bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased Transglutaminase Activity in Elicited and Activated Macrophages: Relationship to Production of Superoxide Anion
Authors: Harris Lesley K , Pabst Michael J , Johnston Richard B 
Published: January 2018

Abstract
To evaluate whether transglutaminase (TG) might be involved in production of oxygen metabolites, TG activity was measured in resident, in activated, and in elicited murine peritoneal macrophages. These various types of macrophages show a wide diversity in their ability to generate oxygen metabolites. Like other transglutaminases, the macrophage enzyme was found to be a calcium-dependent enzyme that was stabilized by dithiothreitol and inhibited by dansylcadav- erine. The TG activity was approximately six-times higher in lysates of LPS- elicited macrophages compared with lysates of resident macrophages; this paralleled the six-fold increase in phorbol myristate acetate-stimulated release of superoxide anion (O2). From mixing experiments, the difference in TG activity was not due to an endogenous cellular inhibitor in the resident cells. The apparent Km of TG for putrescine was similar in lysates of resident and LPS-elicited macrophages, but the Vmax was significantly greater in lysates of LPS-elicited cells. Macrophages obtained from mice injected with either viable bacillus Calmette-Guérin, muramyl dipeptide, or killed Corynebacterium parvum released three- to six- times more O2 than did resident macrophages. The TG activity in these macrophages was also two- to six- times higher than in resident cells. However, macrophages that were primed by exposure to LPS in vitro exhibited increased production of O2 but no increase in TG activity. We conclude that enhanced TG activity is not a prerequisite for the enhanced O2 production observed in activated macrophages.
Modulation of Endotoxin-Induced Neutrophil Alveolitis by Captopril and by Hyperoxia
Authors: Rinaldo J E , Dauber J H 
Published: January 2018

Abstract
We compared survival and the intensity of bronchoalveolar inflammation reflected by lung lavage after the intraperitoneal injection of endotoxin from Escherichia coli serotype 055B5 in rats breathing air and those breathing 60% oxygen for six days after endotoxin injection. Survival following 7.5 mg/kg of endotoxin was comparable in air-breathing rats (50%) and in oxygen-breathing rats (63%). Endotoxin caused a dose-dependent increase in the recovery of polymorphonuclear leukocytes from the lung. Oxygen breathing reduced the percentage of neutrophils recovered by lavage 24 hr after endotoxin from 17% to 9% after 2.5 mg/kg of endotoxin and from 34% to 12% after 7.5 mg/kg of endotoxin. The absolute number of neutrophils recovered was also significantly decreased in oxygen-breathing rats. The activity of pulmonary angiotensin- converting enzyme (ACE) has been reported to be affected by oxygen tension, and ACE degrades bradykinin, a proinflammatory mediator. Therefore, we questioned whether the salutary effect of increased inspired oxygen tension on the magnitude of neutrophil influx into the airspaces could be related to changes in ACE activity. We found that after 48 hr of peroral pretreatment of the rats with captopril, a specific ACE inhibitor, there was increased recovery of neutrophils by lavage 24 hr after injection of endotoxin in air-breathing rats. Captopril pretreatment also increased the chemotactic activity of bronchoalveolar lavage fluid (BALF). There was no concomitant alteration in the accumulation of 125l albumin in the lung following captopril pretreatment either in endotoxin-treated rats or in controls. Thus, breathing 60% oxygen decreased the accumulation of neotrophils in airspaces after intraperitoneal endotoxin injection and pharmacologic inhibition of ACE had the opposite effect. Alterations in the activity of pulmonary angiotensin-converting enzyme related to alveolar oxygen tension is a potential speculative mechanism for modulation of alveolar inflammation by the inspired oxygen concentration in this model.
A Lectinlike Receptor on Murine Macrophage Cell Line Cells, Mm1: Involvement of Sialic Acid-Binding Sites in Opsonin-Independent Phagocytosis for Xenogeneic Red Cells
Authors: Kyoizumi Seishi , Masuda Tohru 
Published: January 2018

