Dyslipidemia and coronary artery disease. Prevalence and treatment in patients referred for coronary arteriography

We report a case with adult respiratory distress syndrome (ARDS) associated with increased levels of squamous cell carcinoma-related antigen (SCC) in the serum and bronchoalveolar lavage fluid (BALF). ARDS was likely induced by ibuprofen, based on the presence of pancytopenia and a weakly positive drug lymphocyte stimulating test (DLST). High serum and BALF levels of interleukin (IL)-8, neutrophil elastase as well as SCC were detected. Corticosteroid therapy resulted in clinical improvement, resolution of pulmonary infiltrates on chest roentgenogram and normalization of serum and BALF levels of IL-8, neutrophil elastase and SCC.     

Platelet activating factor and tumor necrosis factor-alpha in bronchoalveolar lavage fluid of patients with ARDS

Platelet activating factor (PAF) and tumor necrosis factor alpha (TNF-alpha) were examined in the bronchoalveolar lavage fluid (BALF) of 21 ARDS patients to clarify the role of these factors in ARDS. Neutrophil percentages and albumin concentrations in the BALF of the ARDS group were markedly elevated compared with those in the control group (p < 0.01), showing a significant correlation (r = 0.596, p < 0.01). PAF was detected in 14 of 19 ARDS patients (237.5 +/- 86.0 pg/ml) and TNF-alpha was detected in 7 of 16 ARDS patients (24.9 +/- 13.6 pg/ml), whereas these factors were not detected in control subjects. Neither PAF nor TNF-alpha showed a significant correlation with neutrophil percentage, neutrophil number or albumin concentration. They do not seem to be contributing factors to the prognosis of ARDS patients. However the existence of PAF and TNF-alpha in the BALF of some ARDS patients suggests that they might play a role in the pathogenesis of ARDS.     

High levels of interleukin-8 in the blood and alveolar spaces of patients with pneumonia and adult respiratory distress syndrome

There is ample experimental evidence that polymorphonuclear neutrophils (PMN) play a critical role in the pathogenesis of the adult respiratory distress syndrome (ARDS). Since interleukin-8 (IL-8) is a strong chemotactic factor for PMN, we measured IL-8 levels in plasma and bronchoalveolar lavage (BAL) fluid of 18 patients, 12 with ARDS and 6 with severe pneumonia uncomplicated by ARDS, all of whom had an increased number of PMN in BAL fluid. Seven healthy subjects served as controls. We found elevated levels of IL-8 in the alveolar spaces of all patients tested. Elevated BAL IL-8 levels were related to a fatal outcome and the presence of shock and correlated with a general clinical severity index (simplified acute physiological score). BAL fluid levels of IL-8 were significantly higher in patients with ARDS than in patients with pneumonia. In plasma, IL-8 levels were increased similarly in all patients and did not correlate with survival or the presence of shock. The BAL fluid-to-plasma ratio of IL-8 was significantly greater than that of tumor necrosis factor alpha, indicating higher local production of IL-8. Moreover, the presence of a primed subpopulation of blood PMN with respect to H2O2 production indicates that IL-8 may contribute to the neutrophil-mediated process in the pathogenesis of ARDS and pneumonia.     

Procollagen III in bronchoalveolar lavage fluid of patients with allergic alveolitis and sarcoidosis

In 12 patients with sarcoidosis and 11 patients with allergic alveolitis concentration of procollagen III peptide in bronchoalveolar lavage fluid (in bronchial and alveolar fraction) was estimated using RIA method. In studied populations procollagen III levels were higher in comparison to control. In patients with allergic alveolitis and with DLCO < 60% pred. procollagen III peptide concentrations in BAL fluid were significantly higher than in patients with sarcoidosis. In patients with allergic alveolitis a positive correlation between BAL lymphocytes number and procollagen III peptide concentration was observed.     

