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Q N Myrvik

Publications and source records attributed to Q N Myrvik.

At least 55 records · Page 3Linked to original sources
PubMed1986

Induction of a macrophage migration enhancement factor after desensitization of tuberculin-positive rabbits with purified protein derivative.

The production of a macrophage migration enhancement factor (MEF) has been achieved as a consequence of administering a desensitizing dose of purified protein derivative (PPD) to Mycobacterium bovis BCG-sensitized rabbits. The migration-enhancing effect was first demonstrated when alveolar macrophages (AM) harvested from desensitized rabbits exhibited marked migration stimulation; whereas maximum migration enhancement was observed 8 days after the administration of PPD, migration enhancement of the AM from these rabbits persisted for up to 12 days. Sera from BCG-sensitized, PPD-desensitized animals exhibited a peak of MEF activity 4 days after desensitization. Maximal MEF activity was demonstrated in culture supernatants of nonadherent spleen cells harvested 8 days after the intravenous desensitizing dose of PPD was given. Control spleen cell culture supernatants did not produce detectable MEF. The route of desensitization with PPD was critical. When PPD was administrated intratracheally, MEF activity was not induced. The intravenous administration of BCG after PPD desensitization reversed migration enhancement to strong migration inhibition. Ammonium sulfate fractionation indicated that two fractions contained MEF activity. MEF activity was retained by dialysis membranes with a 15,000-molecular-weight cutoff but passed through dialysis membranes with a 25,000-molecular-weight cutoff. The mixture of migration inhibition factor with MEF-containing supernatants resulted in the mutual cancellation of both activities. These observations suggest that MEF may be a modulator of macrophage effector responses mediated by migration inhibition factor.

Animals↗
PubMed1985

Demonstration of a macrophage migration enhancement factor in the sera of young rabbits.

Alveolar macrophages (AM), harvested from the lungs of untreated normal young rabbits (New Zealand White) 14 days to 8 weeks of age, exhibited a state of migration stimulation compared to AM from normal adult rabbits (5 to 6 months of age). Migration of AM from normal adult rabbits (New Zealand White) was stimulated 2.0- to 2.5-fold when incubated with sera from 39- to 46-day-old rabbits compared with sera from normal adult rabbits. Furthermore, 4-day spleen cultures obtained from animals 28 to 59 days of age yielded supernatants that also stimulated the migration of adult AM. The spleen cell culture supernatants from 42- to 49-day-old animals had the greatest activity and stimulated the migration of adult AM 2.5- to 3.2-fold compared to the supernatants from adult normal rabbits. The peak production of migration enhancement factor (MEF) by splenic lymphoid cells coincided with the peak activities found in the sera. It was observed that nonadherent peanut agglutinable lymphoid cells produced MEF. When sera or culture supernatants containing MEF were mixed with MIF-containing adult sera or spleen cell culture supernatants, the respective activities were neutralized. The large migrations of normal neonatal AM were diminished by the addition of MIF-containing sera obtained from BCG-sensitized/challenged rabbits. In contrast, AM from BCG-sensitized rabbits, which exhibited a state of reduced migration, were enhanced by MEF-containing sera from untreated young rabbits. Three peaks of MEF activity were detected in Sephadex G-100 column fractionated sera from 42-day-old rabbits having MWs of approximately (Peak I) 80,000, (Peak II) 43,000, and (Peak III) 8000 to 18,000; most of the activity was found in peaks II and III. Two peaks of MEF activity were detected in Sephadex G-100 column-fractionated spleen cell culture supernatants from 42-day-old rabbits having MWs of approximately (Peak I) 35,000 to 43,000 and (Peak II) 10,000 to 14,000; most of the activity was in peak I which corresponds to peak II of the serum fractionation experiment. Collectively, these data indicate that MEF is a lymphokine that could be important in the modulation of cell-mediated immune effector responses.

Age Factors↗
PubMed1985

Effects of asbestos on the random migration of rabbit alveolar macrophages.

The toxicity of sized and characterized chrysotile, crocidolite, and amosite preparations obtained from Dr. K. R. Spurny have been evaluated using alveolar macrophage (AM) migration inhibition assays and viability tests. These results have been compared with asbestos samples obtained from the National Institute of Environmental Health Sciences (NIEHS). These latter samples are designated chrysotile A (RT), crocidolite (RT), and amosite (RT). In addition, filter-isolated preparations of chrysotile A (RT) that consisted mainly of large nonphagocytosable fibers were also tested. Chrysotile (Spurny) and sonicated chrysotile A (RT) produced 50% migration inhibition at about 115 micrograms/mL. Spurny crocidolite produced 50% migration inhibition at about 340 micrograms/mL, whereas RT crocidolite produced 50% migration inhibition at about 230 micrograms/mL. RT amosite caused 50% migration inhibition at about 180 micrograms/mL, whereas Spurny amosite was inactive up to 500 micrograms/mL. The large nonphagocytosable chrysotile A (RT) fibers produced 50% migration inhibition at about 66 micrograms/mL. This indicates that fibers can be toxic for AM through extracellular membrane contact. In general the results from the viability studies paralleled the migration inhibition observations. None of the asbestos preparations induced a burst in the hexose monophosphate shunt of BCG-immune AM at 1 mg/mL. BCG-immune AM were more susceptible to cell death than normal AM when incubated with chrysotile A (RT), amosite (RT) and zymosan. Migration inhibition induced by asbestos fibers probably reflects toxicity of the asbestos preparations and could play an important role in blocking normal alveolar clearance of inhaled particles.

