PubMed Health⌕ Search

Biomedical subjects

Q N Myrvik

Publications and source records attributed to Q N Myrvik.

At least 19 recordsLinked to original sources
PubMed1997

Alveolar macrophage priming by intravenous administration of chitin particles, polymers of N-acetyl-D-glucosamine, in mice.

Intravenous (i.v.) administration of phagocytosable chitin particles (1 to 10 microm) in C57BL/6 mice and SCID mice primed alveolar macrophages (Mphi) within 3 days to yield up to a 50-fold increase in their oxidative burst when elicited in vitro with phorbol myristate acetate (PMA). C57BL/6 mice pretreated with monoclonal antibodies (MAbs) against mouse gamma interferon (IFN-gamma) or NK1.1 showed a markedly decreased level of alveolar Mphi priming following injection of chitin particles. To confirm IFN-gamma production in vitro, spleen cells isolated from normal C57BL/6 mice and SCID mice were cultured with chitin particles. Significant IFN-gamma production was observed following stimulation with chitin but not with chitosan or latex beads. When spleen cells were treated with anti-NK1.1 MAb, IFN-gamma production was significantly inhibited. Another set of experiments showed that when C57BL/6 mice were pretreated i.v. with a small dose IFN-gamma, a higher level of priming was induced with not only phagocytosable chitin particles but also phagocytosable chitosan and even latex beads. Likewise, the spleen cell cultures preconditioned with IFN-gamma provided an up-regulation of IFN-gamma production by these phagocytosable particles. Taken together, the in vivo and in vitro results suggest that (i) the alveolar Mphi priming mechanism is due, at least in part, to direct activation of Mphi by IFN-gamma, which is produced by NK1.1+ CD4- cells; (ii) IFN-gamma would have an autocrine-like effect on Mphi and make them more responsive to particle priming; and (iii) phagocytosis of particulates, probably by a postmembrane event such as interiorization, appears to be important for the up-regulation of alveolar Mphi priming and IFN-gamma production.

Animals↗
PubMed1995

Simple technique for the preparation of silicone gel particles: the effect of silicone gel particles on oxidative responses of macrophages.

A simple technique was developed to prepare phagocytosable-size particles from the silicone gel used in breast implants. Sonication of silicone gel (1 g) in 5 ml of 20 mM sodium phosphate buffer (pH 7.2) containing 1% (wt/vol) polyoxypropylene-polyethylene block surfactant (F-68 or F-108) produced silicone gel particles ranging from 1-50 microns in diameter. Passage of the suspension through a series of filters yielded phagocytosable particles (1-5 microns in diameter) at a concentration of ca. 2 x 10(9) particles/ml. The particles remained as individual particles, did not coalesce to form large clumps, and were not pelleted by centrifugation (2000 x g, 20 min). They were not toxic for rabbit alveolar macrophages (AM) during 24 h of incubation at 37 degrees C, did not elicit an oxidative burst from AM in vitro in a luminol-enhanced chemiluminescent assay, and did not significantly increase the phorbol myristate acetate (PMA)-elicited oxidative burst by AM. AM isolated from rabbits 2 days after the intravenous injection of silicone particles were not primed or activated (i.e., the AM did not show an enhanced oxidative burst when elicited with PMA in vitro). However, AM isolated from rabbits 2 days after intratracheal injection of the particles were primed but only exhibited a 4-6-fold increase in the oxidative burst elicited with PMA.

Animals↗
PubMed1995

Biomaterial-induced dysfunction in the capacity of rabbit alveolar macrophages to kill Staphylococcus epidermidis RP12.

The effect of poly(methyl methacrylate) (PMMA), titanium alloy, and silicone discs on the capacity of rabbit alveolar macrophages (AM) to kill RP12 strain of Staphylococcus epidermidis (RP12) was studied in vitro. When freshly harvested AM were preincubated with PMMA discs for 3 h and subsequently assayed for RP12 killing, there was no change in the RP12 killing capacity of AM. However, when AM were incubated with PMMA discs for 6 or 18 h at 37 degrees C in 5% CO2, the RP12 killing capacity of AM was reduced to 15% and 4%, respectively. Preincubation of AM with titanium alloy for 6 h reduced RP12 killing capacity of AM to 30%, and to 21% in 18-h incubation. Silicone discs did not affect the RP12 killing by AM at 6 h of preincubation, but reduced RP12 killing (35%) by AM when preincubated for 18 h. Preincubation of AM with PMMA discs for 3 or 6 h did not affect the level of PMA-elicited oxidative burst of AM as measured by a luminol-enhanced chemiluminescent assay. Superoxide dismutase, which eliminated the oxidative burst of AM by 90%, did not affect the RP12 killing by AM.

