Effects of respiratory viruses on pulmonary alveolar macrophages.
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Antigen-Presenting Cells↗
Biomedical subjects
S F Quan
Publications and source records attributed to S F Quan.
Bronchoalveolar lavage fluid cytology reflects airway inflammation in beagle puppies with acute bronchiolitis.
Beagle puppies infected with both canine parainfluenza virus type 2 (CPI2) and Bordetella bronchiseptica (Bb) develop more severe acute bronchiolitis and airways hyperresponsiveness than do those infected with CPI2 or Bb alone. The aim of our study was to characterize the inflammatory response associated with airway hyperresponsiveness, and to determine whether the inflammatory cell response of bronchoalveolar lavage fluid (BALF) reflected changes in the bronchioles in this model. We investigated 25 beagle puppies (ages 76 +/- 5 days, mean +/- SEM) in four groups: controls (n = 6), or puppies inoculated with both CPI2 and Bb (CPI2-Bb) (n = 11), with only CPI2 (n = 4), or only Bb (n = 4). The puppies were killed 3-4 days after inoculation, the lungs excised, the intermediate lobe lavaged, and BALF and the bronchiolar wall tissue examined for neutrophils and other inflammatory cells. Control puppies had no evidence of inflammation. However, the CPI2-Bb puppies had developed cough and rhinitis, positive cultures for CPI2 and Bb, and a neutrophilic cellular response in both the bronchioles and the BALF. Puppies inoculated with only CPI2 or Bb had milder illnesses and no significant bronchiolar and BALF neutrophilic response. For all groups, the severity of bronchiolar wall inflammation correlated with the total number of BALF inflammatory cells, and bronchiolar wall neutrophil counts correlated with the percentage of neutrophils in the BALF. The illness and the airway hyperresponsiveness observed in the CPI2-Bb group were associated with airway neutrophilia. Our studies support the hypothesis that neutrophils are associated with airway dysfunction in this model, and the use of BALF to study the process.
Acute Disease↗
Risk factors associated with complaints of insomnia in a general adult population. Influence of previous complaints of insomnia.
BACKGROUND: Insomnia is a common complaint both in the general population and also in physician's offices. However, risk factors for the development of insomnia complaints have not been completely identified. METHODS: To identify population characteristics associated with increased prevalence of insomnia complaints, we surveyed a large general adult population in 1984 through 1985. We evaluated the relationship among current complaints of initiating and maintaining sleep and obesity, snoring, concomitant health problems, socioeconomic status, and documented complaints of difficulty with insomnia 10 to 12 years previously. RESULTS: The strongest risk factor for complaints of initiating and maintaining sleep was previous complaints of insomnia (odds ratio, 3.5). In addition, female gender (odds ratio, 1.5), advancing age (odds ratio, 1.3), snoring (odds ratio, 1.3), and multiple types of concomitant health problems (odds ratios, 1.1 to 1.7) were all risk factors associated with an increased rate of complaints of initiating and maintaining sleep. CONCLUSION: Complaints of insomnia tend to be a persistent or recurrent problem over long periods of time. Female gender, advancing age, and concomitant health problems also are important risk factors.
Adult↗
Changes in lung mechanics and histamine responsiveness after sequential canine adenovirus 2 and canine parainfluenza 2 virus infection in beagle puppies.
We determined the effects of an immediately antecedent viral lower respiratory tract infection (LRI) on the severity of clinical illness, changes in lung function and airway histamine responsiveness produced by a subsequent LRI in 9-12 week old beagle puppies inoculated with canine adenovirus 2, followed in 2 weeks by inoculation with canine parainfluenza 2 virus (CAV2-CP12, n = 7). We compared their acute responses to puppies infected with CP12 alone (n = 5), CAV2 alone (n = 7), and no infection (control, n = 6). Puppies inoculated with either virus alone developed a LRI 3 to 6 days after inoculation which resolved by 12-14 days after inoculation. However, the illness was more severe in the CAV2 group. In the CAV2-CP12 group, CP12 infection following CAV2 infection resulted in a clinical illness nearly comparable to that observed with CAV2 alone. Whereas in control and CP12 puppies, lung resistance (RL) decreased and dynamic lung compliance (Cdyn) increased during the study due to normal growth, RL increased and Cdyn remained unchanged in the CAV2 group. In contrast, RL did not change and Cdyn increased in the CAV2-CP12 group. Airway histamine responsiveness in the CAV2-CP12 group increased during infection with CP12 and was similar to that observed with CAV2 alone. In contrast, infection with CP12 alone produced a small, but non-significant increase in histamine responsiveness. The duration of the increase in histamine responsiveness was not prolonged in the CAV2-CP12 group in comparison to CP12 or CAV2 alone. However, the length of clinical illness was extended in the CAV2-CP12 group in comparison to the other infected groups. These data suggest that an immediately antecedent viral LRI can potentiate the clinical and physiologic effects of a subsequent viral LRI.