High levels of elastolytic activity in bronchoalveolar lavage fluid from a patient with idiopathic interstitial pneumonia]

A 63-year-old female with acure exacerbution of idiopathic interstitial pneumonia (IIP) showed high levels of elastolytic activity in bronchoalveolar lavage fluid (BALF). She was admitted to our hospital with progressive dyspnea. Arterial blood gas analysis and pulmonary function tests were abnormal. Examination of the bronchoalveolar lavage fluid revealed an increased numbers of neutrophils. Despite the administration of corticosteroids, the patient died of respiratory failure. A high level of elastolytic activity was present in the BALF. Western immunoblot analysis, using an anti-alpha 1-protease inhibitor (PI) antibody, revealed a truncated alpha 1-PI in the BALF. These findings suggest that an imbalance between protease and PI in the lower respiratory tract contribute to lung tissue damage in patients with IIP.     

Serial prognostic capabilities of electrocardiographic indices of infarcted and hibernating myocardium in predicting short- and long-term outcome following coronary artery bypass surgery

Concentrations and ex vivo production of interleukin 1 beta (IL-1), tumour necrosis alpha (TNF), interleukin 6 (IL-6), interleukin-1 receptor antagonist (IL-1RA) and TNF soluble receptors (sTNF-receptors, P55 and P75) were measured in bronchoalveolar lavage (BAL) fluid and blood in 23 HIV-seropositive (HIV+) patients with Pneumocystis carinii pneumonia (PCP) and compared with values found in healthy HIV-seronegative (HIV-) controls and asymptomatic HIV+ subjects. Concentrations of the proinflammatory cytokine IL-1 beta were increased in BAL fluid of HIV+ patients with PCP (184 +/- 47 pg mL-1) compared with undetectable levels in healthy control subjects (P = 0.0001). In plasma of these patients higher concentrations of the anti-inflammatory cytokine IL-1RA were found during acute PCP than after recovery (2.1 +/- 0.7 vs. 0.5 +/- 0.2 ng mL-1, P = 0.01). No correlations could be found between cytokine concentrations and clinical severity of the infection. Corticosteroid treatment did not influence cytokine concentrations in BAL or blood, nor did it suppress the production in alveolar cells. In whole-blood cultures, however, lipopolysaccharide (LPS)-stimulated production was significantly suppressed for IL-1 (1.3 vs. 5.5 ng mL-1, P = 0.009) and for IL-6 (0.6 vs. 2.5 ng mL-1, P = 0.01). The overall data show that in HIV+ patients with PCP (similar to what we had found previously in HIV-patients with PCP) proinflammatory cytokines are more prominently present in BAL, whereas anti-inflammatory reaction is predominant in the circulation.     

Pneumocystis carinii alters surfactant protein A concentrations in bronchoalveolar lavage fluid

To understand better the interaction between surfactant protein A (SP-A), human immunodeficiency virus (HIV) and Pneumocystis carinii pneumonia (PCP), we measured SP-A from bronchoalveolar lavage (BAL) fluid in immunosuppressed patients (HIV-positive [HIV+] and HIV noninfected [HIV-]) who were examined for possible pneumonia. Forty-five HIV+ patients, 16 with PCP and no other pathogen (HIV+/Pc) and 29 with no evidence of pulmonary pathogen (HIV+ controls), were compared with 6 HIV- patients with PCP (HIV-/Pc) and 11 control patients with no underlying disease (controls). Despite a similar inflammatory response in the HIV-infected patients whether they had PCP or not, we found increased BAL SP-A concentrations in HIV+/Pc patients as compared with HIV+ control patients (HIV+/Pc: median, 10.3 micrograms/ml; range, 2.8 to 24.3 micrograms/ml; HIV+ control: median, 1.9; range, 0.06 to 3.83 micrograms/ml; p < 0.05). The amount of SP-A in the HIV+ control group was significantly lower than healthy, uninfected volunteers, suggesting that HIV itself may lower SP-A levels. Six HIV+/Pc patients underwent BAL after 21 days of therapy and showed complete resolution of the P. carinii organism. There was a significant drop in the amount of SP-A at follow-up lavage (initial mean, 14.1 micrograms/ml; follow-up mean, 7.4 micrograms/ml; p < 0.02). We also found a significant correlation between the amount of P. carinii and the amount of SP-A in the BAL fluid (Spearman rank, 0.74; p < 0.01). We conclude that SP-A content is increased in HIV+ patients with PCP. The relationship between SP-A concentration and the abundance of P. carinii present in the BAL fluid may be related to SP-A binding to P. carinii or to alterations in surfactant protein homeostasis.     