Animals↗
PubMed1994

Inhibition of Staphylococcus adherence to biomaterials by extracellular slime of S. epidermidis RP12.

Adherence of selected strains of coagulase-negative staphylococci to various biomaterials, and the inhibition of their adherence by extracellular slime obtained from the RP12 strain of Staphylococcus epidermidis were studied in vitro. S. epidermidis RP12 adhered considerably more to polymethylmethacrylate (PMMA) discs than did the SP2 strain of S. hominis and the SE-360 strain of S. hyicus. Strain RP12 was less adherent to titanium alloy, ultrahigh molecular weight polyethylene (UHMWPE), and Teflon discs than to PMMA discs. Exposure of PMMA discs to extracellular slime extracted from strain RP12 greatly reduced adherence of strain RP12, SP2, SE-360, and S. epidermidis RP-62A. The active component(s) was present in the > 10 kD mol wt fraction obtained by Amicon YM10 ultrafiltration of crude slime; heat treatment of the fraction did not affect its inhibitory activity. When the bacteria and RP12 slime fractions were added simultaneously to the PMMA discs, the > 10 kD mol wt fraction of slime competitively inhibited adherence of strain RP12 to PMMA discs; in contrast, the < 10 kD mol wt fraction enhanced adherence of strain RP12 to PMMA discs.

Alloys↗
PubMed1994

Site-specific adhesion of Staphylococcus epidermidis (RP12) in Ti-Al-V metal systems.

Staphylococcus epidermidis (RP12) adhesion patterns were studied on the following titanium (Ti)-aluminium (Al)-vanadium (V) metal systems: (i) microfabricated samples consisting of Ti, Al and V islands deposited onto Ti or V substrata, (ii) pure Ti, Al and V metals, and (iii) medical grade Ti6Al4-V alloy. All of these surfaces were covered with their respective oxides formed upon exposure of the metals to air. Quantitative analysis of the number of cells bound per unit area indicates that S. epidermidis (RP12) exhibits greatest adhesion to pure V surfaces. When exposed to surfaces having controlled spatial variations in chemical composition on the 10 microns scale (microfabricated samples), the bacteria preferentially populate V islands versus Ti or Al substrata. In the case of the biphasic Ti6Al4V alloy, the bacteria tend to adhere to V-rich, mixed phase regions and phase boundaries. These findings demonstrate that enhanced and preferential adhesion of S. epidermidis (RP12) occurs on V surfaces in Ti-Al-V metal systems and suggest that bacterial interactions are influenced by surface oxide composition.

Alloys↗
PubMed1993

Particle-induced in vivo priming of alveolar macrophages for enhanced oxidative responses: a novel system of cellular immune augmentation.

A novel system for priming adult rabbit alveolar macrophages (AMs) in vivo for markedly enhanced oxidative responses is described. When adult rabbits were injected intravenously (i.v.) with 1- to 5-microns particles such as zymosan, latex particles, or heat-killed bacille Calmette-Guérin, AMs were primed in 1-3 days for greatly enhanced phorbol myristate acetate (PMA)- or opsonized zymosan (Op-zym)-elicited chemiluminescent (CL) responses. Intratracheal (i.t.) injection of zymosan particles also primed AMs for enhanced PMA- or Op-zym-elicited CL responses. AMs obtained from particle-injected rabbits showed up to 100-fold higher levels of PMA-elicited CL responses than AMs from normal rabbits. In contrast, Op-zym failed to prime normal AMs in vitro for enhanced CL responses. Whereas AMs could not be primed in vivo with an i.v. injection of particles of approximately 24 microns diameter. AMs could be primed if the particles were administered by the i.t. route. The priming appears to be independent of particle types. The priming effect was of short duration and declined after 5 to 7 days. The possibility that this system represents the primitive cellular immune response found in invertebrates is discussed. The potential use of this system as a means of immune augmentation prompts further investigation.

Animals↗
PubMed1993

Altered oxidative responses and antibacterial activity of adult rabbit alveolar macrophages exposed to poly(methyl methacrylate).