Adenoviridae Infections↗
Canine parainfluenza type 2 and Bordetella bronchiseptica infection produces increased bronchoalveolar lavage thromboxane concentrations in beagle puppies.
Acute infections in beagle puppies with canine parainfluenza virus type 2 (CP12), and CP12 in combination with Bordetella bronchiseptica (Bb) produce bronchiolitis and increased airways responsiveness to aerosolized histamine during the acute infection. In order to determine whether these observations were associated with increased levels of eicosanoids, the stable metabolites of thromboxane A2 and prostacylin, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF 1 alpha) respectively, and leukotriene B4 were measured in the bronchoalveolar lavage (BAL) fluid of 25 beagle puppies (age = 76 +/- 1 days, mean +/- SEM) 3-4 days after no infection (control, n = 6), inoculation with both CP12 and Bb (CP12-Bb, n = 11), inoculation with CP12 alone (CP12, n = 4), and inoculation with Bb alone (Bb, n = 4). In addition, plasma levels of TXB2 and 6-keto-PGF1 alpha were measured before and after infection in the CP12-Bb and control groups. The BAL concentration of thromboxane B2 was increased in the CP12-Bb group (520 +/- 120 pg/ml), but not in the CP12 (88 +/- 40 pg/ml), Bb (235 +/- 100 pg/ml), or control groups (120 +/- 60 pg/ml, p less than 0.01). There also was a borderline increase in BAL concentration of LTB4 in the CP12-Bb group. No differences were observed in the BAL concentration of 6-keto PGF1 alpha. Furthermore, neither TXB2 nor PGF1 alpha was elevated in the plasma of control or CP12-Bb puppies. These data suggest that increased thromboxane concentrations in BAL fluid are associated with histamine hyperresponsiveness during acute infection in the CP12-Bb group.
6-Ketoprostaglandin F1 alpha↗
Effect of smoke inhalation on immediate changes in lung chemical mediators.
We studied the effects of acute smoke exposure on lung and alveolar macrophage (AM) function in New Zealand white rabbits. Six rabbits were exposed to smoke (SE, N = 6) and a control group of rabbits (SS, N = 6) were exposed to sham smoke. The smoke exposure consisted of 60 tidal volume breaths of air and smoke which were aspirated by syringe from a sampling port of a smoke chamber. The smoke was generated by the combustion of 20 ml diesel fuel and 0.2 g polycarbonate plastic shavings. The smoke was administered in 8-9 min. The rabbits were then killed and the lungs were removed for lavage. Acute smoke exposure caused a significant (p = 0.037) increase in bronchoalveolar lavage fluid levels of leukotriene B4 in the SE rabbits; 643 (+/- 30, SEM) pg/ml compared to 539 (+/- 43, SEM) pg/ml for SS rabbits at 3-4 min post-exposure. Lung surfactant, measured as mumoles/kg phosphatidylcholine, was decreased (p = 0.039) in SE rabbits' bronchoalveolar lavage fluid, 1.07 (+/- 0.12, SEM) -vs- 1.45 (+/- 0.15, SEM) for SS. Furthermore, cultured SE alveolar macrophage superoxide secretion after stimulation with phorbol myristate acetate was significantly decreased versus SS alveolar macrophage superoxide values at 40 min in culture. We conclude that acute smoke exposure causes immediate increases in bronchoalveolar lavage fluid levels of LTB4, and decreases in alveolar macrophage superoxide production and lung surfactant. These changes in chemical mediators may contribute to the lung injury caused by the smoke insult.