Abstract
The recognition mechanism of xenogenic red cells by mouse macrophages was studied by using established cell lines. Approximately 30% of cell line cells Mm1, which lack la antigen, as well as of thioglycollate-induced peritoneal macrophages from SL/Am mice (TGC-Mφ) could ingest unopsonized quail red cells (QRC). In contrast, an undifferentiated type of cell line, M1″, and another type of macrophage cell line, Mk1C, possessing accessory cell activity in association with the expression of la antigen, had no phagocytic activity for QRC. Approximately 80% of Mm1, cells, as well as TGC-Mφ formed rosettes with QRC, whereas M1 and Mk1 C cells did not; indicating that specific binding sites for QRC are expressed on a large portion of Mm1 and TGC-Mφ but not on M1 - and Mk1,-C cells. No requirement of divalent cation (Mg++, Ca++) and metabolic energy was observed for rosette formation between Mm1 cells and QRC. Protease treatment of Mm1 cells eliminated the rosetting activity, whereas periodate oxidation or glycosidase treatment slightly enhanced this activity, suggesting the involvement of surface protein in binding sites of Mm1, cells. In contrast to these findings on Mm1 cells, binding components of QRC were sensitive to periodate oxidation or neuraminidase treatment but resistant to protease, suggesting that the terminal sialic acid residues of carbohydrate of QRC are recognized by Mm1, cells. Furthermore, N-acetylneuraminic acid (NeuNAc) inhibited the rosette formation and promoted the dissociation of rosettes already formed. N-Acetylneuramin lactose (NeuNAc-Lact) was more efficient in rosette inhibition than NeuNAc. These sugars also blocked the phagocytosis of QRC by Mm1 cells but had no effect on either Fc-mediated phagocytosis or latex ingestion. These results suggest that phagocytosis of QRC by murine macrophages is mediated by protease-sensitive binding sites recognizing terminal sialic acid residues of QRC in conjunction with additional carbohydrates.
Antileukocyte Activity II. Induction of Tolerance to Systemic Anti-Inflammation Associated With Local Irritation and Major Surgery
Authors: Normann S J , Schardt M , Sorkin E 
Published: January 2018

Abstract
Anergy associated with cancer or major surgery may derive from the systemic antileukocyte effect induced by local inflammatory reactions (counter-irritation). Since the mechanism of the latter phenomenon is unknown, we approached the problem by asking if tolerance develops to repeated local irritant injections. Our results demonstrate that both tolerance and cross-desensitization occur rapidly to inflammatory agents (inflammagens) such as proteose peptone, thioglycollate, and carrageenan but not to the mitogens Con A, PHA-P, or LPS which also induce local inflammation. We interpret this data as supporting the notion that a common mechanism underlies the counter-irritant action of inflammagens but that injection of mitogens induces an additional mechanism of anti-inflammation distinguished from the former by its lack of tolerance induction. Based upon cross-desensitization experiments, we show that the anti-inflammatory effect of surgical amputation is analogous to that induced by inflammagens. In contrast, the systemic anti-inflammatory effect of tumor bearing, like that induced by mitogens, resists cross-desensitization suggesting that its mediation is not caused solely by the mechanism common to the counter-irritant action of inflammagens or major surgery.
Enhancement of Hamster Alveolar Macrophage Phagocytic Activity by Lymphokines
Authors: Widen Raymond H , Paradise Lois J 
Published: January 2018

Abstract
Modulation of phagocytic activity of resident hamster pulmonary alveolar macrophages was accomplished by incubation of the cells in lymphokines prepared by stimulation of hamster splenocytes with concanavalin A or alloantigens in mixed lymphocyte cultures. Alveolar macrophages preincubated in either of these lymphokine preparations possessed significantly greater ability to ingest IgG or IgM plus complement-coated sheep erythrocytes, via their Fc or complement receptors, respectively, than macrophages exposed to control preparations. Ingestion of yeast particles also was enhanced with macrophages incubated in supernatants from cultures of stimulated splenocytes. Supernatant fluids from either mitogen- or alloantigen-stimulated splenocytes possessed migration inhibitory activity with characteristics similar to MIF from other animals; the phagocytosis-enhancing activity shared some of these characteristics.
Effects of N-Nitrosodimethylamine on Tumor Susceptibility
Authors: Duke Scherer S , Schook Lawrence B , Holsapple Michael P 
Published: January 2018

