elastin and Pneumonia

Topics: Adenovirus Infections, Human; Antioxidants; Apoptosis; Collagen; DNA Damage; Elastin; Endopeptidases; Humans; Oxidants; Pneumonia; Protease Inhibitors; Protein Denaturation; Pulmonary Disease, Chronic Obstructive; Virus Latency

The diagnosis of ventilator-associated pneumonia (VAP) is difficult for several reasons. Firstly, clinical markers show a large percentage of false-positive and false-negative results. Secondly, microbiological diagnosis based on quantitative cultures of protected specimen brush (PSB), bronchoalveolar lavage (BAL), and endotracheal aspirates also present false-positive and false-negative results. Furthermore, definite results are delayed for 48-72 hours. For all these reasons it would be an advantage to have a biological marker of ventilator-associated pneumonia in clinical practice. Since clinical features of pneumonia in mechanically ventilated patients are neither specific nor sensitive, rapid markers of pneumonia might be of great assistance to the clinician in deciding whether to start an empiric antibiotic regimen. A marker of ventilator-associated pneumonia could be a rapid alternative diagnostic method which permits the definite diagnosis of pneumonia. Accordingly, specific markers of VAP, namely the presence of intracellular microorganisms, the detection of elastin fibres, the antibody-coated bacteria test, the level of endotoxin in bronchoalveolar lavage fluid, the local production of interleukin-8, the levels of lactate dehydrogenase, and decreased surfactant protein A, may be important as they can provide a rapid diagnosis of VAP. Among the markers alluded to above, the search for intracellular bacteria in polymorphonuclear leukocytes or macrophages is the most widely validated technique with an excellent specificity, provided that prior antibiotics are not given. However, this technique has its own limitations; it requires a considerable time effort for the microbiologist, and also compels the performance of BAL, a technique not always harmless to the patient.

Topics: Antibody-Coated Bacteria Test, Urinary; Bacteriological Techniques; Biomarkers; Bronchoalveolar Lavage Fluid; Elastin; Endotoxins; Glycoproteins; Humans; Interleukin-8; L-Lactate Dehydrogenase; Pneumonia; Proteolipids; Pulmonary Surfactant-Associated Proteins; Pulmonary Surfactants; Ventilators, Mechanical

In this review article, the effects of old age on lung structure and function are discussed. Changes in lung morphology and biochemistry are correlated with changes in lung mechanics and gas exchange, as well as with the respiratory system's adaptability to the stresses of exercise and sleep. The effects of aging on the lungs' defense mechanisms are related to pulmonary diseases of the elderly.

Topics: Adaptation, Physiological; Aging; Animals; Asthma; Carcinoma, Bronchogenic; Closing Volume; Collagen; Diaphragm; Elastin; Humans; Lung; Lung Neoplasms; Maximal Expiratory Flow-Volume Curves; Nucleic Acids; Pneumonia; Proteins; Proteoglycans; Pulmonary Circulation; Pulmonary Diffusing Capacity; Pulmonary Gas Exchange; Residual Volume; Respiration; Total Lung Capacity; Tuberculosis, Pulmonary; Vital Capacity

Topics: Animals; Chemotaxis; Collagen; Connective Tissue; Connective Tissue Diseases; Elastin; Fibronectins; Humans; Lung; Phagocytosis; Pneumonia; Proteoglycans; Pulmonary Emphysema; Pulmonary Fibrosis

Topics: Animals; Elastin; Histocytochemistry; Humans; Hyaline Membrane Disease; Infant, Newborn; Infant, Newborn, Diseases; Lung; Lung Diseases; Pneumonia; Pulmonary Surfactants; Respiratory Therapy