Animals↗
Effects of intravenous and aerosolized arachidonic acid on alveolar epithelial permeability in rabbits.
To determine whether arachidonic acid (AA) alters alveolar epithelial permeability, we studied the effect of both continuous intravenous and aerosolized AA on clearance of [99m]Tc-DTPA from lung to blood in rabbits. Although intravenous AA increased prostacyclin production and aerosolized AA decreased systemic blood pressure, neither continuous intravenous nor aerosolized AA augmented alveolar epithelial permeability.
Aerosols↗
Changes in lung mechanics and reactivity with age after viral bronchiolitis in beagle puppies.
We measured changes with growth in lung function and airway reactivity after acute canine parainfluenza virus type 2 (CPI2, n = 5), canine adenovirus type 2 (CAV2, n = 7), and sequential CAV2-CPI2 (n = 6) infections or no infection (controls, n = 6) in beagle puppies (age approximately 79 days). In the CPI2 and CAV2 groups, a lower respiratory illness developed by day 3 postinfection with clinical recovery by day 14. In the CAV2-CPI2 group, puppies were inoculated initially with CAV2 and 12 days later with CPI2. In this group, illness persisted until day 14 after infection with CPI2. Lung resistance (RL), dynamic (Cdyn) and static (Cst) lung compliance, functional residual capacity (FRC), and responsiveness to aerosolized histamine were measured before infection and at periodic intervals until 239 +/- 43 days of age. Lung function data were analyzed using a longitudinal random effects model. In all groups, FRC, Cst, and Cdyn increased with age. In all infected groups, the regression slopes for Cdyn were steeper than in controls. RL decreased linearly with age without group slope differences. Histamine reactivity increased with age, but there were no differences in slope among groups. Lung pathological studies showed areas of obliterative bronchiolitis and chronic small airways inflammation particularly in the CAV2 and CAV2-CPI2 groups. Thus, viral bronchiolitis produces chronic small airways inflammation in beagle puppies and alters the changes in lung function occurring with growth. Histamine reactivity increases with age and is not modified by viral infection.
Adenoviridae Infections↗
Canine parainfluenza type 2 bronchiolitis increases histamine responsiveness in beagle puppies.
Histamine hyperresponsiveness with viral bronchiolitis may depend on previous exposures to viruses or to other pathogens. We studied 32 outbred beagle puppies 80 to 155 days of age who were raised in isolation and who were specific pathogen-free. Puppies were inoculated with canine parainfluenza type 2 (CPI2, n = 8), Bordetella bronchiseptica (Bb, n = 7), or both CPI2 and Bb (CPI2-Bb, n = 9). Control puppies (C, n = 8) were not inoculated. The puppies were anesthetized with sodium thiopental (5 mg/kg) and chloralose (80 mg/kg) and were ventilated mechanically. Lung resistance (RL), dynamic lung compliance (Cdyn), functional residual capacity (FRC), and responsiveness to aerosolized histamine were measured 3 days prior to inoculation (Day -3), on the day of inoculation (Day 0), and on Days 3-4, 6, 8-10, and 12-14 after inoculation. Histamine responsiveness was measured as: (1) the concentration of histamine base that increased RL to 150% (PC 150% RL) or decreased Cdyn to 75% (PC 75% Cdyn) of the response to saline (RL sal and Cdyn sal, respectively), and (2) the change in RL or Cdyn after inhalation of 11 mg/ml of histamine when compared with RL sal and Cdyn sal. On Day 0 there were no significant (p greater than 0.05) differences among groups with regard to age-corrected weights, FRC, RL, Cdyn, or histamine responsiveness. Control puppies remained healthy, and their pulmonary function and histamine responsiveness did not change. CPI2-Bb puppies increased RL and decreased FRC on Day 3-4, and were moderately ill and histamine-hyperresponsive on Day 3-4 and on Day 6.(ABSTRACT TRUNCATED AT 250 WORDS)
Airway Resistance↗
Acute canine adenovirus 2 infection increases histamine airway reactivity in beagle puppies.
