Modeling the acute- and late-phase responses to peripheral airway cooling and desiccation

2002 ◽  
Vol 93 (1) ◽  
pp. 195-200 ◽  
Author(s):  
Michael S. Davis ◽  
Chris M. Royer ◽  
Mark Payton ◽  
Brian Buttress
Keyword(s):  
Acute Phase ◽  
Bronchoalveolar Lavage Fluid ◽  
Polynomial Function ◽  
Late Phase ◽  
Lavage Fluid ◽  
Canine Model ◽  
Phase Response ◽  
Linear Relationships ◽  
Peripheral Airway ◽  
Isocapnic Hyperpnea

Acute bronchoconstriction after isocapnic hyperpnea can be produced in most asthmatic individuals. However, the existence of a late-phase response is less certain. We used a canine model of isocapnic hyperpnea to test the hypothesis that this discrepancy is due to differences in the challenge threshold for the responses. Acute-phase and late-phase bronchoconstriction was measured in nine dogs after peripheral airway exposure to unconditioned air. Additionally, bronchoalveolar lavage fluid (BALF) was obtained during the late-phase response. The acute-phase response was a polynomial function with a decreasing slope at higher challenges, whereas the late-phase response suggested that a minimum threshold of challenge severity was needed to produce late-phase bronchoconstriction. BALF leukocyte and eicosanoid concentrations had linear relationships with challenge severity. Our data support the hypothesis that acute- and late-phase posthyperpnea responses have different dose-response relationships, a fact that may explain the frequent lack of a late-phase response. However, our data suggest that mild inflammation can be induced with relatively lower challenge severity.

A Study of Peripheral Airway Findings Using an Ultrathin Bronchofiberscope and Bronchoalveolar Lavage Fluid with Diffuse Panbronchiolitis

Respiration ◽  
1998 ◽  
Vol 65 (6) ◽  
pp. 433-440 ◽  
Author(s):  
Masayuki Kikawada ◽  
Yuichi Ichinose ◽  
Kazushige Minemura ◽  
Masaru Takasaki ◽  
Keisuke Toyama
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Diffuse Panbronchiolitis ◽  
Peripheral Airway

Eicosanoids modulate hyperpnea-induced bronchoconstriction in canine peripheral airways

1996 ◽  
Vol 81 (3) ◽  
pp. 1255-1263 ◽  
Author(s):  
C. Omori ◽  
P. Tagari ◽  
A. N. Freed
Keyword(s):  
Bronchoalveolar Lavage ◽  
Wall Temperature ◽  
Airway Resistance ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Airway Wall ◽  
Airway Reactivity ◽  
Dry Air ◽  
Peripheral Airways ◽  
Peripheral Airway

We examined the role of leukotrienes (LTs) in the development of dry air-induced bronchoconstriction (AIB) in canine peripheral airways. Airway reactivity to exogenous LTs was first tested by using an LTD4 aerosol challenge: peripheral airway resistance increased approximately 130 +/- 51% (n = 4) above baseline when compared with its vehicle control. AIB was then assessed by measuring peripheral airway resistance after, and airway wall temperature during, a dry air challenge (DAC). Treatment with a peptidoleukotriene biosynthesis inhibitor (MK-0591) attenuated AIB by approximately 65% without altering airway wall temperature. The fact that MK-0591 did not alter airway reactivity to aerosolized acetylcholine and completely inhibited Ca2+ ionophore-induced LTB4 generation in canine whole blood attests to the specificity of the drug. Treatment with MK-0591 did not affect the increased number of epithelial cells recovered in bronchoalveolar lavage fluid 5 min after DAC. Concentrations of LTs and other eicosanoids in bronchoalveolar lavage fluid from vehicle-treated DAC airways were increased above baseline values; only LTs were reduced by MK-0591. Before MK-0591, AIB was significantly correlated with the dry air-induced generation of LTC4, LTD4, and LTE4. After treatment with MK-0591, AIB was correlated with thromboxane B2, prostaglandin (PG) F2 alpha, and PGE2. We conclude that hyperpnea with dry air stimulates local production and release of LTs in canine bronchi and, alone with the generation of bronchoconstricting and bronchodilating PGs, plays a central role in the modulation of AIB.