Cytokine storm invoked during acute and chronic lung injury promotes alveolar damage and remodeling. The current study shows that degraded elastin-targeted nanoparticles releasing doxycycline (Doxy NPs) are potent in mitigating cytokines storm, migration of immune cells in the lungs, and inhibiting inflammasome pathways in the LPS mouse model.. Cytokine storm and lung injury were induced using LPS and elastase in C57BL/6 mice (rodent model for emphysema). The mice were then treated with I.V. Doxy NPs, blank NPs, or Doxy a day before LPS administration. Cytokine levels, immune cell population, and MMP activity were analyzed in broncheo-alveolar lavage fluid (BALF) 4 hours after LPS administration. Additionally, gene expression of IL-6, IL-1beta, MCP-1, NLRP3, Caspase 1 and MMPs were investigated in alveolar cells on day 3 after LPS administration.. Doxycycline NPs but not Doxycycline significantly decreased IL-6, TNF-α, IL-23 and were significantly more effective in decreasing the percentage of immune cells in the BALF. This is the first in-vivo study to demonstrate that Doxycycline can effectively inhibit inflammasome pathways in the lungs.. IV administration of elastin antibody conjugated Doxycycline-loaded albumin NPs can effectively modulate the local immune environment in the lungs, which is not achieved by IV Doxycycline even at 100-fold higher dose. This novel method of drug delivery can effectively lead to the repurposing of traditional Doxycycline as a potential adjunct treatment for managing the cytokine storm in the lungs in COPD and viral infections.

Topics: Animals; Cytokine Release Syndrome; Cytokines; Elastin; Inflammasomes; Interleukin-6; Lipopolysaccharides; Lung; Lung Injury; Mice; Mice, Inbred C57BL; Nanoparticles; Pneumonia

Acute lung injury (ALI) is characterized by hypoxemia, enhanced permeability of the air-blood barrier, and pulmonary edema. Particularly in the elderly, ALI is associated with increased morbidity and mortality. The reasons for this, however, are poorly understood. We hypothesized that age-related changes in pulmonary structure, function, and inflammation lead to a worse prognosis in ALI. ALI was induced in young (10 wk old) and old (18 mo old) male C57BL/6 mice by intranasal application of 2.5 mg lipopolysaccharide (LPS)/kg body wt or saline (control mice). After 24 h, lung function was assessed, and lungs were either processed for stereological or inflammatory analysis, such as bronchoalveolar lavage fluid (BALF) cytometry and qPCR. Both young and old mice developed severe signs of ALI, including alveolar and septal edema and enhanced inflammatory BALF cells. However, the pathology of ALI was more pronounced in old compared with young mice with nearly sixfold higher BALF protein concentration, twice the number of neutrophils, and significantly higher expression of neutrophil chemokine Cxcl1, adhesion molecule Icam-1, and metalloprotease-9, whereas the expression of tight junction protein occludin significantly decreased. The old LPS mice had thicker alveolar septa attributable to higher volumes of interstitial cells and extracellular matrix. Tissue resistance and elastance reflected observed changes at the ultrastructural level in the lung parenchyma in ALI of young and old mice. In summary, the pathology of ALI with advanced age in mice is characterized by a greater neutrophilic inflammation, leakier air-blood barrier, and altered lung function, which is in line with findings in elderly patients.

Topics: Acute Lung Injury; Aging; Animals; Blood-Air Barrier; Body Weight; Bronchoalveolar Lavage Fluid; Cell Count; Collagen; Disease Progression; Elastin; Extracellular Matrix; Flow Cytometry; Gene Expression Regulation; Lipopolysaccharides; Lung; Male; Mice, Inbred C57BL; Pneumonia; Pulmonary Alveoli; Respiratory Function Tests

Receptors for advanced glycation end-products (RAGE) are multiligand surface receptors detected abundantly in pulmonary tissue. Our previous work revealed increased RAGE expression in cells and lungs exposed to tobacco smoke and RAGE-mediated cytokine expression via proinflammatory mechanisms involving NF-κB. RAGE expression is elevated in various pathological states, including chronic obstructive pulmonary disease; however, precise contributions of RAGE to the progression of emphysema and pulmonary inflammation in the adult lung are unknown. In the current study, we generated a RAGE transgenic (RAGE TG) mouse and conditionally induced adult alveolar epithelium to overexpress RAGE. RAGE was induced after the period of alveologenesis, from weaning (20 d of age) until animals were killed at 50, 80, and 110 days (representing 30, 60, and 90 d of RAGE overexpression). Hematoxylin and eosin staining and mean chord length revealed incremental dilation of alveolar spaces as RAGE overexpression persisted. TUNEL staining and electron microscopy confirmed increased apoptosis and blebbing of alveolar epithelium in lungs from RAGE TG mice when compared with control mice. Immunohistochemistry for matrix metalloproteinase 9 revealed an overall increase in matrix metalloproteinase 9, which correlated with decreased elastin expression in RAGE TG mice. Furthermore, RAGE TG mice manifested significant inflammation measured by elevated bronchoalveolar lavage protein, leukocyte infiltration, and secreted cytokines. These data support the concept that innovative transgenic mice that overexpress RAGE may model pulmonary inflammation and alveolar destabilization independent of tobacco smoke and validate RAGE signaling as a target pathway in the prevention or attenuation of smoke-related inflammatory lung diseases.