Acute infection with canine adenovirus was studied in 23 specific pathogen-free outbred beagle puppies (median age = 78 days, range = 67 to 86 days) to determine its effects on pulmonary function and airway responsiveness to aerosolized histamine. The following groups were studied: uninoculated (n = 6, Control); inoculated with canine adenovirus type 2 (CAV2) (n = 11, Infected); and subclinical spontaneous infection with CAV2 (n = 6, Subclinical). While anesthetized with chloralose and mechanically ventilated, lung function and responsiveness to aerosolized histamine were measured 3 days before inoculation (Day -3), the day of inoculation (Day 0), and 3 to 4 (Day 3-4), 6 (Day 6), 8 to 10 (Day 8-10), and 12 to 14 (Day 12-14) days after inoculation. Histamine responsiveness was assessed by calculating the provocation concentration of histamine diphosphate to increase lung resistance (RL) to 150% (PC 150% RL), or decrease dynamic lung compliance (Cdyn) to 75% (PC 75% Cdyn) of the response to saline [RL(sal) and Cdyn(sal), respectively]. Arterial blood gases, functional residual capacity (FRC), specific static lung compliance (spCst), RL, Cdyn, and histamine responsiveness were not significantly different on Day 0 among the groups (p greater than 0.05). Control and Subclinical puppies remained healthy, had a mean weight gain of 0.7 kg, and did not change their histamine responsiveness during the study period. Infected puppies developed moderate to severe clinical illnesses, had poor weight gain, and were histamine hyperresponsive on Days 3-4 and 6. One infected puppy died on Day 3-4, and two died on Day 6 of their illness.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Localization of inflammation and virions in canine adenovirus type 2 bronchiolitis.
Beagle puppies develop bronchiolar inflammation and histamine hyperresponsiveness with canine adenovirus type 2 (CAV2) infections. We determined the distribution of bronchiolar lesions and correlated inflammation with virions and bronchoalveolar lavage fluid (BALF) cytology. Nineteen beagle puppies were inoculated with tissue culture fluid (control puppies, n = 8), or CAV2 (CAV2, n = 11). The puppies had clinical assessments and measurements of lung resistance (RL), and dynamic compliance (Cdyn) immediately before inoculation (Day zero) and 3 days later (Day 3). The puppies were killed on Day 3, the lungs were removed, and the right intermediate lobe was lavaged. The BALF was assessed for total and differential cell counts. Bronchiolar inflammation was quantitated by bronchiolar inflammation scores (BIS). CAV2 was localized by immunofluorescent antibody staining and electron microscopy. The control puppies remained healthy. The CAV2 puppies had positive cultures for CAV2, respiratory symptoms, and generalized necrotizing bronchiolitis. Alveolar inflammation was quantitatively less prominent than bronchiolar inflammation, and RL and Cdyn were unchanged. The BALF neutrophilia correlated with the BIS. CAV2 was present within bronchiolar epithelium, alveolar epithelial type 2 cells, neutrophils, and macrophages. CAV2 was not found in airways smooth muscles or nerves, nor in any noninflamed tissues of CAV2 puppies or in control animals. Our data suggest that acute CAV2 in beagle puppies produces an inflammation of most bronchioles. Intracellular CAV2 was found in bronchiolar epithelium, macrophages, neutrophils, and alveolar epithelial type 2 cells. Bronchiolar inflammation was reflected in BALF cytology. We conclude that bronchiolar inflammation as indicated by BIS and BALF cytology is related temporarily to histamine hyperresponsiveness in our beagle puppies.
Adenoviridae↗
Bilateral paramediastinal post-traumatic lung cysts.
Unilateral post-traumatic and paramediastinal lung cysts are uncommon. Conservative therapeutic measures are usually sufficient. This report describes a patient whose bilateral post-traumatic paramediastinal lung cysts, a previously undescribed entity, were presumed to be bilateral hemidiaphragmatic hernias and, consequently, led to unnecessary surgery.
Adult↗
A ghost from the past. Low tidal volume mechanical ventilation revisited.
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Humans↗
Airway responses to inhaled Ascaris suum antigen in naturally sensitized beagle dogs.