The effect of poly(methyl methacrylate) (PMMA) on the oxidative responses and antibacterial activity of adult rabbit alveolar macrophages (AM) was studied. PMMA beads (ca. 0.3 micron diameter) elicited an acute respiratory burst within 6-8 min after the addition of the beads. In contrast. Teflon beads of comparable size (ca. 0.2 micron diameter) did not elicit an oxidative burst of AM. An oxidative response was elicited only by those PMMA samples that had affinity for AM adherence. Incubation of AM with PMMA beads reduced the subsequent phorbol myristate acetate (PMA)-elicited oxidative burst by more than 80%. The Staphylococcus epidermidis--RP12 killing capacity of AM was greatly increased when PMMA beads (ca. 0.3 micron) were added to the challenge dose of bacteria. Pre-incubation of freshly harvested AM with PMMA beads, which greatly reduced subsequent PMA-elicited chemiluminescent (CL) responses did not significantly affect the RP12 killing capacity of AM. Our data also suggest that killing of the RP12 strain of S. epidermidis does not involve reactive oxygen intermediates.

Animals↗
PubMed1993

Cell biology and molecular mechanisms in artificial device infections.

Biomaterials are being used with increasing frequency for tissue substitution. Complex devices such as total joint replacement and the total artificial heart represent combinations of polymers and metal alloys for system and organ replacement. The major barrier to the extended use of these devices is bacterial adhesion to biomaterials, which causes biomaterial-centered infection, and the lack of successful tissue integration or compatibility with biomaterial surfaces. Adhesion-mediated infections are extremely resistant to antibiotics and host defenses and frequently persist until the biomaterial or foreign body is removed. The pathogenesis of adhesive infections is related, in part, to preferential colonization of "inert" substrate whose surfaces are not integrated with healthy tissues composed of living cells and intact extracellular polymers. Tissue integration is an interesting parallel to microbial adhesion and is a desired phenomenon for the biocompatibility of certain implants and biomaterials. Tissue integration requires a form of eukaryocytic adhesion or compatibility with possible chemical integration to an implant surface. Many of the fundamental principles of interfacial science apply to both microbial adhesion and to tissue integration and are general to and independent of the substratum materials involved. Interactions of biomaterials with bacteria and tissue cells are directed not only by specific receptors and outer membrane molecules on the cell surface, but also by the atomic geometry and electronic state of the biomaterial surface. An understanding of these mechanisms is important to all fields of medicine and is derived from and relevant to studies in microbiology, biochemistry, and physics.(ABSTRACT TRUNCATED AT 250 WORDS)

Alloys↗
PubMed1992

Pulmonary surfactant phospholipids modulate priming of rabbit alveolar macrophages for oxidative responses.

We investigated the effect of individual phospholipids contained in pulmonary surfactant (PS) on the macrophage-activating factor (MAF)-induced priming of rabbit alveolar macrophages (AMs) for oxidative responses elicited by phorbol myristate acetate (PMA) or opsonized zymosan (Op-Zym). AMs were incubated with MAF with or without phospholipids for 18 h. After incubation, oxidative responses were elicited with PMA (0.5 micrograms/ml) or Op-Zym (250 micrograms/ml) and monitored by chemiluminescence (CL) assays. The data indicate that natural surfactant inhibited MAF-induced priming of rabbit AMs for PMA- or Op-Zym-elicited oxidative responses. Artificial surfactant inhibited PMA-elicited CL responses but enhanced Op-Zym-elicited CL responses. Individual phospholipids differed in modulative activities. Dioleoyl phosphatidylcholine (DOPC), dipalmitoyl phosphatidylglycerol (DPPG), and phosphatidylinositol (PI) inhibited MAF-induced priming when the oxidative responses were elicited with PMA. Whereas DPPG inhibited Op-Zym-elicited oxidative responses, dipalmitoyl phosphatidylcholine (DPPC) and DOPC primed AMs for increased Op-Zym-elicited oxidative responses. DOPC did not affect the binding of phorbol dibutyrate to AMs, which suggests that reduced cell binding of phorbol ester was not responsible for the inhibition of PMA-elicited oxidative responses in AMs treated with DOPC. Similarly, DPPC, DOPC, and DPPG did not affect the number of zymosan particles phagocytosed by AMs compared to the control, which suggested that enhanced or reduced Op-Zym-elicited oxidative responses by phospholipids were not due to altered phagocytic activity of AMs. In conclusion, our data indicate that individual surfactant phospholipid differently modulates priming of AMs for oxidative responses, and the effect of individual phospholipids does not account for the effect of complete PS on priming of AMs.

Animals↗
PubMed1991

Priming of rabbit alveolar macrophages for enhanced oxidative responses by herpes simplex virus type 2 infection.