Topics: Animals; Apoptosis; Doxycycline; Elastin; Gene Expression Regulation; Immunohistochemistry; In Situ Nick-End Labeling; Lung; Matrix Metalloproteinase 9; Mice; Mice, Transgenic; Microscopy, Electron; Pneumonia; Proteolysis; Pulmonary Alveoli; Pulmonary Emphysema; Receptor for Advanced Glycation End Products; Receptors, Immunologic; Staining and Labeling; Up-Regulation; Weaning

Cystic fibrosis (CF) lung disease is characterized by structural changes and remodeling in airway architecture and lung parenchyma. Neutrophilic inflammation and infection lead to injury and breakdown of airway matrix constituents, including elastin. The non-invasive measurement of urinary desmosine (UDes), a breakdown product of elastin, may be reflective of ongoing lung injury and may serve as a biomarker of active short-term damage during pulmonary exacerbation. Our objectives were to measure desmosine in the urine of CF patients hospitalized for treatment of a pulmonary exacerbation and to explore the correlation between desmosine concentration and other markers of clinical improvement, including lung function and inflammatory mediators.. Urine and blood samples plus lung function measurements were collected at up to three points during hospitalization for treatment of a CF pulmonary exacerbation. We used a repeated measures model, adjusted for age and time between measurements, to compare log transformed urine desmosine concentrations across multiple time points and to correlate those concentrations with related clinical variables. Change in UDes concentration was investigated using a statistical model that incorporated normalization factors to account for variations in urinary concentration.. Desmosine was measured by radioimmunoassay (RIA) in 155 spot urine samples from 53 CF patients hospitalized for 63 pulmonary exacerbations (range of results: 0-235 pmol Des/ml). Specific gravity (SG) adjusted UDes concentration decreased significantly during admission for CF pulmonary exacerbation, P < 0.01 (average length of stay = 11 days). No correlation was observed between UDes concentration and lung function or inflammatory markers.. UDes decreased significantly following treatment for an acute pulmonary exacerbation and may be a useful biomarker of short-term injury to the CF lung. Further investigation is needed to evaluate the utility of UDes concentration in the long-term progression of CF lung disease.

Topics: Airway Remodeling; Biomarkers; C-Reactive Protein; Cohort Studies; Cystic Fibrosis; Desmosine; Disease Progression; Elastin; Female; Humans; Interleukin-8; Lung Injury; Male; Pneumonia; Prospective Studies; Respiratory Function Tests

Smoking is the major etiologic factor in COPD, yet the exact underlying pathogenetic mechanisms have not been elucidated. Since a few years, there is mounting evidence that a specific immune response, partly present as an autoimmune response, contributes to the pathogenesis of COPD. Increased levels of anti-Hep-2 epithelial cell and anti-elastin autoantibodies as well as antibodies against airway epithelial and endothelial cells have been observed in COPD patients. Whether the presence of these autoantibodies contributes to the pathogenesis of COPD is unclear.. To test whether induction of autoantibodies against lung matrix proteins can augment the smoke-induced inflammatory response, we immunized mice with a mixture of the lung extracellular matrix (ECM) proteins elastin, collagen, and decorin and exposed them to cigarette smoke for 3 or 6 months. To evaluate whether the immunization was successful, the presence of specific antibodies was assessed in serum, and presence of specific antibody producing cells in spleen and lung homogenates. In addition, the presence of inflammatory cells and cytokines was assessed in lung tissue and emphysema development was evaluated by measuring the mean linear intercept.. We demonstrated that both ECM immunization and smoke exposure induced a humoral immune response against ECM proteins and that ECM immunization itself resulted in increased macrophage numbers in the lung. The specific immune response against ECM proteins did not augment the smoke-induced inflammatory response in our model.. By demonstrating that smoke exposure itself can result in a specific immune response and that presence of this specific immune response is accompanied by an influx of macrophages, we provide support for the involvement of a specific immune response in the smoke-induced inflammatory response as can be seen in patients with COPD.