Effect of different doses of inhaled nitric oxide on pulmonary capillary pressure and on longitudinal distribution of pulmonary vascular resistance in ARDS

Inhaled nitric oxide lowers pulmonary capillary pressure (PCP) in animals and in patients with acute respiratory distress syndrome (ARDS). A dose-response relationship in patients with ARDS has not yet been established. Therefore, we studied the effects of four concentrations of nitric oxide (1, 10, 20 and 40 volumes per million (vpm)) in random order, on PCP in 19 patients with ARDS. PCP was estimated by visual analysis of the pressure decay curve after balloon inflation of the pulmonary artery catheter. Haemodynamic and gas exchange variables were measured at each nitric oxide concentration. Patients were classified as responders when PCP decreased by at least 2 mm Hg after nitric oxide 20 vpm. In responders (n = 8), nitric oxide decreased PCP and post-capillary vascular resistance dose-dependently and changed longitudinal distribution of pulmonary vascular resistance with a maximum effect at 20 vpm. In non-responders (n = 11), PCP did not change. In both groups, the nitric oxide-induced decrease in pre-capillary vascular resistance was small with a maximum effect at 1 vpm. In ARDS, vasodilatation of pre-capillary vessels is achieved at low concentrations of nitric oxide, whereas the effect of nitric oxide on postcapillary vessels is variable. Higher concentrations may be required for optimal post-capillary vasodilatation in a subgroup of ARDS patients.     

Diagnosis of pneumocystis carinii pneumonia in AIDS patients

BACKGROUND: Based on the changing disease pattern of human immunodeficiency virus (HIV) associated pulmonary complications we conducted a prospective study in order to compare the value of laboratory tests in patients with Pneumocystis (P.) carinii pneumonia (PCP) and other pulmonary complications and of different identification methods of P. carinii in bronchoalveolar lavage fluid (BALF) in PCP patients. PATIENTS AND METHODS: In 217 HIV-1-infected patients we evaluated the following parameters: platelets, serum lactat dehydrogenase (LDH), total serum protein (TP), hemoglobin (Hb), and CD4+ and CD8+ T-lymphocyte count. P. carinii was identified in BALF by May Grünwald Giemsa stain (MGG), direct immunofluorescence test (DIFT), and polymerase chain reaction (PCR). We correlated these parameters in patients with a presumptive diagnosis of PCP and compared them with those of patients suffering from other pulmonary complications. RESULTS: All patients underwent bronchoscopy. 55 patients (25.3%) had a presumptive diagnosis of PCP. The sensitivity values of MGG stain, DIFT, and PCR differed considerably (79.1%, 56.1%, and 65.9%, respectively), but specificity values did not (99.2%, 97.3%, and 98.2%, respectively) as well as accuracy values (93.8%, 86.2%, and 89.7%, respectively). The mean values of platelets, of LDH, and of total serum protein of PCP patients and those of patients with other pulmonary diseases differed statistically significant as well as the mean values of these parameters of PCP patients and those of patients with bacterial pneumonia. Logistic-regression analysis revealed the number of platelets and the amount of total serum protein as independent, significant prognostic factors. Moreover, each PCP patient had a CD4+ T-lymphocyte count of less than 200 cells/mm3 blood. The CD4/CD8 ratio of PCP patients was statistically significant lower than that of patients with bacterial pneumonia. CONCLUSIONS: A detection of P. carinii in BALF is inevitable for a definitive diagnosis of a PCP. The most efficient identification method in this case is the MGG stain. Platelets, total serum protein, and CD4+ T-lymphocyte count should be included into the criteria for the presumptive diagnosis of PCP.     