scholarly journals Exhausted and Apoptotic BALF T Cells in Proinflammatory Airway Milieu at Acute Phase of Severe Mycoplasma Pneumoniae Pneumonia in Children

2022 ◽  
Vol 12 ◽  
Author(s):  
Xi Chen ◽  
Fang Liu ◽  
Baoying Zheng ◽  
Xiaohui Kang ◽  
Xiaolin Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Mycoplasma Pneumoniae ◽  
Acute Phase ◽  
Cell Activation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Clinical Complications ◽  
First Time ◽  
Mycoplasma Pneumoniae Pneumonia ◽  
Activation Status

Severe mycoplasma pneumoniae pneumonia (MPP) in children presents with serious clinical complications. Without proper and prompt intervention, it could lead to deadly consequences. Dynamics of the inflammatory airway milieu and activation status of immune cells were believed to be the hallmark of the pathogenesis and progress of the disease. In this study, by employing the T-cell sorting and mRNA microarray, we were able to define the main feature of the chemokine/cytokine expression and the unique characteristics of T cells in the bronchoalveolar lavage fluid (BALF) from severe MPP patients at acute phase. Our study for the first time delineated the molecular changes in isolated BALF T cells in severe MPP children with respect to the cytokine/chemokine expression, cell activation, exhaustion, and apoptosis. By comparing the BALF aqueous expression of cytokines/chemokines with that in sorted T cells, our data give a preliminary clue capable of finishing out the possible cell source of the proinflammatory cytokines/chemokines from the BALF mixture. Meanwhile, our data provide a distinctively pellucid expression profile particularly belonging to the isolated BALF T cells demonstrating that in the inflammatory airway, overactivated T cells were exhausted and on the verge of apoptotic progress.

scholarly journals Acute-phase protein concentration in bronchoalveolar lavage fluid from healthy horses

2020 ◽  
Vol 40 (12) ◽  
pp. 1073-1076
Author(s):  
Paula Alessandra Di Filippo ◽  
Luiza Maria F. Ribeiro ◽  
Marcos Aurélio D. Meireles ◽  
Francielli P. Gobbi ◽  
Andressa Francisca S. Nogueira
Keyword(s):  
Bronchoalveolar Lavage ◽  
Acute Phase ◽  
Immunoglobulin G ◽  
Gel Electrophoresis ◽  
Bronchoalveolar Lavage Fluid ◽  
Acute Phase Proteins ◽  
Polyacrylamide Gel Electrophoresis ◽  
Lavage Fluid ◽  
Polyacrylamide Gel ◽  
Sds Page

ABSTRACT: Bronchoalveolar lavage fluid (BALF) was analyzed to obtain information on leakage of acute-phase proteins from the blood into the respiratory lumen and about local synthesis. Ceruloplasmin, transferrin, albumin, α1-antitripsin, immunoglobulin G heavy, immunoglobulin G light, immunoglobulin A, haptoglobin, acidic glycoprotein, and P23 were measured in BALF from 30 horses without inflammatory disease by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). In serum, the same proteins were identified except for α1-antitrypsin. In conclusion, this study demonstrated that polyacrylamide gel electrophoresis (SDS-PAGE) can be used for the determination of acute-phase proteins in BALF samples from horses. In healthy horses, the values are very low, but they can be compared with reference values to assist in the diagnosis of animals with respiratory diseases.