The effect of herpes simplex virus type 2 (HSV-2) infection on the oxidative response in infant and adult rabbit alveolar macrophages (AM) was studied using either phorbol myristate acetate (0.5 microgram PMA/ml) or latex (250 micrograms/ml) as eliciting agents in a chemiluminescence (CL) assay. Results indicated that uninfected infant AM responded to a latex-elicited but not PMA-elicited CL response. HSV-2 infection (moi = 1.0) of infant AM for 2 hr at 37 degrees C did not alter the PMA or latex-elicited CL responses. In contrast, uninfected adult AM exhibited a markedly increased CL response when elicited with either PMA or latex. HSV-2 infection (moi = 1) of adult AM for 2 hr further increased both PMA- and latex-elicited CL responses. Increasing the moi to 10 inhibited both PMA- and latex-elicited CL responses. Incubation of uninfected control and HSV-2 infected adult AM for 18 hr at 37 degrees C resulted in spontaneous priming of the cells for increased CL responses. In the absence of PMA HSV-2 alone failed to elicit a CL response in adult AM. Infection with heat-inactivated HSV-2 (moi = 1.0 before heat inactivation) did not prime adult AM for enhanced CL responses. AM from BCG immunized adult rabbit produced a considerably higher level CL response that nonimmunized AM; however, HSV-2 infection of these cells did not further enhance the response. In summary, these data indicate that adult AM but not infant AM can be primed by active HSV-2 infection for an increased CL response elicited by either PMA or latex.

Animals↗
PubMed1991

Mechanisms of musculoskeletal sepsis.

Musculoskeletal infection is extraordinarily resistant to treatment. Bacterial colonization is discussed as well as host defense systems and antibiotic resistance.

Anti-Bacterial Agents↗
PubMed1990

Human immunodeficiency virus type 1 (HIV-1) and herpes simplex virus type 2 (HSV-2) can coinfect and simultaneously replicate in the same human CD4+ cell: effect of coinfection on infectious HSV-2 and HIV-1 replication.

Experiments were designed to determine whether HIV-1 and herpes simplex virus type 2 (HSV-2) coinfection leads to simultaneous replication of both viruses in the same human CD4+ cell (MT-4 cell line) and the possible effects of coinfection on infectious virus production. Results from transmission electron microscopy analysis revealed replication of typical HSV-2 nucleocapsids in the nucleus and budding of HIV-1 particles through the plasma membrane and through intracytoplasmic vacuoles containing enveloped HSV-2 particles in the same coinfected cell. Coinfection of HIV-1 persistently infected H9IIIB or promonocytic U1 cells with HSV-2 did not alter total production of infectious HSV-2 or the percentage of HSV-2 infectious centers compared with control H9 and U937 cells infected with HSV-2 alone. However, in coinfected promonocytic U1 cells HSV-2 induced infectious HIV-1 production measured by syncytial plaque assay. In summary, both HIV-1 and HSV-2 can coinfect and simultaneously replicate in the same human CD4+ cell. Interactions between HIV-1 and HSV-2 appear to be unidirectional, resulting in accelerated replication of HIV-1 as reported by Albrecht et al. (J Virol 1989;63:1861-1868), but not HSV-2 as shown by us.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Musculoskeletal infection, microbial adhesion, and antibiotic resistance.

Osteomyelitis and intra-articular infection are septic diseases that present pathogenic features characteristic of molecular mechanisms involving adhesion to substrata. In this review, mechanisms of microbial adhesion to bone and cartilage as substrata are presented and related to host tissue response and to antibiotic treatment.

Anti-Bacterial Agents↗
PubMed1989

Oxidative responses of rabbit alveolar macrophages: comparative priming activities of MIF/MAF, sera, and serum components.

The comparative abilities of various reagents to prime rabbit alveolar macrophages (AM) to produce reactive oxygen intermediates (ROI) in a chemiluminescent (CL) assay were investigated. It was noted that AM from normal rabbits cultured in a serum-free medium for 18 hr exhibited a "spontaneous" priming response following a challenge with phorbol myristate acetate (PMA); however, "spontaneous" priming was not evident when the AM were cultured for only 3 hr. It was further established that pretreatment of normal AM for 3 or 18 hr with MIF/MAF preparations (serum-free), fetal bovine serum (FBS), or bovine serum albumin (BSA) exhibited marked increases in their CL responses following challenge with PMA. When FBS was used in the culture medium, the priming activity of MIF/MAF was masked because of the high CL responses of controls due to the priming effects of FBS. BSA at concentrations approximately equivalent to the amount in FBS also displayed marked priming activity. Bacterial products (lipopolysaccharide and muramyl dipeptide), latex particles, rabbit IgG, PMA, and opsonized as well as nonopsonized zymosan and bacteria (BCG and Staphylococcus epidermidis) were inactive as priming agents. In comparison, AM from BCG-immune rabbits that were primed in vivo yielded a very large CL response when challenged with PMA. Opsonized zymosan and bacteria produced twofold increases in the CL responses in BCG-immune AM compared to nonopsonized preparations. The marked priming effect of serum on AM cultured for even a short period (3 hr) indicates that normal AM undergo marked changes in culture that complicate the interpretation of AM function when AM are cultured in vitro in media containing serum.

