Angiotensin converting enzyme concentrations in the lung lavage of normal rabbits and rabbits treated with nitrogen mustard exposed to hyperoxia.

Increased concentrations of angiotensin converting enzyme (ACE) were found in lung lavages from rabbits exposed to hyperoxia for 72 h and the concentrations of ACE were correlated with ratios of extravascular lung water to body weight (r = 0.69, p less than 0.05) and albumin concentrations in lung lavages (r = 0.

Hydrogen peroxide kills Staphylococcus aureus by reacting with staphylococcal iron to form hydroxyl radical.

Two lines of investigation supported the premise that killing of Staphylococcus aureus, 502A, by hydrogen peroxide involves formation of the more toxic hydroxyl radical (.OH) through the iron-dependent Fenton reaction. First, growing S.

Serum from patients with invasive fungal infections inhibits the adherence of polymorphonuclear leukocytes and alveolar macrophages.

Adherence of various combinations of polymorphonuclear leukocytes (PMN) or alveolar macrophages (AM) and serum from nonimmunosuppressed patients wit culture-proved, invasive fungal infections or control subjects was evaluated in vitro using the standard nylon fiber pipette technique. In autologous serum, adherence of PMN from patients with wide variety of untreated fungal infections, including blastomycosis, histoplasmosis, cryptococcosis, coccidiodomycosis, and spirotrichosis, was significantly (p less than 0.001) decreased when compared with PMN from uninfected control subjects or patients with untreated bacterial infections.

Platelets increase neutrophil adherence in vitro to nylon fiber.

The effect of platelets on the adherence of neutrophils to nylon fiber was assessed in whole blood samples and purified neutrophil suspensions in the presence or absence of plasma. In whole blood samples, increasing numbers of platelets were associated (r = 0.47, p less than 0.

Pulmonary inflammation due to oxygen toxicity: involvement of chemotactic factors and polymorphonuclear leukocytes.

Although the pathogenesis of pulmonary oxygen toxicity is not fully understood, the fact that increased numbers of polymorphonuclear leukocytes (PMN) are found in the lung and that these increases coincide with the massive endothelial damage raises the possibility that PMN may contribute to lung injury caused by hyperoxia. In order to begin to elucidate a mechanism for this influx of PMN, we measured the chemoattractant activity for PMN of lung lavages of rats exposed to greater than 95% oxygen for various durations. We found that the chemoattractant activity of the lavages of the lungs of rats exposed to hyperoxia for 66 h was markedly increased (9.

Effect of staphylococcal iron content on the killing of Staphylococcus aureus by polymorphonuclear leukocytes.

Preincubation of Staphylococcus aureus 502A in broth with increasing concentrations of ferrous sulfate progressively increased their iron content, markedly increased their susceptibility to killing by hydrogen peroxide, and did not alter their susceptibility to killing by polymorphonuclear leukocytes.

Dimethyl sulfoxide prevents DNA nicking mediated by ionizing radiation or iron/hydrogen peroxide-generated hydroxyl radical.

Eighty percent of the single-strand DNA breaks induced by gamma-irradiation were prevented by the hydroxyl radical (.OH) scavenger dimethyl sulfoxide (Me2SO); CH4 was generated in the process as a product of the interaction of .OH and Me2SO.

Dimethyl sulfoxide inhibits killing of Staphylococcus aureus by polymorphonuclear leukocytes.

Increasing concentrations of the highly permeable, hydroxyl radical scavenger dimethyl sulfoxide progressively decreased killing of Staphylococcus aureus 502A by human polymorphonuclear leukocytes; methane, a product of the reaction of the hydroxyl radical with dimethyl sulfoxide, was generated in the process.

Altered oxidative metabolic responses in vitro of alveolar macrophages from asymptomatic cigarette smokers.

Superoxide anion (O2) release by alveolar macrophages (AM) from young asymptomatic cigarette smokers was greater than that by AM from age-matched nonsmokers. Greater O2 release by AM from cigarette smokers was observed before and after stimulation by bacteria or phorbol myristate acetate (PMA). In contrast, oxygen uptake and glucose (1(-14)C) oxidation by unstimulated or stimulated AM from cigarette smokers was the same as that by AM from non-smokers.