Time course of lung ischemia-reperfusion-induced ICAM-1 expression and its role in ischemia-reperfusion lung injury

2002 ◽  
Vol 93 (2) ◽  
pp. 620-628 ◽  
Author(s):  
Yen-Ta Lu ◽  
Pai-Gene Chen ◽  
Shu Fang Liu
Keyword(s):  
Bronchoalveolar Lavage ◽  
Neutrophil Count ◽  
Time Course ◽  
Bronchoalveolar Lavage Fluid ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Late Phase ◽  
Lavage Fluid ◽  
Intercellular Adhesion Molecule ◽  
Microvascular Leakage

Upregulation of intercellular adhesion molecule-1 (ICAM-1) expression is an important mechanism underlying ischemia-reperfusion (I/R) induced neutrophil activation and tissue injury in other organs. However, I/R of the lungs has not been shown to upregulate ICAM-1 expression. We determined the time course profile of lung I/R-induced ICAM-1 expression and assessed the role of ICAM-1 in mediating neutrophil sequestration, transmigration, and I/R injury in the isolated blood-perfused rat lungs. I/R had a biphasic effect on ICAM-1 expression, an early downregulation and a late-phase upregulation. Superoxide dismutase and neutrophil depletion prevented the early ICAM-1 downregulation. The late-phase ICAM-1 upregulation coincided with the I/R-induced increase in pulmonary microvascular leakage index. ICAM-1 monoclonal antibody (MAb) reversed the I/R-induced increase in pulmonary microvascular leakage index, with control antibody being ineffective. Neither I/R nor ICAM-1 MAb affected lung MPO activity and circulating neutrophil count. Lung I/R significantly increased bronchoalveolar lavage fluid neutrophil count and the GSSG-to-(GSSG+GSH) ratio. ICAM-1 MAb blocked the I/R-induced increase in GSSG-to-(GSSG+GSH) ratio but had no effect on bronchoalveolar lavage fluid neutrophil count. Our results demonstrated that lung I/R up- and downregulates ICAM-1 expression depending on the duration of reperfusion. ICAM-1 upregulation is an important mechanism of I/R-induced pulmonary endothelial injury.

Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors

1996 ◽  
Vol 81 (5) ◽  
pp. 2053-2059 ◽  
Author(s):  
Ju-Lun Hong ◽  
Lu-Yuan Lee
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Bronchoalveolar Lavage Fluid ◽  
Smooth Muscles ◽  
Lavage Fluid ◽  
Phase Response ◽  
Second Phase ◽  
Causative Agents ◽  
Thromboxane Receptors

Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors. J. Appl. Physiol. 81(5): 2053–2059, 1996.—Inhalation of cigarette smoke induces a biphasic bronchoconstriction in guinea pigs: the first phase is induced by a combination of cholinergic reflex and tachykinins, whereas the second phase involves cyclooxygenase metabolites (J.-L. Hong, I. W. Rodger, and L.-Y. Lee. J. Appl. Physiol. 78: 2260–2266, 1995). This study was carried out to further determine the causative agents in the smoke and the types of prostanoid receptors and endogenous prostanoids mediating the bronchoconstriction. Inhalation of 10 ml of high-nicotine cigarette smoke consistently elicited the biphasic bronchoconstriction in anesthetized and artificially ventilated guinea pigs. Pretreatment with hexamethonium (10 mg/kg iv) significantly reduced the first-phase bronchoconstriction but did not have any measurable effect on the second-phase response. In sharp contrast, gas-phase smoke did not elicit any bronchoconstrictive effect. Furthermore, when the animals were challenged with low-nicotine cigarette smoke, only a single second-phase response was evoked, accompanied by increases in thromboxane (Tx) B2 (a stable metabolite of TxA2), prostaglandin (PG) D2, PGF2α in the bronchoalveolar lavage fluid. The bronchoconstrictive response induced by low-nicotine smoke was completely prevented by pretreatment with SQ-29548 (0.3 mg/kg iv), a TxA2-receptor antagonist. These results indicate that 1) nicotine is the primary causative agent responsible for the first-phase bronchoconstriction and 2) nonnicotine smoke particulates evoke the release of TxA2, PGD2, and PGF2α, which act on TxA2 receptors on airway smooth muscles and induce the second-phase response to cigarette smoke.