Animals↗
PubMed1989

L-fucose blocks MIF/MAF priming of rabbit alveolar macrophages for a PMA-induced oxidative response.

The effect of L-fucose on the priming of AM from normal adult rabbits and their subsequent chemiluminescent (CL) responses to phorbol myristate acetate (PMA) was investigated. It was observed that 12.5 mM L-fucose, but not D-fucose, blocked the "spontaneous" priming of normal AM during an 18-hr incubation period in serum-free RPMI 1640 medium by about 40% (P less than 0.01) as detected by their CL responses to a PMA challenge. In addition, the optimal concentration of L-fucose (12.5 mM) blocked MIF/MAF priming during the 3- or 18-hr incubation period by 71 or 93% (P less than 0.05), respectively, as determined by their CL responses following PMA challenge. It is of particular significance that D-fucose was inactive. These results, together with previously published data, indicate that L-fucose (a) blocks priming of AM for an oxidative response, (b) stimulates random migration of AM, and (c) reverses migration inhibition produced by migration inhibition factor.

Animals↗
PubMed1989

Comparative in vitro antibiotic resistance of surface-colonizing coagulase-negative staphylococci.

The MBCs of nafcillin, vancomycin, gentamicin and daptomycin (LY146032) were determined for three clinical isolates of coagulase-negative staphylococci grown in suspension and adherent to biomaterials. Strains studied were the slime-producing strain Staphylococcus epidermidis RP-12 (ATCC 35983), S. hyicus SE-360, and the non-slime-producing strain S. hominis SP-2 (ATCC 35982). All three strains were allowed to colonize surgical-grade disks of stainless steel, polymethylmethacrylate, and ultrahigh-molecular-weight polyethylene for 24 h, and the disks were then exposed to various concentrations of antibiotics for 24 h. Surviving adherent bacteria were mechanically dislodged from the disks and quantitated by standard broth dilution plating techniques. Biomaterial-adherent RP-12 and SE-360 yielded approximately 10 times more CFU per disk than non-slime-producing SP-2 did. For all organisms, 10 times more bacteria bound to polymethylmethacrylate disks than to the other biomaterials. In general, bacteria adherent to biomaterials exhibited greater resistance to antibiotics than the same strains in suspension did. Resistance was independent of bacterial slime-producing characteristics and was related to the biomaterial colonized.

Anti-Bacterial Agents↗
PubMed1989

Pulmonary surfactant inhibits priming of rabbit alveolar macrophage. Evidence that surfactant suppresses the oxidative burst of alveolar macrophage in infant rabbits.

We have investigated the possible role of pulmonary surfactant in mediating a deficiency in alveolar macrophages (AM) from infant animals to produce chemiluminescent (CL) responses elicited by phorbol myristate acetate (PMA) or opsonized zymosan (Op-Zym). Freshly harvested AM from rabbits 7 to 28 days of age produced much reduced PMA-elicited CL responses compared to 5- to 6-month-old rabbits. Initially we observed that AM from both infant and adult rabbits exhibited increasing PMA- or Op-Zym-elicited CL responses in a time-dependent manner when they were incubated in RPMI 1640 medium without serum for more than 3 h. In addition, AM from infant rabbits acquired the capacity to become primed with macrophage activation factor (MAF) containing supernatants or fetal bovine serum (FBS) during an 18-h incubation period that was basically equivalent to that of AM from adult rabbits. Our studies reveal that natural and artificial surfactant inhibited "spontaneous" priming as well as priming of AM induced by MAF-containing supernatant or FBS for producing PMA- or OP-Zym-elicited CL responses from both normal infant and adult animals. In addition, these surfactant preparations also suppressed the response of AM from adult BCG-sensitized rabbits during the course of an 18-h incubation period. It is especially noteworthy that AM from infant rabbits appeared to be more susceptible to the inhibitory activity of surfactant than AM from adult animals. Our data indicate that freshly harvested AM from infant rabbits are under greater suppression than AM from adult rabbits in terms of their capacities to produce oxidative responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