bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Macrophage Content of Tumors Is Unrelated to Levels of NK Cell-Mediated Resistance
Authors: Polentarutti Nadia , Acero Raffaella , Bottazzi Barbara , Taraboletti Giulia , Mantovani Alberto 
Published: January 2018

Abstract
Three malignant tumors (3LL carcinoma, mFS6 sarcoma, and B16 F1 melanoma) were transplanted in mice with congenital (beige) or acquired (antiasialo GM1-treated) defects of natural killer cell (NK) activity. The macrophage content of the neoplastic tissues was not influenced by host NK activity levels. These data suggest that NK cell-mediated resistance does not play an appreciable role in the regulation of the levels of tumor-associated macrophages in established malignancy.
Release of Interleukin-1 (IL-1) and IL-1-Like Factors From Rabbit Macrophages With Silica
Authors: Kampschmidt Ralph F , Worthington Martin L , Mesecher Maria I 
Published: January 2018

Abstract
Oil-elicited rabbit macrophages stimulated by endotoxin were found to release increased amounts of interleukin 1 (IL-1) when incubated with silica. The assays used to determine the amount of IL-1 released were uptake of thymidine by mouse thymocytes, fever in rabbits, and neutrophilia in rats. All three assays showed that endotoxin-stimulated macrophages released five to 10 times more IL-1 when incubated with silica. Most of the IL-1 had a molecular weight (MW) of about 14,000 with a smaller amount at a MW of approximately 35,000. All of the neutrophilia-producing activity had an isoelectric point (pl) near 7. Thymocyte proliferation was promoted about equally by activities near pH 5 and 7. Fever was found not only at these two isoelectric points but also at a pl above 8 which had neither of the other two activities.
Rapid Killing of Actinomycin D-Treated Tumor Cells by Mononuclear Phagocytes: Characterization of Effector Cells in Mice
Authors: Colotta Francesco , Polentarutti Nadia , Bersani Laura , Poll Guido , Mantovani Alberto 
Published: January 2018

Abstract
Pretreatment with Actinomycin D (Act D, 1 μg/ml for 3 hr) rendered WEHI 164 tumor cells susceptible to killing by mouse resident or peptone-induced peritoneal exudate cells (PEC) in a 6-hr 51Cr release assay. Cytotoxicity was attributed to cells of the monocyte macrophage lineage on the basis of tissue distribution, separation by adherence on plastic and carbonyl iron, membrane antigens, and expression in mice with defective T cell- or NK cell-mediated immunity. Macrophages from four strains of mice (C3H/HeJ, A/J, P/J, C57BI/10 ScCR) previously shown to have defective “classical” nonspecific tumoricidal activity were examined for killing of Act-D-treated WEHI 164 cells. C3H/HeJ peritoneal macrophages had little or no DDCC, whereas cells from A/J, P/J, and C57BI/10 ScCR mice had normal levels of this reactivity. Tumor cells exposed to ActD were heterogenous in their susceptibility to killing by PEC, with five lines showing significant, though variable, lysis, whereas 12 tumor lines, normal fibroblasts, and lymphoblasts were not appreciably killed under the same conditions. Macrophage-mediated DDCC was also detectable in a colony assay. DDCC could explain how macrophages contribute to the antitumor activity of selected chemotherapeutic agents in murine tumor models.
A Monoclonal Antibody Against Migration Inhibitory Factor (MIF) Obtained by Immunization With MIF From the Human Lymphoblast Cell Line Mo
Authors: Kawaguchi Tsutomu , Mednis Alma , Golde David W , David John R , Remold Heinz R 
Published: January 2018

Abstract
A monoclonal antibody-secreting hybrid cell line, E7, was constructed from myeloma cells and spleen cells from BALB/c mice immunized with partially purified human MIF from culture fluid of the human T-lymphoblast cell line Mo. The hybrid cell line E7 was selected by screening hybridoma cultures for their capacity to adsorb added MIF activity when assayed together with rabbit antimouse IgG-coupled to protein A-Sepharose. The monoclonal antibody produced by the cloned hybridoma E7 also directly neutralized MIF activity from Mo cells and two species of MIF from the culture fluid of human peripheral blood lymphocytes, but did not neutralize IFN-gamma from Mo cells and from human peripheral blood lymphocytes. This antibody reacted also with a component in phytohemagglutinin preparations with an apparent molecular weight of 60,000; however, it did not react with the active tetramer of phytohemagglutinin.
Comparison of Cell-Mediated and Humoral Immunity in the Dog Lung After Localized Lung Immunization
Authors: Galvin Jennifer B , Bice David E , Muggenburg Bruce A 
Published: January 2018