Cytokines and the acute phase response to influenza virus in mice

1995 ◽  
Vol 268 (1) ◽  
pp. R78-R84 ◽  
Author(s):  
C. A. Conn ◽  
J. L. McClellan ◽  
H. F. Maassab ◽  
C. W. Smitka ◽  
J. A. Majde ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Locomotor Activity ◽  
Acute Phase ◽  
Water Intake ◽  
Acute Phase Response ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Phase Response ◽  
Necrosis Factor Alpha ◽  
Food And Water Intake

This study characterized selected aspects of the acute phase response after intranasal inoculation of mice with two doses of mouse-adapted influenza virus differing in lethality. Mice given 140 plaque-forming units (PFU) of virus (58% survival) gradually decreased food and water intake to nearly zero over 6 days; survivors then slowly increased intakes. Declines in these behaviors were parallel to decreases in body temperature and general locomotor activity and were associated with elevated activities of interleukin-6 (IL-6), tumor necrosis factor-alpha, and interferons in lung lavage fluid. Circulating levels of these cytokines were not increased. After 55,000 PFU of virus (100% mortality), food and water intake fell to near zero within 48 h, temperature and locomotor activity decreased significantly, and activities of IL-1 and IL-6 were elevated in lung lavage fluid. These data show that cytokine activities in the lungs are elevated in a time frame that supports the hypothesis that cytokines could mediate behavioral and physiological changes in mice during acute influenza infections.

scholarly journals Activation of Hepatic STAT3 Maintains Pulmonary Defense during Endotoxemia

2015 ◽  
Vol 83 (10) ◽  
pp. 4015-4027 ◽  
Author(s):  
Kristie L. Hilliard ◽  
Eri Allen ◽  
Katrina E. Traber ◽  
Yuri Kim ◽  
Gregory A. Wasserman ◽  
...  
Keyword(s):  
Acute Phase ◽  
Host Defense ◽  
Bronchoalveolar Lavage Fluid ◽  
Acute Phase Proteins ◽  
Ex Vivo ◽  
Reactive Oxygen Species Generation ◽  
Lavage Fluid ◽  
Phase Changes ◽  
Content Type

Pneumonia and infection-induced sepsis are worldwide public health concerns. Both pathologies elicit systemic inflammation and induce a robust acute-phase response (APR). Although APR activation is well regarded as a hallmark of infection, the direct contributions of liver activation to pulmonary defense during sepsis remain unclear. By targeting STAT3-dependent acute-phase changes in the liver, we evaluated the role of liver STAT3 activity in promoting host defense in the context of sepsis and pneumonia. We employed a two-hit endotoxemia/pneumonia model, whereby administration of 18 h of intraperitoneal lipopolysaccharide (LPS; 5 mg/kg of body weight) was followed by intratrachealEscherichia coli(106CFU) in wild-type mice or those lacking hepatocyte STAT3 (hepSTAT3−/−). Pneumonia alone (without endotoxemia) was effectively controlled in the absence of liver STAT3. Following endotoxemia and pneumonia, however, hepSTAT3−/−mice, with significantly reduced levels of circulating and airspace acute-phase proteins, exhibited significantly elevated lung and blood bacterial burdens and mortality. These data suggested that STAT3-dependent liver responses are necessary to promote host defense. While neither recruited airspace neutrophils nor lung injury was altered in endotoxemic hepSTAT3−/−mice, alveolar macrophage reactive oxygen species generation was significantly decreased. Additionally, bronchoalveolar lavage fluid from this group of hepSTAT3−/−mice allowed greater bacterial growthex vivo. These results suggest that hepatic STAT3 activation promotes both cellular and humoral lung defenses. Taken together, induction of liver STAT3-dependent gene expression programs is essential to countering the deleterious consequences of sepsis on pneumonia susceptibility.

scholarly journals The Acute Phase Response Is a Prominent Renal Proteome Change in Sepsis in Mice