Abstract
Dimethylnitrosamine (DMN) exposure altered the activity of the macrophage and natural killer (NK) cell defense mechanisms against the B16F10 melanoma In B6C3F1 adult female mice as assessed by several immunologic assays. Following 14 daily exposures (i.p.) to 1.5, 3.0, or 5.0 mg DMN/kg, mice were injected (i.v.) with B16F10 melanoma. The incidence and number of lung nodules, determined 18 days after challenge, were decreased in the DMN-exposed animals. The initial observation indicated the mice exposed to 3 mg/kg DMN were afforded the greatest protection. However, when mice exposed to the highest dose of DMN were divided into subgroups of mice with or without ascites, there was a degree protection seen in the 5-mg/kg-treated mice without ascites that was comparable to that of the 3-mg/kg group. The development of ascites is an overt toxic effect reflecting damage to the liver and was frequently associated with exposure to 5 mg/kg DMN. Exposure to DMN produced only slight changes in the activity of splenic NK cells as determined by the cytotoxicity of 51Cr-labelled YAC-1 cells. The activity was significantly increased only in mice exposed to 3 mg/kg DMN and only at effectortarget (E:T) ratios of 30:1 and 10:1. Interestingly, the activity of the NK cells was significantly decreased at all E:T ratios in mice exposed to 5 mg/kg that developed ascites. The number of peritoneal exudate cells was decreased, albeit nonsignificantly, in a dose-related fashion. The phagocytic activity, as measured by the uptake of fluorescent latex beads, was increased in a dose- related fashion with significance noted at the highest dose of DMN. The role of the macrophage in the increased resistance to the tumor challenge was assessed with bone marrow derived macrophages. The cytostatic activity versus B16F10 tumor cells, as measured by the uptake of 3H-thymidine, was markedly increased in the bone marrow derived macrophages from DMN (5 mg/kg) mice when compared to vehicle controls. These results suggest that exposure to DMN alters bone marrow, particularly the differentiation of effector tumoricidal cells, which renders the host more resistant to metastatic tumor formation.
The Effect of Local Antibody Responses on In Vivo and In Vitro Phagocytosis by Pulmonary Alveolar Macrophages
Authors: Harmsen Allen G , Bice David E , Muggenburg Bruce A 
Published: January 2018

Abstract
This study used both in vitro and in vivo techniques to determine if local antigen deposition in the lung has a localized effect on immune phagocytosis by pulmonary alveolar macrophages (PAM). Using a fiberoptic bronchoscope, dogs were immunized in the left cardiac and left diaphragmatic lobes with sheep red blood cells (sRBC). The right cardiac and right diaphragmatic lobes of the same animals received saline as controls. Unimmunized dogs served as additional controls. On days 2, 6, 9, 13, and 16 after immunization, the left and right diaphragmatic lobes were lavaged, and the cells and fluids were analyzed in vitro. Opsonizing antibody in lavage fluids was first detectable at 6 days, peaked at 9–13 days, and was significantly higher in the immunized lobe than in the control lobe. Phagocytosis of sRBC caused by cytophilic antibody on PAM also peaked at 9 to 13 days. Significantly more cytophilic antibody activity was detected on day 9 in the immunized lobes, than in the control lobes. In vivo phagocytosis of sRBC was evaluated in the alveoli of immunized and control lobes of immunized dogs and a control lobe of unimmunized dogs. Phagocytosis of sRBC by PAM in the immunized lobes was about four times greater than that of the control lobes and about 40 times greater than that of a control lobe of an unimmunized dog. These results indicate that the local deposition of a particulate antigen in the lung had a localized effect on immune phagocytosis. These data suggest that the accumulation of antibody-secreting cells in the alveolus may play a critical role in pulmonary defense mechanisms.
Reactivity of Anti-Asialo GM1 Serum With Tumoricidal and Non-Tumoricidal Mouse Macrophages
Authors: Wiltrout Robert H , Santoni Angela , Peterson Erik S , Knott Denise C , Overton W Roy , Herberman Ronald B , Holden Howard T 
Published: January 2018