To characterize the airway responses to inhaled Ascaris suum antigen in a group of adult Beagle dogs with cutaneous Ascaris sensitivity, 9 dogs were challenged with aerosolized Ascaris antigen and 6 were subsequently challenged 1 to 2 weeks later with aerosolized saline. Changes in lung resistance, dynamic lung compliance, and responsiveness to aerosolized histamine were measured during the ensuing 6 hours. Inhalation of Ascaris antigen produced immediate bronchoconstriction, but no spontaneous late bronchoconstrictive responses were noted. Two dogs demonstrated increased histamine responsiveness 6 hours after Ascaris challenge, and 4 dogs were histamine hyperresponsive 1 to 2 weeks later. We conclude that exposure to Ascaris antigen in naturally sensitized Beagle dogs produces an immediate asthmatic response and may result in airway hyperresponsiveness for several weeks. However, spontaneous late responses do not occur.
Airway Resistance↗
Pressure support compensation for inspiratory work due to endotracheal tubes and demand continuous positive airway pressure.
We evaluated the use of pressure support to compensate for the added inspiratory work of breathing due to the resistances of endotracheal tubes and a ventilator demand-valve system for continuous positive airway pressure (CPAP). A mechanical model was used to simulate spontaneous breathing at five respiratory rates through 7-mm, 8-mm, and 9-mm endotracheal tubes with and without a ventilator demand CPAP circuit. Added work was measured as the integral of the product of airway pressure and volume during inspiration. Additional work was a function of the tube's size, and each 1-mm decrease in the tube's diameter resulted in a 67 to 100 percent increase in work. Adding the ventilator CPAP circuit further increased work and was responsible for 30 to 50 percent of the total work resulting from a tube and CPAP circuit together. Pressure support was added to a level at which net work on the airway was zero, and a relationship between mean inspiratory flow (VT/TI) and the optimal level of pressure support was established for each endotracheal tube. The inspiratory work of breathing was then measured in normal subjects breathing with and without each endotracheal tube plus the demand CPAP circuit. Work per liter of minute ventilation due to the endotracheal tube and CPAP circuit was increased from 54 to 240 percent over levels measured while breathing through an open airway. For each endotracheal tube and VT/TI, a level of pressure support (range, 2 to 20 cm H2O) was found which eliminated added work in the spontaneously breathing subject. This level correlated well with that predicted from the data derived using the mechanical model. We conclude that when adjusting for an endotracheal tube's diameter and VT/TI, pressure support can be used to compensate for the added inspiratory work due to artificial airway resistances.
Airway Resistance↗
Risk factors in a general population for snoring. Importance of cigarette smoking and obesity.
In order to study risk factors associated with snoring in a general adult population, 2,187 subjects in the Tucson Epidemiologic Study of Obstructive Airways Disease were surveyed to determine the prevalence of snoring. Major independent risk factors for snoring were male gender, age between 40 and 64 years, obesity, and current cigarette smoking. Furthermore, greater intensity of cigarette smoking also was associated with higher snoring prevalence rates. Snoring prevalence remained elevated in subjects who recently quit smoking, but declined in ex-smokers to the level of never smokers within four years of smoking cessation. The presence of cough or sputum production was associated with an increase in snoring prevalence especially in ex-smokers. Snoring prevalence was slightly increased in subjects who regularly used alcohol or medications as aids to sleep. We conclude that cigarette smoking, obesity, male gender, age over 40, and use of alcohol or sleep medications are important risk factors for snoring. We propose that the effect of smoking may be related to the production of upper airway inflammation and edema by cigarette smoke, and that smoking cessation may eventually reduce snoring risk.
Adult↗
Acute cigarette smoke exposure alters lung eicosanoid and inflammatory cell concentrations in rabbits.