Topics: Animals; Autoantibodies; Collagen; Cytokines; Decorin; Disease Models, Animal; Elastin; Extracellular Matrix Proteins; Female; Immunization; Lung; Mice; Mice, Inbred C57BL; Pneumonia; Pulmonary Emphysema; Smoking

Elastin fibres in sputum have been described as a more sensitive marker of pulmonary necrosis than plain chest X-rays. This study aimed to determine the prevalence of elastin fibres using non-directed non-protected mini-bronchoalveolar lavage (BM-BAL) in mechanically ventilated patients in the intensive care unit. Patients admitted to the general intensive care unit of a tertiary referral hospital requiring more than 48 hours of mechanical ventilation had surveillance BM-BAL performed on admission and were then examined weekly using potassium hydroxide wet preparations for the presence of elastin fibres. All positive and a random selection of 16 negative preparations from patients with acute respiratory distress syndrome or pneumonia were fixed and examined using Weigert's staining method for elastin. Of 412 patients enrolled, 130 (32%) had pneumonia on admission, 50 (12%) developed 58 episodes of ventilator-associated pneumonia and acute respiratory distress syndrome was diagnosed in 86 patients (21%). No chest X-ray showed cavitating infiltrates. Of 985 specimens examined, only seven had elastin fibres. Elastin fibres are uncommonly found using BM-BAL in general screening, acute respiratory distress syndrome or pneumonia in the intensive care unit, the incidence too low to be a useful indicator of pulmonary necrosis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Bronchoalveolar Lavage; Bronchoalveolar Lavage Fluid; Elastin; Female; Humans; Intensive Care Units; Lung Diseases; Male; Middle Aged; Necrosis; Pneumonia; Pneumonia, Ventilator-Associated; Respiration, Artificial; Respiratory Distress Syndrome

Increased numbers of T lymphocytes are observed in the lungs of patients with chronic obstructive pulmonary disease, but their role in the disease process is not known. We investigated the role of CD8+ T cells in inflammatory cell recruitment and lung destruction in a cigarette smoke-induced murine model of emphysema. In contrast to wild-type C57BL/6J mice that displayed macrophage, lymphocyte, and neutrophil recruitment to the lung followed by emphysema in response to cigarette smoke, CD8+ T cell-deficient (CD8-/-) mice had a blunted inflammatory response and did not develop emphysema when exposed to long-term cigarette smoke. Further studies supported a pathogenetic pathway whereby the CD8+ T cell product, IFN-gamma-inducible protein-10, induces production of macrophage elastase (matrix metalloproteinase 12) that degrades elastin, both causing lung destruction directly and generating elastin fragments that serve as monocyte chemokines augmenting macrophage-mediated lung destruction. These studies demonstrate a requirement for CD8+ T cells for the development of cigarette smoke-induced emphysema and they provide a unifying pathway whereby CD8+ T cells are a central regulator of the inflammatory network in chronic obstructive pulmonary disease.

Topics: Animals; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Chemotaxis, Leukocyte; Disease Models, Animal; Elastin; Lung; Matrix Metalloproteinase 12; Mice; Mice, Inbred Strains; Monocytes; Nicotiana; Pneumonia; Pulmonary Emphysema; Smoke

Macrophage and neutrophil proteinases damage lung elastin, disrupting alveolar epithelium and filling alveoli with inflammatory exudate. Alveolar collapse and regional hypoxia occur. Whether low oxygen tension alters fibroblast-mediated lung repair is unknown. To determine the effect of chronic hypoxia on repair of enzyme-induced elastin disruption, primary rat lung fibroblasts produced elastin matrix for 5 wk before treatment with porcine pancreatic elastase (PPE). After exposure to PPE or saline, cultures recovered for 2 wk in normoxia (21% O(2)) or hypoxia (3% O(2)). Hypoxia suppressed regeneration of hot alkali-resistant elastin, achieving only 49% of the repair achieved in normoxic cultures. Vascular smooth muscle cells and lung fibroblasts repair elastin by two pathways: de novo synthesis and salvage repair. Although both pathways were affected, hypoxia predominantly inhibited de novo synthesis, decreasing formation of new elastin matrix by 63% while inhibiting salvage repair by only 36%. Prolonged hypoxia alone downregulated steady-state levels of elastin mRNA by 45%, whereas PPE had no significant effect on elastin gene expression. Electron microscopy documented preservation of intracellular organelles and intact nuclei. Together, these data suggest that regional hypoxia limits lung elastin repair following protease injury at least in part by inhibiting elastin gene expression.