Bactericidal function of neutrophils from patients with acute bacterial infections and from diabetics.

Killing of Staphylococus aureus by neutrophils from untreated patients with acute bacterial infection was increased compared with neutrophils from uninfected controls or the same patients after antibiotic treatment. In contrast, neutrophils from diabetics failed to increase their bactericidal activity in response to infection to the same degree as neutrophils from nondiabetic subjects. The latter abnormality was pronounced in poorly controlled (plasma glucose level, greater than 130 mg/100 ml), but was also present in well-controlled (plasma glucose levels, less than 130 mg/100 ml), diabetics.

Phagocytosis by human alveolar macrophages and neutrophils: qualitative differences in the opsonic requirements for uptake of Staphylococcus aureus and Streptococcus pneumoniae in vitro.

The opsonic requirements for uptake of 3H-adenine-labeled Staphylococcus aureus (strains 502A, Wood 46, or 209) or Streptococcus pneumoniae (Type VII) by human alveolar macrophages (AM) or neutrophils (PMN) were evaluated and compared using a quantitative assay of phagocytosis. AM readily engulfed S. aureus organisms preopsonized with 1% albumin, serum, or serum that had been heated (56 degrees C for 30 min) to inactivate complement, whereas uptake of S.

Production of hydroxyl radical by human alveolar macrophages.

Stimulated human alveolar macrophages were demonstrated to oxidize B-methyl proprionaldehyde (methional) or 2-keto-4-thiomethylbutyric acid to ethylene (C2H4). Agents which are believed to scavenge the hydroxyl radical (.OH), sodium benzoate, and mannitol, as well as scavengers of superoxide anion (O2-) or hydrogen peroxide, decreased C2H4 production, implicaing .

Generation of hydroxyl radical by enzymes, chemicals, and human phagocytes in vitro. Detection with the anti-inflammatory agent, dimethyl sulfoxide.

Methane (CH(4)) production from the anti-inflammatory agent, dimethyl sulfoxide (DMSO), was used to measure .OH from chemical reactions or human phagocytes. Reactions producing .

Defective oxidative metabolic responses in vitro of alveolar macrophages in chronic granulomatous disease.

After stimulation with bacteria, alveolar macrophages (AM) from uninfected normal subjects or persons with pneumonia approximately doubled their rates of O2 consumption, superoxide anion generation, and glucose (1(-14)C) oxidation. In contrast, bacteria-stimulated AM from a patient with chronic granulomatous disease (CGD) failed to consume more O2, make superoxide anion, or oxidize glucose. In addition, AM from the patient with CGD did not respond to stimulation by a chemical agent, phorbol myristate acetate, which increased the metabolic activities of AM from control subjects.

An improved nitroblue tetrazolium test using phorbol myristate acetate-coated coverslips.

The endotoxin--nitroblue tetrazolium (NBT) slide test was modified by precoating coverslips with phorbol myristate acetate instead of endotoxin. The percentage of control polymorphonuclear leukocytes reducing NBT was significantly (P less than .05) greater on phorbol myristate acetate-coated coverslips (99 +/- 0.

Influence of cationic local anesthetics on the metabolism and ultrastructure of human alveolar macrophages.

The concentrations of cationic local anesthetics present in effluents from subsegmental bronchoscopic lavage were determined. Subsequently, the effect of these agents on lavaged human AM was evaluated in vitro. The results indicate that concentrations of LDC that may alter human AM function are present in effluents during routine subsegmental bronchopulmonary lavage.

The Chediak-Higashi syndrome: quantitation of a deficiency in maximal bactericidal capacity.

The maximum bactericidal capacity of neutrophils from a patient with the Chediak-Higashi syndrome (CHS) was measured by a quantitative assay in which the neutrophils were challenged with increasing multiples of Staphylococcus aureus, 502A. At various bacterial challenges from 0.5 to 65 bacteria per neutrophil, the CHS cells killed normal numbers of bacteria in 60 minutes.