Abstract
All peritoneal macrophage (pMφ) populations studied exhibited some binding of the anti-asGM1 serum as assessed by flow cytometry. The levels of reactivity varied quantitatively among populations, depending on the combination of eliciting and activating agents employed prior to the harvest of pMφ. Resident pMφ contained a very small percentage (4%) of cells that were strongly asGM1 +. Any treatment of these cells that induced them to become stimulated or activated increased the percentage of highly asGM1 + cells. Treatments that enhanced anti-asGMi binding including eliciting pMφ with proteose peptone (16% asGM1+) or Brewer's thioglycollate medium (66% asGM1+), treatment with the activating biological response modifiers (BRMs) MVE-2 (12% asGM1 +) and P acnes (18% asGM1 +), or treatment with both peptone + MVE-2 (37% asGM1 +) or peptone + poly IC/LC (33%). Increased expression of anti-asGM1 was accompanied by some increase in the reactivity of the various pMφ populations to treatment with anti-asGMj serum. This conclusion was based on the reduced viabilities of cells treated with both an eliciting agent and an activating agent prior to in vitro treatment with anti-asGM1 + C, as well as by reductions in cytolytic activity of pMφ elicited with peptone and activated by MVE-2, following anti-asGM1 treatment in vitro or administration in vivo. Conversely, the cytolytic activity of resident pMφ activated in vivo by MVE-2 or heat-killed P acnes, agents that induced relatively small increases in the percentage of asGM1φ cells, was resistant to the effects of in vivo and/or in vitro treatment with doses of anti-asGM1 serum that inhibit NK activity. These results indicate that stimulation of pMφ by eliciting or activating agents can increase the level of expression of asGM1 This increased expression of asGM1may be a useful marker for some aspects of macrophage heterogeneity, but increased expression is not necessarily directly related to expression of tumor- icidal activity. In fact, the results of this study demonstrate that anti-asGM1 serum can be used for specific depletion of NK activity in vivo in normal mice and in mice treated with at least some BRMs. However, the results also demonstrate that the use of eliciting agents, particularly thioglycollate, or eliciting agents in conjunction with activating agents can cause pMφ to become reactive with anti-asGM1 serum.
Effect of Prostaglandins on Complement Production by Tissue Macrophages
Authors: Rediske J J , Pickering R J 
Published: January 2018

Abstract
Tissue macrophages produce several proteins of the complement system. The mechanisms that regulate this process are poorly understood. The established ability of certain prostaglandins to influence macrophage secretory activity suggests that these lipid mediators may also modulate complement production (CP). Using the guinea pig peritoneal macrophages, we determined the effects of selected prostaglandins on in vitro CP and found that 1) PGE2 inhibited production of complement proteins but not lysozyme; 2) the response of elicited and resident peritoneal cells to PGE2 was identical; and 3) PGE1 PGF2 and PGI2 had no detectable effect. PGE2 may contribute to regulation of CP in vivo.
Interferon Produced Endogenously in Response to CSF-1 Augments the Functional Differentiation of Progeny Macrophages
Authors: Moore Robert N , Pitruzzello Frank J , Robinson Richard M , Rouse Barry T 
Published: January 2018

Abstract
The role of endogenously produced interferon α/β in the functional maturation of newly derived mononuclear phagocytes was investigated. Addition of highly specific anti-interferon α+ βantiserum to murine marrow cultures stimulated with colony-stimulating factor-1 (macrophage growth factor) markedly suppressed the capacity of resulting progeny mononuclear phagocytes to ingest opsonized sheep erythrocytes (EAlgG). This impairment was corrected either by direct addition of interferon α+ βat a concentration in excess of that neutralized by the antiserum or by the addition of lesser amounts of interferon (33 U/ml) following removal of the anti-interferon from the cultures. Conditioned media from control colony-stimulating factor-stimulated cultures similarly reversed the impairment of maturation resulting from 5 days of growth in the presence of anti-interferon. This enhancement of EA|gG ingestion reflected upon the interferon activity in the conditioned media and was neutralized by anti-interferon. Lastly, the endogenous interferon was found to enhance EAlgG ingestion by a majority of the mononuclear phagocyte progeny and not by a limited subpopulation.
Reactivation of Tritonated Models of Human Polymorphonuclear Leukocytes (PMNs): A Computer-Assisted Analysis
Authors: Cheung Anthony T W , Miller Michael E , Donovan Richard M , Goldstein Elliot , Kimura Gregory M 
Published: January 2018