Abstract
This study evaluated cell-mediated immunity (CMI) and antibody production serially in control and immunized lung lobes of beagle dogs. A fiberoptic bronchoscope was used to immunize selected airways in the left cardiac lung lobe with 1010 sheep red blood cells (SRBC); the right cardiac lobe received saline as control. The immune responses produced by this localized lung immunization were evaluated in cells and fluids obtained from blood and serial bronchial washings of the immunized and control lung lobes from 5 to 21 days after immunization. The antigen-specific production of procoagulant activity (LPCA) and inhibition of migration of alveolar macrophages by SRBC antigen were used to measure CMI in lavage cells from immunized and control lung lobes. The level of specific IgM and IgG antibody in lavage fluid from the control and immunized lung lobes was evaluated with the enzyme-linked immunosorbent assay (ELISA). The results of this study showed a significantly greater percentage of neutrophils and lymphocytes in the lavage fluid from the immunized lung lobes than from the control lung lobes. The increased number of lymphocytes in the immunized lung lobes showed a positive correlation with increased antibody concentrations. In contrast to the antibody response, CMI as measured by LPCA and MIF assays was positive, with nearly equal responses in control and immunized lung lobes. Even though there were only a few lymphocytes in the control lung lobes, there were apparently enough specific immune lymphocytes present that produced mediators after antigen stimulation to result in positive CMI responses.
The In Vitro Mitogenic Response to Intact Bacteria by Murine B Cells Does Not Predict In Vivo Susceptibility to Salmonella typhimurium
Authors: Elkins Karen , Metcalf Eleanor S 
Published: January 2018

Abstract
We are interested in developing in vitro culture systems that will permit immune responses to intact Salmonella typhimurium, since these systems would have certain advantages over in vivo infection models for the characterization of the host's responding cell types. In this report, the in vitro proliferative response of nonimmune murine spleen cells to four different killed preparations of S. typhimurium, strain TML (TML), are examined. These studies show that UV-killed TML, heat-killed TML, glutaraldehyde-killed TML, and acetone-killed and dried TML, all elicit a nonspecific mitogenic spleen cell response in vitro, as does a live, avirulent, temperature-sensitive mutant of TML, TS27. This response reaches a maximum on day 2 after initiation of culture, which is similar to the time course of a conventional lipopolysaccharide (LPS) response. Unlike the LPS response, little 3H-thymidine incorporation is observed in low-density cultures (2 × 105 cells/well), which suggests a critical role for accessory cells. The responding cell types include, but are not necessarily limited to, the B-cell population. The response cannot be readily inhibited by polymyxin B, which binds specifically to the lipid A portion of LPS. Thus, the bacterial components required for mitogenicity are not yet definitively identified. A survey of the mitogenic responses of lymphocytes from various inbred mouse strains, including the C3H/HeJ LPS hyporesponsive strain, indicates that all B cells tested are capable of proliferating vigorously in response to intact TML, regardless of the in vivo susceptibility to virulent infection. These results also emphasize the importance of assessing the nonspecific components of the immune response when studying the specific immune response to intact S. typhimurium.
The Relationship Between Intracellular Cyclic AMP Concentrations and the In Vitro Growth of Macrophages
Authors: Inouye L K , Wharton Walker 
Published: January 2018

Abstract
The addition of cholera toxin, prostaglandins, or one of a series of xanthine phosphodiesterase inhibitors to bone marrow-derived macrophages maintained in liquid culture caused a dose-dependent decrease in colony formation measured 7–10 days following seeding. The growth inhibitory effects of xanthines were in the same order of potency (caffeine &lt; theophylline &lt; isobutylmethylxanthine) as their reported ability to inhibit cyclic AMP phosphodiesterase. The relationship between the magnitude of the increases in intracellular concentrations of cyclic AMP observed following the addition of the drugs and the degree of growth inhibition was complex. Combinations of cholera toxin and phosphodiesterase inhibitors caused synergistic elevations in cyclic AMP levels after a lag of approximately 3 days. However, the growth rate was decreased immediately following the addition of the combination of drugs, and thus seemed to be independent of the nucleotide levels. A cyclic AMP-resistant variant of a cloned nontransformed macrophage cell line was found to be also resistant to the growth inhibitory actions of both cholera toxin and prostaglandins. However, resistance to the inhibitory effects of cyclic AMP did not render the cells resistant to a xanthine-induced growth inhibition.
Heterogeneity in Chronic Granulomatous Disease Detected With an Improved Nitroblue Tetrazolium Slide Test
Authors: Meerhof Louis J , Roos Dirk 
Published: January 2018