Animals↗
PubMed1985

Characterization and maturation of alveolar macrophages procured from BCG-induced pulmonary granulomas.

Pulmonary macrophages from BCG-induced granulomas were separated according to their densities into six fractions by the use of discontinuous gradients of Percoll. A comparative study of distribution profiles of lavaged rabbit alveolar cells obtained 16 or 28 days after vaccination revealed that 16 days after vaccination there were small numbers of low-density cells (fractions 1 and 2) and large numbers of high-density cells (fractions 4 and 5). In contrast, 28 days after vaccination there was a marked increase in the numbers of macrophages in fractions 1 and 2 and relatively small numbers of high-density cells in fractions 4 and 5. Macrophages of fractions 1 and 2 (densities of 1.030-1.050) were large and mature in appearance and expressed low levels of acid phosphatase and beta-glucuronidase. Although macrophages in fraction 1 commonly showed signs of degeneration, they were the most active in terms of reducing nitroblue tetrazolium (NBT). Macrophages of fractions 3 and 4 (densities of 1.050-1.068) were smaller, appeared intact and fully mature, showed no signs of degeneration, and expressed the highest levels of the above enzymes, although their ability to reduce NBT was less than that in cells from fractions 1 and 2. The cells of fractions 5 and 6 (densities of 1.068-1.074) were small, expressed low levels of the above enzymes, and their ability to reduce NBT was minimal. These results indicate that density may be a reliable correlate of the maturity of macrophages harvested from BCG-induced granulomas.

Acid Phosphatase↗
PubMed1984

Phagosomal membranes of Mycobacterium bovis BCG-immune alveolar macrophages are resistant to disruption by Mycobacterium tuberculosis H37Rv.

Data obtained in this study reaffirm that virulent Mycobacterium tuberculosis H37Rv has a potent phagosome-destroying capacity when ingested by normal alveolar macrophages. In contrast, Mycobacterium bovis BCG-immune alveolar macrophages are highly resistant to this virulence mechanism. BCG-immune sera incubated with BCG-immune alveolar macrophages did not increase resistance of BCG-immune alveolar macrophages as compared with the data obtained from experiments with normal sera. BCG-immune sera failed to confer resistance to normal alveolar macrophages against the phagosomal membrane-destroying H37Rv virulence mechanism.

Animals↗
PubMed1984

Disruption of phagosomal membranes of normal alveolar macrophages by the H37Rv strain of Mycobacterium tuberculosis. A correlate of virulence.

The H37Rv and H37Ra strains of Mycobacterium tuberculosis were incubated with normal rabbit alveolar macrophages and examined by electron microscopy at 5 to 6 and 18 to 24 h of incubation. At the 18- to 24-h incubation interval, 60 to 100% of the endocytosed organisms of the H37Rv strain disrupted the phagosomal membranes and appeared free in the cytoplasm of the macrophages. In contrast, the H37Ra strain lacked this putative virulence characteristic, and greater than 99% of the organisms appeared within intact phagosomes. Heating the organisms of the H37Rv strain abrogated to a large extent, but not completely, their capacity to disrupt phagosomal membranes. In the course of the interaction of organisms of the virulent H37Rv strain with phagosomal membranes of normal rabbit alveolar macrophages, adherence of the phagosomal membrane to the surface of the organisms was a prominent feature that was followed by fragmentation and apparent disintegration of the membrane. This potential virulence characteristic could explain why there is essentially no resistance expressed in the lung during the early postinfectious period of primary infection to M. tuberculosis.

Animals↗
PubMed1982

Increased hyaluronic acid is associated with dermal delayed-type hypersensitivity.

