, we assessed allergic inflammatory responses of mice induced by TR-PM. PM2.5 was collected from a roadside with heavy traffic, and its soluble extract was prepared. Mice were treated with OVA, TR-PM alone, and OVA + TR-PM. The inflammatory cells were counted, and inflammation-related cytokines IL-4, IL-17A, and IL-10 in bronchoalveolar lavage fluid (BALF) were determined by the radioimmunity assay. Allergy-induced inflammation and lung injury were investigated by histopathological analyses. The expression of IL-4, IL-17A, and IL-10 mRNA was analyzed by RT-PCR. Our results revealed that TR-PM exposure, combined with OVA allergen sensitization, increased the inflammatory cells in BALF as well as levels of IgE in lung tissue; increased the IL-4 and IL-17A levels in BALF significantly, but decreased IL-10 level. The histopathologic results demonstrated that TR-PM markedly exacerbated the OVA-induced neutrophilic granulocyte, lymphocyte, and macrophage infiltration. Furthermore, the expression of IL-4, IL-17A and IL-10 mRNA was well in agreement with the results of the inflammatory cytokines. In conclusion, during the sensitization to allergic antigens, TR-PM exposure triggers severe allergic inflammation and lung injury. These findings suggest that commuters should use public transportation instead of riding motorcycles or walking during rush hours.

Sign in / Sign up

Export Citation Format

Share Document