Abstract
The microscopic nitroblue tetrazolium (NBT) slide test, used to score the ability of individual phagocytic leukocytes to produce superoxide, was improved according to the following procedure. Purified granulocyte suspensions are incubated with NBT and fixed in suspension, thereafter centrifuged on microscope slides and stained with nuclear fast red. This method precludes stimulation and selection of cells by adherence and washing. The number of formazan grains per cell can be judged in a semiquantitative way. In parallel incubations, the cells are stained with May-Grünwald/Giemsa, allowing identification of formazan-positive and -negative cells. The test discriminates well between cells from normal individuals, cells from patients with chronic granulomatous disease (CGD), and cells from heterozygotes for the X-linked form of CGD. Several patients and heterozygotes with an autosomal or variant form of CGD were detected with decreased NBT-reducing activity in their neutrophils and/or eosinophils. The relation between NBT-reductase activity of the phagocytes and the clinical situation is discussed.
Therapeutic effect of Lipoxin A4 in malaria-induced acute lung injury
Authors: Pádua Tatiana A , Torres Natalia D , Candéa André L P , Costa Maria Fernanda Souza , Silva Johnatas D , Silva-Filho João Luiz , Costa Fabio T M , Rocco Patricia R M , Souza Mariana C , Henriques Maria G 
Published: January 2018

Abstract
Acute lung injury (ALI) models are characterized by neutrophil accumulation, tissue damage, alteration of the alveolar capillary membrane, and physiological dysfunction. Lipoxin A4 (LXA4) is an anti-inflammatory eicosanoid that was demonstrated to attenuate lipopolysaccharide-induced ALI. Experimental models of severe malaria can be associated with lung injury. However, to date, a putative effect of LXA4 on malaria (M)-induced ALI has not been addressed. In this study, we evaluated whether LXA4 exerts an effect on M-ALI. Male C57BL/6 mice were randomly assigned to the following five groups: noninfected; saline-treated Plasmodium berghei-infected; LXA4-pretreated P. berghei-infected (LXA4 administered 1 h before infection and daily, from days 0 to 5 postinfection), LXA4- and LXA4 receptor antagonist BOC-2-pretreated P. berghei-infected; and LXA4-posttreated P. berghei-infected (LXA4 administered from days 3 to 5 postinfection). By day 6, pretreatment or posttreatment with LXA4 ameliorate lung mechanic dysfunction reduced alveolar collapse, thickening and interstitial edema; impaired neutrophil accumulation in the pulmonary tissue and blood; and reduced the systemic production of CXCL1. Additionally, in vitro treatment with LXA4 prevented neutrophils from migrating toward plasma collected from P. berghei-infected mice. LXA4 also impaired neutrophil cytoskeleton remodeling by inhibiting F-actin polarization. Ex vivo analysis showed that neutrophils from pretreated and posttreated mice were unable to migrate. In conclusion, we demonstrated that LXA4 exerted therapeutic effects in malaria-induced ALI by inhibiting lung dysfunction, tissue injury, and neutrophil accumulation in lung as well as in peripheral blood. Furthermore, LXA4 impaired the migratory ability of P. berghei-infected mice neutrophils.
Effect of Human Recombinant Tumor Necrosis Factor on the Growth of Different Human and Mouse Long-Term Hematopoietic Cell Lines
Authors: Hahn Cathy J , Ovak Geraldine M , Donovan Renea M , Pauly John L 
Published: January 2018

Abstract
Previous studies have demonstrated that one of the most salient features of tumor necrosis factor (TNF) is its ability to induce tumor necrosis in vivo, and the specificity of its cytotoxic/cytostatic activity for tumor cells has been demonstrated in in vitro studies in which this lymphokine has been shown to kill cultured cells of malignant lines and to have no effect on cells of normal diploid lines. Studies described herein defined the effect of highly purified human recombinant TNF on cells of 34 different human and murine hematopoietic cell lines, particularly human leukemic T and B cells of long-term lymphoblastoid cultures. Results of these studies demonstrated that TNF at concentrations of 3,600 U/ml had no significant effect on the growth of these cells as defined by cytotoxicity, measured with the use of the trypan blue dye-exclusion assay and as defined by cytostasis, assayed by the enumeration of cells and the uptake of [3H]-thymidine and -uridine. In contrast, positive control cultures of TNF-sensitive cells from a murine tumor (L-M/clone L-929, connective tissue) displayed at 50% (LD50) reduction in growth by TNF at ~ 5 U/ml. Likewise, human tumors (MCF-7, breast, and HT-29, colon) were also highly sensitive (LD50 &lt; 100 U/ml). These studies demonstrate that T and B cells of lymphoblastoid lines as well as cells of other hematopoietic lines display little or no sensitivity to TNF.
Ganglioside Identification on Human Monocyte Membrane With Clostridium perfringens Delta-Toxin
Authors: Cavaillon J M , Jolivet-Reynaud C , Fitting C , David B , Alouf J E 
Published: January 2018