Rabbits sensitized subcutaneously with heat-killed bacilli Calmette-Guerin (BCG) and challenged intradermally with heat-killed BCG or purified protein derivative (PPD) demonstrated classical dermal delayed-type hypersensitivity which peaked two days postchallenge. Animals challenged with BCG developed dermal granulomas as measured by induration and gross observation. Challenge with either PPD or BCG resulted in increased levels of dermal hyaluronic acid (HA) by two days postchallenge. Dermal HA returned to normal levels by seven days postchallenge regardless of the challenge antigen. These results indicated that increased HA is associated with dermal delayed-type sensitivity, but increased HA is not associated with dermal granulomatous hypersensitivity. These results are in contrast to previously reported work which indicates that increased HA is associated with both pulmonary delayed hypersensitivity and pulmonary granulomatous hypersensitivity.

Animals↗
PubMed1981

Deacylation of dipalmitoyllecithin by phospholipases A in alveolar macrophages.

Optimal conditions in vitro were established for the assay of phospholipases A of Bacillus Calmette Guerin-induced alveolar macrophages that deacylated dipalmitoyllecithin in the alkaline pH range. Sodium deoxycholate and Ca++ were found to stimulate both phospholipases A1 and A2, whereas sodium dodecylsulfate strongly inhibited both enzyme activities. Other detergents like Triton X-100, Triton WR-1339, and Tween-20 activated phospholipase A1, whereas they had no effect on or slightly inhibited the phospholipase A2 enzyme. These phospholipases preferentially removed palmitic acid regardless of the position of palmitic acid on the phospholipid molecule and were more active on phosphatidylcholines than phosphatidylethanolamines. This suggests a role for macrophage phospholipases A in the clearance of saturated lecithins in the pulmonary surfactant complex.

Animals↗
PubMed1980

Selective suppression of granuloma formation and delayed hypersensitivity in rabbits.

The relationship between dermal delayed hypersensitivity (DH) and granulomatous hypersensitivity was studied in rabbits sensitized with killed mycobacteria. Specific antigen challenge of sensitized animals resulted in extensive pulmonary granulomatous inflammation and induced suppression of both dermal DH and dermal granuloma formation. Whereas suppression of DH was concomitant with pulmonary granuloma formation, as is the case in a number of granulomatous diseases, a causal relationship between the two did not exist. Both DH and dermal granulomatous hypersensitivity were significantly suppressed whether or not the antigen challenge was of a granulomagenic (particulate) or nongranulomagenic (soluble) form. The data presented indicate that granulomatous hypersensitivity and DH are selectively suppressed with regard to different anatomical sites.

Animals↗
PubMed1980

Characterization of the early phase of the tuberculin reaction in rabbits.

The dermal response to purified protein derivative (PPD) in rabbits sensitized with Mycobacterium bovis strain Bacille Calmette Guèrin (BCG) is composed of at least two distinct phases. The early phase occurs within 24 h after injection of tuberculin and is characterized by accumulation of polymorphonuclear leukocytes. The second phase is delayed in onset, depending on mononuclear cell accumulation, and constitutes the classic delayed hypersensitivity reaction. The early component of the reaction of PPD is not immunologically specific, in that it can be elicited in either BCG-sensitized or nonsensitized rabbits and appears to be induced by pyrogenic components present in tuberculin preparations. Rabbit fever index assays indicated the presence of sufficient pyrogen in tuberculin PPD to account for the observed reactions; however, Limulus amebocyte pyrogen assays were negative. These findings suggest that tuberculin contains pyrogenic components other than endotoxin. Radiometric assays for mononuclear cell accumulation as well as desensitization experiments indicated that the early phase was independent of the delayed mononuclear phase.

Animals↗
PubMed1980

Participation of hyaluronic acid in the macrophage disappearance reaction.

Hyaluronic acid accumulates in the peritoneal cavity of mice during the macrophage disapperance reaction. Macrophages reappear in the exudates during the depletion of hyaluronate. The disappearance reaction is simulated by the intraperitional (i.p.) injection of hyaluronic acid into normal mice. The disapperance reaction largely is inhibited by the simultaneous injection (i.p.) of specific hyaluronidase with the challenge dose of BCG. We propose that hyaluronic acid makes a major contribution to the macrophage disappearance reaction.

Animals↗
PubMed1979

Phagocytosis-induced injury of normal and activated alveolar macrophages.

The present study tested the hypothesis that BCG-activated macrophages become injured when they phagocytose certain particulates. The data indicate that alveolar macrophages obtained from Mycobacterium bovis BCG-sensitized animals were more susceptible to cell death after in vitro incubation with BCG or zymosan than were macrophages from normal animals. Increased susceptibility was dependent on phagocytosis, since incubation with cytochalasin B, a phagocytosis inhibitor, abrogated the effect. Catalase, cytochrome c, and ascorbic acid offered partial protection to the macrophage, suggesting the involvement of free radicals in the generation of cytotoxicity. Not all of the cells from the alveolar populations were equally susceptible to cell death, thus suggesting either heterogeneity in the cell population or a requirement of more than one cell type in the induction of necrosis or both.

Animals↗