Chronic K depletion inhibits renal brush border membrane Na/sulfate cotransport

Conversion of the highly surface-active subtype of pulmonary surfactant known as large surfactant aggregates (LA) to small aggregates (SA) with poor surface activity has recently been shown to occur upon cyclic changes of the air-liquid interface area in vitro. By subjecting pooled rabbit bronchoalveolar lavage fluid (BALF) to this maneuver, we found that conversion of LA to SA was accompanied by a marked decline in the ability of the remaining LA fraction to reduce surface tension by adsorption and during film compression on a pulsating bubble surfactometer. SA obtained by centrifugation of noncycled rabbit BALF had a similar phospholipid (PL) but different neutral lipid (NL) composition than did the LA. Upon cycling, the increased formation of SA obliterated this difference. No substantial difference in the PL, NL, or fatty acid profile of LA was noted before and after cycling. In contrast, the content of surfactant apoprotein-B (SP-B) in the LA decreased dramatically to nearly undetectable levels during the cycling maneuver, and this decline in SP-B content was closely correlated with the decrease in proportional appearance of LA and loss of surface activity of this fraction. Reconstitution of LA with intact SP-B after cycling virtually fully restored the surface activity of this surfactant subtype. When comparing lavage samples from adults with acute respiratory distress syndrome (ARDS; n = 10) with samples from healthy controls (n = 11), we noted a marked reduction of SP-B in the LA fraction. There was a significant correlation between the SP-B content of the LA fraction and the relative percentage of LA in BALF or the lower surface activity of this surfactant subtype. We conclude that an SP-B-related loss of LA integrity and function may substantially contribute to the decline of this surfactant subtype and the loss of its surface activity during cycling in vitro and in clinical ARDS.     

Acute respiratory distress syndrome due to methicillin-resistant Staphylococcus aureus sepsis in hyper-IgE syndrome

We report the case of a 34 year old woman with acute respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) due to methicillin-resistant Staphylococcus aureus (MRSA) sepsis with hyperimmunoglobulin E syndrome (HIES). Although chemotactic activity of neutrophils was impaired in this patient, neutrophils accumulated in the lungs as assessed by bronchoalveolar lavage fluid (BALF) counts. In addition to antibiotics and oxygen therapy, the administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) resulted in a remarkable recovery.     

Studies of lymphocyte subpopulations of bronchoalveolar lavage fluid in HTLV-I seropositive patients with uveitis

To determine whether HTLV-I infection is associated with uveitis, we investigated the bronchoalveolar lavage fluid (BALF) cells in 23 patients with uveitis. Of these, sarcoidosis was diagnosed in 13 patients, but could not be confirmed in the remaining 10 patients (non-sarcoidosis). Three of 13 patients (23.1%) with sarcoidosis and 7 of 10 non-sarcoidosis patients (70.0%) were HTLV-I seropositive. In BALF, no significant differences were observed between the HTLV-I seropositive and seronegative patients. However, in non-sarcoidosis patients, total cell counts, CD3+ and CD+ HLA-DR+ cells in BALF were significantly higher in seropositive patients than in seronegative patients. CD3+ CD25+ cells in BALF were markedly increased in 3 of 7 non-sarcoidosis seronegative patients. These findings indicated that BALF lymphocytes in HTLV-I seropositive non-sarcoidosis patients were more activated than those in seronegative non-sarcoidosis patients, supporting the hypothesis that HTLV-I infection may be associated with uveitis.     