Abstract
Clostridium perfringens delta-toxin was first described as a hemolysin with a restricted lytic spectrum. A selective cytotoxicity of the delta-toxin was then found on rabbit leukocytes: peritoneal and alveolar macrophages were uniformly killed, whereas thymocytes were essentially resistant. The toxin was shown to be specific for GM2 ganglioside or a GM2-like structure. In the present study we report the interaction of delta-toxin with human monocytes. A specific, saturable, and irreversible binding of 125I-delta-toxin was demonstrated. Binding was inhibited by preincubation of the radiolabeled toxin with GM2 and with high amount of GM1 ganglioside. As judged by dye exclusion, no cytotoxicity was observed on freshly isolated monocytes, but when added at the beginning of a culture of human adherent cells, the cytotoxic effect was detected after 48 hours of culture. Taken together, these data indicate the presence of monosialoganglioside(s) at the surface of human monocytes, and suggest a possible reorganisation of such structure into the cell membrane when monocytes mature in vitro toward macrophage-like cells.
Gender-Related Variations and Interaction of Human Neutrophil Cyclooxygenase and Oxidative Burst Metabolites
Authors: Mallery Susan R , Zeligs Barbara J , Ramwell Peter W , Bellanti Joseph A 
Published: January 2018

Abstract
Gender-related variations in human neutrophil membrane bound oxidative metabolism were evaluated employing the calcium ionophore A23187. These included the measurement of cyclooxygenase metabolites of arachidonate by specific RIA determination of thromboxane B2 (TxB2), prostaglandin E2 (PGE2), and 6-Keto PGF1 (6KPGF) as well as the initiation of the oxidative burst by the quantitative evaluation of superoxide (O2−) reduction of nitroblue tetrazolium (NBT). Neutrophils from women generated 30% less TxB2 and PGE2 than those obtained from men. In contrast, the neutrophils from women demonstrated relatively higher O2− production with a cyclic pattern of both TxB2 and O2− which correlated with their menstrual cycle. The elevated O2− generation appeared to inversely correlate with TxB2 production. Further, introduction of an intracellular oxygen centered radical (OCR) scavenger, sodium benzoate, for the hydroxyl (OH) radical was observed to affect cyclooxygenase metabolism in a dose-response manner. At higher concentrations of sodium benzoate, i.e., 10-2M, TxB2 production was inhibited; in contrast, 10-3M sodium benzoate enhanced neutrophil TxB2 generation which was particularly marked during times of increased oxidative burst activity, i.e. O2− production. We conclude that the decreased production of cyclooxygenase metabolites observed in neutrophils from women in part derive from an increased oxidative burst activity. This suggests that a regulatory mechanism may exist between the neutrophil membrane bound oxidative system(s) involving oxygen centered radicals generated during both the oxidative burst and prostaglandin cyclic endoperoxide reduction. Further, these gender-related differences may be partially attributable to variations in circulating endogenous sex steroids.
Monocyte-Derived Growth Factors for Human Tumor Clonogenic Cells
Authors: Hamburger Anne W , White Christine P , Lurie Karin , Kaplan Richard 
Published: January 2018

Abstract
Human peripheral blood monocytes secrete a soluble factor that enhances the ability of human epithelial tumor cell lines to clone in soft agar. Monocytes increased colony growth in a concentration-dependent manner, although inhibition of cell growth was observed in the presence of high concentrations of monocytes. Addition of indomethacin to monocytes did not abrogate this inhibition. Exposure of monocytes to endotoxin increased their ability to secrete stimulatory factors. Nonadherent lymphocytes were unable to support colony growth. Conditioned media from unstimulated monocytes also increased colony growth. Growth-promoting activity was detected in the media within the first 24 hr of culture, reaching a peak at 72 hr. Activity was not observed in monocyte lysates. Monocytes released this activity when cultured in the presence of both serum-free and serum-containing media. The activity was nondialyzable, relatively heat stable, and failed to adhere to CM-Sephadex. The demonstration of a monocyte-derived factor that enhances growth of epithelial tumor colonies supports findings indicating that inflammatory products may enhance tumor cell growth in vitro.
Tumor Growth Stimulatory Macrophages Induced by a Subclinical Bacterial Infection In Vivo
Authors: De Groot Jan W , Compier-Spies Philome I , Wilbrink Bert , Dullens Hub F J , De Weger Roel A , Rademakers Louk H P M 
Published: January 2018