Abstract
The orientation (chemotaxis) and locomotion (chemokinesis) of human polymorphonuclear leukocytes (PMNs) are generated by an internal movement mechanism that involves active cytoplasmic movement; they are influenced by external environmental and ionic conditions. We have studied the degree to which the orientation and movement mechanisms of PMNs are self-contained within the cell and the degree to which they are under membrane control.
PMNs were partially and selectively demembranated by treatment with the non-ionic detergent, octyl-phenoxyl-polyethoxyethanol (commercially known as Triton X-100) under controlled conditions. The tritonated PMNs (referred to in the literature as models) were non-motile and non-locomotory. Addition of ATP/Mg+ + with a trace amount of Ca+ + to the medium was followed by reactivation of the tritonated PMN models to move again as motile cells. Although these reactivated PMN models actively locomoted, they could no longer orient to chemoattractants. Thus, the reactivation process restored the physical self-contained movement parameters but could not reestablish the orientation capacity (chemotactic responsiveness) that was characteristic of live PMNs. The demembranation process apparently destroyed the chemotactic receptors and/or eradicated the coordination function of the membrane.
Videotapes of normal (control) as well as reactivated PMN movement were analyzed for movement characteristics. These characteristics were objectively analyzed with a newly designed computer-assisted micro-image-processing technique whereby the videotapes were digitized and quantified and the actual PMN movement printed out in computer-graphics and tracings (Freeman codes) for confirmation of orientation and movement arising as a result of reactivation.
Isolation of Canine Neutrophil Plasma Membranes
Authors: O'Donnell Robert T , Andersen Burton R 
Published: January 2018

Abstract
This paper describes the isolation of plasma membrane vesicles formed by nitrogen cavitation of canine neutrophils. Plasma membranes from disrupted cells were separated from other membranes and organelles by Percoll-density gradient centrifugation. Transmission electron microscopic examination of membrane preparations chromatographed on either Sephacryl S-1000 or Sepharose 4B revealed that two populations of plasma membrane vesicles were formed: large (176 ± 22nm), and small (119 ± 11 nm). Purified large vesicles were separated from Percoll and contaminating cytosol by Sephacryl S-1000 chromatography. Small vesicles were obtained free of Percoll by recavitating purified large vesicles. Problems encountered due to the presence of a soluble 5′-nucleotidase inhibitor also are discussed. Large and small membrane vesicles were separated into adherent and non-adherent populations by affinity chromatography on either concanavalin A-Sepharose or lentil lectin-Sepharose columns.
Accessory Cells Provide More Than One Signal for Lectin Mitogen-Stimulated Proliferation of Human Lymphocytes
Authors: Kern Jeffrey A , Daniele R P , Nowell P C 
Published: January 2018

Abstract
A culture system was developed in which human peripheral blood mononuclear cells (PBMC) depleted of la-expressing cells did not proliferate in response to the lectin mitogen phytohemagglutinin (PHA). These cells were able to respond to mitogen if purified autologous accessory cells were added back to the culture, thus showing an absolute requirement for la-expressing accessory cells in mitogen-driven T-cell proliferation. The identity of these accessory cells was shown to be not only monocytes but also la-expressing B cells and possibly other unidentified la-bearing cell types.
Human interleukin-1 (IL-1) in the lectin mitogen-unresponsive culture system was found unable to reconstitute normal human T-cell proliferation. This suggests that those cells with la surface antigen acting as accessory cells must deliver more than an IL-1 signal for T-cell proliferation.
The phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was tested for its ability to replace necessary la-expressing accessory cells. TPA was able to replace accessory cells in culture, thus mimicking the la-expressing accessory cells and all their delivered signals in the triggering of human lymphocytes.
Continuous Expression of I-A Antigen by Peritoneal Macrophages From Mice Resistant to Mycobacterium bovis (Strain BCG)
Authors: Johnson Sarah C , Zwilling Bruce S 
Published: January 2018

Abstract
Monoclonal antibodies were used to monitor the expression of I-A antigen on the surface of macrophages obtained from mice immunized to Mycobacterium bovis (strain BCG). Unlike the transient nature of I-A expression by macrophages from Listeria-injected mice, peritoneal macrophages from mice injected 28 days previously with 104 BCG expressed I-A continuously. The continued expression was not due to the presence of antigen or of contaminating lymphocytes. When we compared the kinetics of I-A expression from different strains of mice, the continuous expression of I-A correlated with the genetic resistance of the mice to BCG. Macrophages from mice that were resistant to BCG expressed I-A continuously, while macrophages from BCG susceptible mice expressed I-A transiently. Injection of resistant mice with Salmonella typhimurium did not result in the induction of a population of macrophages that expressed I-A continuously. This suggests that the Bcg gene may not be the same as that responsible for resistance to Salmonella (Ity) or Leishmania (Lsh).