Relationship between lipid peroxidase and superoxide dismutase in bronchoalveolar lavage fluid and pulmonary qi deficiency syndrome

Investigating the levels of lipid peroxidase (LPO) and superoxide dismutase (SOD) in serum, bronchoalveolar lavage fluid (BALF) and alveolar macrophage (AM) were determined in 40 chronic bronchitis patients with Pulmonary Qi Deficiency (PQD) Syndrome and 36 normal subjects. Results showed: (1) No significant differences were found between PQD syndrome and normal subjects on serum SOD or LPO levels. (2) Patients with PQD Syndrome. LPO level in BALF was significantly higher, and SOD significantly lower, when compared with normal subjects. (3) Through correlation analysis, it was found in BALF that SOD level was markedly correlated with AM, while LPO was significantly correlated with neutrophil. In short, SOD and LPO in BALF play an important role in the development of the PQD Syndrome, and are good indications in evaluating the PQD Syndrome.     

Analysis of neurological sequelae from radiosurgery of arteriovenous malformations: how location affects outcome

The present study evaluated the clinical significance of hepatocyte growth factor (HGF) in patients with pulmonary fibrosis. Twenty-one patients with a diagnosis of pulmonary fibrosis [14 with idiopathic pulmonary fibrosis (IPF) and seven with pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD]) and 21 normal subjects as control were studied. HGF levels in sera of patients with pulmonary fibrosis (0.34 +/- 0.02 ng ml-1) were elevated significantly as compared with normal subjects (0.21 +/- 0.01 ng ml-1) (P < 0.0001). HGF/albumin levels in broncho-alveolar lavage fluid (BALF) of patients with pulmonary fibrosis (72 +/- 17 ng g-1 albumin) were also significantly elevated as compared with normal subjects (under the detection limit) (P < 0.01). HGF levels in sera correlated significantly with elastase levels in sera and C-reactive protein, and correlated negatively with PaO2. HGF levels in sera were significantly higher in smokers with pulmonary fibrosis (0.42 +/- 0.03 ng ml-1) as compared with non-smokers with pulmonary fibrosis (0.29 +/- 0.03 ng ml-1) (P < 0.005). HGF/albumin levels in BALF correlated significantly with elastase/albumin levels in BALF, lactate dehydrogenase/albumin in BALF, Immunoglobulin A/albumin in BALF, total cell count/albumin in BALF, total number of alveolar macrophage/albumin in BALF, total number of neutrophil/albumin in BALF, CEA/albumin in BALF, CA19-9/albumin in BALF, and SCC/albumin in BALF. These results suggest that following lung injury, HGF may be a mediator involved in the repair which leads to pulmonary fibrosis.     

Protein patterns of human nasal and bronchoalveolar lavage fluids analyzed with two-dimensional gel electrophoresis

We have previously described the protein patterns of human nasal lavage fluid (NLF) and bronchoalveolar lavage fluid (BALF) after two-dimensional gel electrophoresis (2-DE). We now report the identification of a number of additional proteins in these 2-DE patterns. Several plasma proteins (alpha2-macroglobulin, haptoglobin alpha1-chain, IgA S chain, ceruloplasmin, alpha1-microglobulin, amyloid P and apolipoprotein A-1) could be included both in the BALF and NLF spot pattern data bases by matching with a master plasma 2-DE pattern (SWISS-2DPAGE). Furthermore, lysozyme, lactoferrin and the antiinflammatory proteins lipocortin-1 and Clara cell protein 16 (CC-16) were identified by matching with reference proteins and Western immunoblots. Significant differences in the levels of some of the identified proteins were found between NLF and BALF, and between BALF from smokers and nonsmokers. Transferrin, hemopexin and haptoglobin alpha1 were lower in NLF than BALF, while IgA, lysozyme and lactoferrin were higher in NLF than BALF. One form of alpha1-microglobulin was more abundant in NLF than in BALF, while the opposite was found for a second form of the same protein. Moreover, the levels of IgA, ceruloplasmin and the pro-form of apolipoprotein A-1 in BALF were lower in smokers than in nonsmokers. The possibility to describe and analyze differences in NLF and BALF 2-DE patterns at the protein spot level may have wide clinical applications.     