Abstract
Nonelicited peritoneal macrophages obtained from normal mice from our animal house unexpectedly expressed a strong tumor growth stimulatory effect in vitro. Macrophages expressing this stimulatory effect had an aberrant morphology compared to the morphology of normal macrophages as observed by electron microscopy.
The results of immunization of these affected mice with tumour cells led to the usual lymphocyte sensitization. No external symptoms were observed, and the mice looked healthy.
Treatment of the affected macrophage donors with antibiotics resulted in the abolishment of the tumor growth stimulatory effect by the macrophages. Thus, this tumor cell growth stimulation by marcrophages was probably due to a subclinical infection of the mice.
Biochemical Events Associated With the Stimulation of Rabbit Neutrophils by Platelet-Activating Factor
Authors: Naccache Paul H , Molski Marshall M , Volpi Mario , Shefcyk Jean , Molski Thaddeus F P , Loew Leslie , Becker Elmer L , Sha'afi Ramadan I 
Published: January 2018

Abstract
The functional and biochemical responses evoked by the addition of platelet-activating factor (PAF) to a suspension of rabbit neutrophils have been characterized in an effort to define the mode of action of this lipid mediator. PAF was found to elicit a secretory response and to stimulate a rapid breakdown of the polyphosphoinositides, an increase in the cytoplasmic level of free calcium (as monitored by quin2), a decrease in the fluorescence of cell-associated chlortetracycline, an enhanced activity of the sodium/hydrogen antiport, a transient depolarization, and an increase in the level of cytoskeletal actin. The quin2 response to PAF was found to be detectable at concentrations as low as 0.01 nM, to be very dependent on the presence of extracellular calcium, and to be sensitive to inhibition by phorbol esters. On the other hand, the increase in free calcium induced by PAF in the presence of extracellular calcium was essentially unaffected by pertussis toxin. PAF-induced neutrophil degranulation was similarly extracellular calcium dependent and phorbol ester sensitive. The secretory activity of PAF was evident only at concentrations in excess of 1 nM. All of the other effects of PAF were found to be independent of the presence of external calcium and to be demonstrable only at concentrations larger than 1 nM. In addition, all neutrophil responses to PAF (with the above noted exception of quin2) were potently inhibited by pertussis toxin. These results are interpreted in terms of the possible existence of two functionally distinct populations of receptors. The occupation of one set (of apparent high affinity) induces an increase in permeability to calcium in a phorbol-ester-, but not pertussis-toxin-, sensitive manner. The activation of the other set of receptors at higher concentrations of PAF stimulates the polyphosphoinositide-specific phospholipase C and induces the attendant biochemical responses. These latter responses appear to be mediated by a guanine-nucleotide-binding regulatory protein.
Effects of Diethylstilbestrol on Propionibacterium acnes Immunomodulation: Inhibition of Macrophage Activation and Antitumor Activity
Authors: Ackermann Michael F , Mark Raymond , Chakraborty Prasanta R , Morahan Page S 
Published: January 2018

Abstract
Exposure of mice to diethylstilbestrol (DES) inhibited Propionibacterium acnes-induced antitumor activity in vivo against the B16F10 subcutaneous tumor. The inhibitory effect was associated with inhibition by DES of the characteristic P. acnes induced splenomegaly and changes in splenic and peritoneal macrophages (Mφ) cell populations. The characteristic P. acnes induced reductions in Mφ alkaline phosphodiesterase I (APD) ectoenzyme activity and in total RNA synthesis, proposed biochemical markers of tumoricidal Mφ, were partially or completely reversed in DES-treated mice. As predicted from these in vivo and in vitro results, DES treatment significantly decreased P. acnes activation of Mφ antitumor activity in vitro against B16F10 melanoma and Lewis lung carcinoma cells. These data suggest a macrophage activation defect may be involved in the reduced resistance that DES-treated animals exhibit to a variety of neoplastic and microbial challenges.