We studied lung clearance of technetium-labeled diethylenetriamine pentaacetic acid [( 99mTc]DTPA), plasma and bronchoalveolar lavage fluid (BALF) concentrations of 6-keto-PGF1 alpha (stable metabolite of prostacyclin, prostaglandin I2, PGI2), TxB2 (stable metabolite of thromboxane A2, TxA2), and leukotriene B4 (LTB4), and inflammatory cells as indices of lung injury in rabbits exposed to cigarette smoke (CSE). Thirty-one rabbits were randomly assigned to four groups: control sham exposure (SS, n = 6), sham smoke ibuprofen-pretreated (SS-I, n = 7), CSE (n = 6), and CSE ibuprofen-pretreated (CSE-I, n = 12). Ibuprofen, a cyclooxygenase eicosanoid inhibitor, was administered as a single daily intramuscular injection (25 mg/kg) for 7 d before the experiment. Cigarette or sham smoke was delivered by syringe in a series of 5, 10, 20, and 30 tidal volume breaths with a 15-min counting period between each subset of breaths to determine [99mTc]DTPA biological half-life (T1/2). The CSE-I group was retrospectively divided into rabbits who survived the 30-breath subset (CSE-IL, n = 6) and those who died during the 30-breath CSE (CSE-ID, n = 6). In the CSE, CSE-IL, and CSE-ID groups, [99mTc]DTPA T1/2 as well as BALF LTB4 levels were significantly decreased. Plasma and BALF 6-keto-PGF1 alpha increased in CSE rabbits compared to the other groups. Alveolar macrophages were lower in the CSE-ID rabbits than in the CSE-IL group. CSE and CSE-IL BALF lymphocyte levels were decreased compared to SS values. Our data indicate that acute CSE is associated with significant increases in 6-keto-PGF1 alpha and decreases in LTB4 as well as a significant reduction in lymphocytes. Furthermore, pretreatment with ibuprofen before CSE was associated with severe lung injury in half of the rabbits. The severity of lung injury may be related to a combination of a lower number of alveolar macrophages and blockade of lung PGI2.
6-Ketoprostaglandin F1 alpha↗
Effects of intravenous prostaglandins F2 alpha and E2 in hypoxic and non-hypoxic rabbits with elastase induced emphysema.
To determine whether the pulmonary and circulatory effects of intravenous Prostaglandins F2 alpha and E2 are altered in the presence of emphysema and/or hypoxia, 19 New Zealand White rabbits were treated with 3 doses of intratracheal porcine pancreatic elastase (100 U/kg) administered at 4 day intervals to induce panacinar emphysema, and 19 were treated on a similar schedule with saline to serve as controls. Thirty days after their last elastase or saline treatment, rabbits were divided randomly into hypoxic and non-hypoxic breathing subgroups, so that there were 4 experimental groups: control/non-hypoxic (n = 10), control/hypoxic (n = 9), elastase/non-hypoxic (n = 11), and elastase/hypoxic (n = 8). All rabbits underwent pulmonary physiologic studies and received rapid intravenous infusions of PGF2 alpha (6, 12, 14 micrograms) and PGE2 (1,3,6 micrograms). Lung resistance (RL), dynamic lung compliance (Cdyn), right ventricular systolic pressure (Prv), and mean aortic pressure (Paorta) were measured before, and 1 and 5 min. after prostaglandin infusions. At the conclusion of these studies, all rabbits were killed for morphometric and light microscopic analysis of their lungs. Elastase treated rabbits and physiologic, morphometric, and light microscopic evidence of panacinar emphysema. In the control/non-hypoxic group, PGF2 alpha had no effect on Cdyn, but produced a decline in Paorta and an increase in RL and Prv after the 24 micrograms dose. In the same group, PGE2 had no effect on RL or Cdyn, but a decrease in Paorta was observed with all 3 doses. In addition, Prv increased after 6 micrograms of PGE2. These effects were produced by doses of PGF2 alpha and PGE2 which were 12 and 3 times greater respectively than effects of similar magnitude in dogs. Except for the absence of an increase in RL after PGF2 alpha 24 micrograms, the presence of emphysema did not alter the effects of PGF2 alpha or PGE2. However, hypoxia irrespective of emphysema produced greater physiologic effects from both prostanoids. These findings indicate that rabbits are more resistant to the effects of PGF2 alpha and PGE2 on pulmonary mechanics, and pulmonary and systemic vascular pressures. Furthermore, they suggest that hypoxia is a more important factor influencing pulmonary prostaglandin catabolism than anatomic pulmonary emphysema.
Animals↗