2019 ◽  
Vol 21 (1) ◽  
pp. 200 ◽  
Author(s):  
Beáta Róka ◽  
Pál Tod ◽  
Tamás Kaucsár ◽  
Matej Vizovišek ◽  
Robert Vidmar ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mrna Expression ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Acute Phase Proteins ◽  
Late Phase ◽  
Kidney Injury ◽  
Phase Response ◽  
Complement C3 ◽  
Saline Control

(1) Background: Sepsis-induced acute kidney injury (AKI) is the most common form of acute kidney injury (AKI). We studied the temporal profile of the sepsis-induced renal proteome changes. (2) Methods: Male mice were injected intraperitoneally with bacterial lipopolysaccharide (LPS) or saline (control). Renal proteome was studied by LC-MS/MS (ProteomeXchange: PXD014664) at the early phase (EP, 1.5 and 6 h after 40 mg/kg LPS) and the late phase (LP, 24 and 48 h after 10 mg/kg LPS) of LPS-induced AKI. Renal mRNA expression of acute phase proteins (APP) was assessed by qPCR. (3) Results: Renal proteome change was milder in EP vs. LP. APPs dominated the proteome in LP (proteins upregulated at least 4-fold (APPs/all): EP, 1.5 h: 0/10, 6 h: 1/10; LP, 24 h: 22/47, 48 h: 17/44). Lipocalin-2, complement C3, fibrinogen, haptoglobin and hemopexin were the most upregulated APPs. Renal mRNA expression preceded the APP changes with peak effects at 24 h, and indicated renal production of the majority of APPs. (4) Conclusions: Gene expression analysis revealed local production of APPs that commenced a few hours post injection and peaked at 24 h. This is the first demonstration of a massive, complex and coordinated acute phase response of the kidney involving several proteins not identified previously.

scholarly journals Influence of sensitization and allergen provocation procedures on the development of allergen-induced bronchial hyperreactivity in conscious, unrestrained guinea-pigs

1995 ◽  
Vol 4 (2) ◽  
pp. 149-156 ◽  
Author(s):  
R. E. Santing ◽  
C. G. Olymulder ◽  
B. van Diepen ◽  
H. Meurs ◽  
J. Zaagsma
Keyword(s):  
Bronchoalveolar Lavage ◽  
Guinea Pigs ◽  
Bronchoalveolar Lavage Fluid ◽  
Late Phase ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Bronchial Hyperreactivity ◽  
Cellular Activation ◽  
Allergen Provocation ◽  
Similar Development

The effects of different sensitization and allergen provocation regimens on the development of allergen-induced bronchial hyperreactivity (BHR) to histamine were investigated in conscious, unrestrained guinea-pigs. Similar early and late phase asthmatic reactions, BHR for inhaled histamine after the early (6 h) as well as after the late reaction (24 h), and airway inflammation were observed after a single allergen provocation in animals sensitized to produce mainly IgG or IgE antibodies, respectively. Repeating the allergen provocation in the IgE-sensitized animals after 7 days, using identical provocation conditions, resulted in a similar development of BHR to histamine inhalation. Repetition of the allergen provocation during 4 subsequent days resulted in a decreased development of BHR after each provocation, despite a significant increase in the allergen provocation dose necessary to obtain similar airway obstruction. The number of inflammatory cells in the bronchoalveolar lavage was not significantly changed after repeated provocation, when compared with a single allergen provocation. Finally, we investigated allergen-induced bronchial hyperreactivity by repetition of the sensitization procedure at day 7 and 14 (booster), followed by repeated allergen provocation twice a week for 5 weeks. Surprisingly, no BHR to histamine could be observed after either provocation, while the number of inflammatory cells in the bronchoalveolar lavage fluid after 5 weeks was enhanced compared with controls. These data indicate that both IgE and IgG sensitized guinea-pigs may develop bronchial hyperreactivity after a single allergen provocation. Repeated allergen exposure of IgE sensitized animals causes a gradual fading of the induced hyperreactivity despite the on-going presence of inflammatory cells in the airways, indicating a mechanism of reduced cellular activation.

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