Utility of low mA 1.5 pitch helical versus conventional high mA abdominal CT

We treated nine patients of mycoplasmal pneumonia with sparfloxacin (SPFX) the clinical efficacy, safety and usefulness of SPFX were evaluated. SPFX was administered orally at doses of 200 or 300 mg once daily, and we performed bronchoalveolar lavage (BAL) examinations in five patients. BAL was performed 5 hours after oral administration of 100 mg in one case, 19 hours after oral administration of 200 mg in four cases. Concentrations of SPFX and alubumine were measured in serum and in BALF (bronchoalveolar lavage fluid). The following results were obtained. 1. Nine patients were evaluated; eight patients judged as Good, one patient as Excellent. 2. The serum and BALF levels of SPFX was 0.79 microgram/ml, 0.107 microgram/ml 5 hours after single oral administration of 100 mg in one case and 19 hours after oral administration of 200 mg in four cases, those of levels of SPFX were 0.835 +/- 0.274 microgram/ml and 0.081 +/- 0.033 microgram/ml, respectively. 3. The ratio of SPFX/albumin in BALF was significantly higher than in the serum. From these results, we consider that SPFX is a useful antimicrobial agent for mycoplasmal pneumonia.     

Oligo-2',5'-adenylate synthetase in pulmonary sarcoidosis and idiopathic pulmonary fibrosis

Oligo-2',5'-adenylate synthetase (2,5AS) is an enzyme induced by all types of interferon (IFN). We measured the levels of 2,5AS activity in peripheral blood mononuclear leukocytes (PBML) and bronchoalveolar lavage fluid (BALF) cells of patients with pulmonary sarcoidosis (SAR), idiopathic pulmonary fibrosis (IPF), and normal controls (NC). In NC, the levels of BALF cell 2,5AS activity were approximately seven times as high as the levels of PBML 2,5AS activity. The measurement 2,5AS activity from isolated cells showed that the levels of 2,5AS activity are independent of cell differential from PBML and BALF cells. The levels of PBML and BALF cell 2,5AS activity in SAR were both significantly high in comparison with those in NC. In patients with IPF, the levels of PBML 2,5AS activity were significantly increased as compared with those in NC, whereas there was no significant difference regarding the levels of BALF cell 2,5AS activity between patients with IPF and NC. These results suggest the following: (1) in patients with SAR, IFN production is enhanced both in the alveolar space and peripheral circulation; (2) in patients with IPF, IFN production is greatly enhanced in the circulation, whereas IFN production is not enhanced in the alveolar space; and (3) IFN may contribute to the pathogenesis of SAR and IPF.     

Glutathione depletion in epithelial lining fluid of lung allograft patients

The lower respiratory tract is protected against reactive oxygen species (ROS) by a complex antioxidant system. In the epithelial lining fluid (ELF), glutathione (L-alpha-glutamyl-L-cysteinylglycine, GSH) is essential for adequate protection of pneumocytes from potential toxicity mediated by extracellular hydrogen peroxide (H2O2). We assessed the concentration of total GSH in bronchoalveolar lavage fluid (BALF) in lung allograft patients in the absence and presence of acute rejection. Bronchoalveolar lavage (BAL) and biopsies were performed concurrently on 36 occasions in 17 patients who had undergone lung transplantation. BALF samples were divided into two groups on the basis of presence or absence of acute lung rejection on transbronchial biopsy. Seven BALF samples were obtained from control subjects for comparison. The BALF data demonstrated significantly lymphocyte recruitment and evidence of lung injury during acute rejection episodes. Transplant allografts without rejection showed significant depletion of total GSH in the ELF as compared with that of normal volunteers (94.0 +/- 9.7 microM versus 302.6 +/- 40.8 microM, p < 0.01). Transplant allografts with acute rejection had a slightly higher GSH concentration in their ELF (179.8 +/- 34.7), but this was still lower than control values. The deficiency of total GSH in the alveolar fluid may predispose lung allografts to extracellular H2O2-mediated toxicity.     