Topics: Animals; Cell Hypoxia; Cells, Cultured; Down-Regulation; Elastin; Fibroblasts; Lung; Lung Injury; Macrophages; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Pancreatic Elastase; Pneumonia; Rats; Rats, Sprague-Dawley; Swine

Topics: Elastin; Humans; Intubation, Intratracheal; Mucus; Pneumonia; Sensitivity and Specificity; Specimen Handling; Ventilators, Mechanical

The thrombospondins are a family of extracellular calcium-binding proteins that modulate cellular phenotype. Thrombospondin-1 (TSP-1) reportedly regulates cellular attachment, proliferation, migration, and differentiation in vitro. To explore its function in vivo, we have disrupted the TSP-1 gene by homologous recombination in the mouse genome. Platelets from these mice are completely deficient in TSP-1 protein; however, thrombin-induced platelet aggregation is not diminished. TSP-1-deficient mice display a mild and variable lordotic curvature of the spine that is apparent from birth. These mice also display an increase in the number of circulating white blood cells, with monocytes and eosinophils having the largest percent increases. The brain, heart, kidney, spleen, stomach, intestines, aorta, and liver of TSP-1-deficient mice showed no major abnormalities. However, consistent with high levels of expression of TSP-1 in lung, we observe abnormalities in the lungs of mice that lack the protein. Although normal at birth, histopathological analysis of lungs from 4-wk-old TSP-1-deficient mice reveals extensive acute and organizing pneumonia, with neutrophils and macrophages. The macrophages stain for hemosiderin, indicating that diffuse alveolar hemorrhage is occurring. At later times, the number of neutrophils decreases and a striking increase in the number of hemosiderin-containing macrophages is observed associated with multiple-lineage epithelial hyperplasia and the deposition of collagen and elastin. A thickening and ruffling of the epithelium of the airways results from increasing cell proliferation in TSP-1-deficient mice. These results indicate that TSP-1 is involved in normal lung homeostasis.

Topics: Animals; Blood Platelets; Cells, Cultured; Collagen; Congenital Abnormalities; DNA; Elastin; Eosinophils; Epithelial Cells; Genetic Vectors; Hemorrhage; Hemosiderin; Homeostasis; Hyperplasia; Leukocyte Count; Lordosis; Lung; Macrophages; Mice; Mice, Knockout; Monocytes; Neutrophils; Platelet Aggregation; Pneumonia; Proteins; Radiography; Recombination, Genetic; Restriction Mapping; Ribonucleases; Thrombin; Thrombospondin 1; Transfection

The diagnosis of nosocomial pneumonia is especially difficult in intubated patients due to the low specificity of their clinico-radiological signs. The objective of this study was to evaluate the usefulness of basing diagnosis on elastin fibers (EF) in bronchoaspirate (BAS) as an indication of pneumonia in mechanically-ventilated (MV) patients. Forty-seven MV patients suspected of having nosocomial pneumonia were studied prospectively. Fiber bronchoscopy was carried out on all patients and samples were obtained using a protected catheter brush (PCB) and bronchoalveolar lavage (BAL). A purulent sample of BAS was also examined, after addition of 40% KOH, to determine the presence of EF. EF was found in 15 patients, 11 of whom had pneumonia while 3 more had necrotizing pneumonia (sensitivity 52%, specificity 85%). Ten of the 17 microorganisms isolated in the cases of EF positive pneumonia were gram negative, although the germ found most often was S. aureus. There were no differences in the prognosis for pneumonia patients who were EF positive and those who were EF negative. In conclusion, once necrotizing pneumopathology has been ruled out, the presence of EF in BAS may offer reasonable support for firm diagnosis in some MV patients with pneumonia.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Bronchoalveolar Lavage Fluid; Bronchoscopy; Chi-Square Distribution; Elastin; Female; Humans; Male; Middle Aged; Pneumonia; Prospective Studies; Respiration, Artificial; Sensitivity and Specificity

We have characterized 20 Pseudomonas aeruginosa strains isolated from pneumonic mink lungs with regard to elastase production and serotype. P. aeruginosa PAO1, a well-characterized elastase-producing strain, and two elastase-deficient mutants of PAO1 were used for comparative purposes. Elastase activity was assayed on elastin agar and by using 14C-elastin coated microtiter plates. Elastase antigen was measured using a double antibody sandwich ELISA (enzyme-linked immunosorbent assay). Total proteolytic activity was determined on skim milk agar plates. The results from ELISA showed that all strains produced antigenically similar elastase, although the amounts produced varied considerably between strains. There was a good correlation regarding elastase assays between ELISA and 14C-elastin, elastin agar and total proteolytic activity on skim milk agar. No correlation was found between serotype and elastase activity. The results showed that the 14C-elastin assay is a simple and sensitive method of determining elastolytic activity of P. aeruginosa strains.

Topics: Animals; Culture Media; Elastin; Enzyme-Linked Immunosorbent Assay; Lung; Milk; Mink; Pancreatic Elastase; Pneumonia; Pseudomonas aeruginosa

This study examines the bronchial alveolar lavage (BAL) samples from a group of patients with acute bacterial pneumonia (n = 13) and makes a comparison with a control group (n = 5). The proteinase inhibitory capacity was examined and found to be composed primarily of alpha 1-proteinase inhibitor (PI, alpha 1-antitrypsin) and, to a lesser extent, bronchial mucosal inhibitor. Although the average PI concentration was elevated approximately 5-fold in the pneumonia group, its inhibitory function against elastase was decreased 15-fold when compared with that in the control group. The pneumonia group showed an increased concentration of immunologically identified elastin-derived peptides. Some of the BAL fluid from patients with pneumonia showed elastolytic activity against amorphous insoluble lung elastin. The majority of the elastase appears to be of neutrophil origin. Bronchial mucosal inhibitor is shown to be a component of both normal and pneumonia BAL fluids by both immunologic quantitation and by its resistance to perchloric acid inactivation. Compared with those from control subjects, BAL samples from patients with acute bacterial pneumonia showed a decreased proteinase inhibitor function and both increased elastolytic activity and elastin-derived peptide concentration.

Topics: Acute Disease; Adult; Aged; alpha 1-Antitrypsin; Bacterial Infections; Bronchoscopy; Cell Count; Elastin; Enzyme-Linked Immunosorbent Assay; Female; Humans; Male; Middle Aged; Pancreatic Elastase; Pneumonia; Protease Inhibitors; Pulmonary Alveoli; Therapeutic Irrigation

Potassium hydroxide (KOH) preparations for elastin fibers on sputum obtained from 80 patients seen over a four-month period at two Cleveland hospitals were performed. The results were compared with roentgenographic evidence of necrosis and case diagnosis. Sixty-one patients had neither elastin in sputum nor roentgenographic evidence of cavitation; 11 had positive results using both methods. Two patients had no elastin fibers in sputum but had parenchymal pulmonary cavities on chest x-ray film. Six patients had elastin observed in KOH preparations of sputum, but no cavitation roentgenographically. The presence of elastin in sputum was strongly correlated with roentgenographic evidence of pulmonary necrosis (p = 5.7 X 10(-8]. Including patients seen before, after, and during the prospective study, we have observed a total of nine with positive sputum preparations for elastin and no cavitation on chest x-ray film for whom tissue was available for study. All had pulmonary necrosis histologically. Our observations suggest that the KOH preparation of sputum for elastin fibers may be more sensitive than the chest roentgenogram in the detection of pulmonary necrosis and may be a useful adjunct in the diagnosis of necrotizing disease.

Topics: Diagnosis, Differential; Elastin; Humans; Lung; Necrosis; Pneumonia; Prospective Studies; Radiography; Sputum

We have observed five patients for whom the presence of fibers of elastin in potassium hydroxide (KOH) preparations of sputum represented the first evidence of necrotizing pulmonary disease. In four cases, the discovery of elastin fibers in sputum provided additional evidence supporting initiation or modification of antibiotic therapy. Necrotizing disease was confirmed in all cases by autopsy or by the development of cavitation on chest x-ray film. Cytochemical staining, electron microscopy, and elastase digestion all suggest that the refractile fibers seen on KOH wet mount of sputum are elastin. The test, first described in 1846, is simple to perform, requires little experience to read, and may be a valuable adjunct to the chest roentgenogram in the diagnosis of pulmonary parenchymal destruction.

Topics: Adult; Aged; Bronchopneumonia; Elastin; Female; Humans; Hydroxides; Male; Middle Aged; Necrosis; Pneumonia; Potassium; Potassium Compounds; Sputum