Neutrophil chemokines in bronchoalveolar lavage fluid and leukocyte-conditioned medium from nonsmokers and smokers

Polymorphonuclear neutrophils (PMN) have been implicated in the pathogenesis of emphysema. The chemokines interleukin-8(IL-8), growth-related oncogene (GRO-alpha) and extractable nuclear antigen (ENA)-78 may be involved in the increased numbers of PMN in smokers' airspaces. The levels of these cytokines in bronchoalveolar lavage fluid (BALF) and bronchoalveolar lavage leukocyte conditioned medium (LCM), along with BALF PMN numbers in 12 smokers who abstained for 12 h (chronic smoking) or continued to smoke until I h before study (acute smoking) and seven nonsmokers were compared. Neutrophils in BALF increased in acute (1.96+/-0.53%, 0.99+/-0.32x10(6) cells) compared with chronic smokers (0.59+/-0.25%, 0.61+/-0.24x10(6) cells, p<0.05 nonsmokers) and nonsmokers (0.79+/-0.29%, 0.05+/-0.01x 10(6) cells, p<0.05). There were no differences in IL-8 or GRO-alpha in BALF between smokers and nonsmokers. ENA-78 levels were lower in smokers (p=0.006). There was no difference in IL-8, GRO-alpha or ENA-78 in LCM from unstimulated cells in smokers versus nonsmokers. After stimulation with lipopolysaccharide (LPS) 10 ng mL(-1), IL-8 release in acute smokers (p=0.04) and GRO-alpha release in smokers (p=0.009) were significantly higher than in nonsmokers. Following stimulation with LPS 100 ng.mL(-1), GRO-alpha release was higher in smokers (p=0.03) and increased further in acute smokers (p=0.02 versus nonsmokers, p=0.04 versus chronic smokers) and ENA-78 release increased in smokers (p=0.02 versus non-smokers). In conclusion, influx of polymorphonuclear neutrophils into smokers' airspaces is an acute phenomenon and neutrophil chemokine release from mixed bronchoalveolar lavage leukocytes is influenced by cigarette smoking and endotoxins.     

Relationship between soluble CD14, lipopolysaccharide binding protein, and the alveolar inflammatory response in patients with acute respiratory distress syndrome

The effects of bacterial endotoxin (lipopolysaccharide, LPS) are amplified by lipopolysaccharide binding protein (LBP) and CD14, resulting in cellular activation at very low concentrations of LPS. To investigate the importance of this pathway in acute lung injury, we measured LPS, LBP, and soluble CD14 (sCD14) in the bronchoalveolar lavage fluid (BAL) of 82 patients with acute respiratory distress syndrome (ARDS). LBP and sCD14 increased markedly in BAL of patients with ARDS. sCD14 and LBP each were strongly related to BAL total protein and polymorphonuclear neutrophil (PMN) concentration, whereas LPS concentration was not. Multivariate analyses showed sCD14 to be strongly related to BAL total protein, even after controlling for LPS and LBP concentrations. sCD14 was strongly and independently related to PMN concentration, after controlling for BAL LPS, LBP, and interleukin-8 (IL-8). The BAL LPS concentration was not strongly related to either BAL total protein or BAL PMN. The BAL sCD14 and LBP values were similar in all subgroups of patients with ARDS, and were not related to survival. The serum LBP and sCD14 were elevated in ARDS, but were not related to BAL total protein, LBP, sCD14, PMN, or clinical outcome. Thus, LBP and sCD14 reach high concentrations in the lungs of patients with ARDS, and BAL sCD14 is strongly related to two major indices of lung inflammation: total protein and PMN concentration. CD14-dependent mechanisms may contribute to lung inflammation in ARDS.