B-1/macrophages as 'living fossils'.
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Animals↗
Biomedical subjects
R Seljelid
Publications and source records attributed to R Seljelid.
Tumour immunology: alternative perspectives.
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Adjuvants, Immunologic↗
Altered IL-1 beta and IL-2 mRNA expression in murine splenic cells after concomitant stimulation by Semliki Forest virus and lipopolysaccharide.
Co-infection with virus and bacteria happens frequently and often results in an exacerbated clinical course of the disease, possibly due to mechanisms including altered cytokine production. In the present study, the authors investigated the combined effects of avirulent Semliki Forest virus (SFV-A7) and bacterial lipopolysaccharide (LPS) on the interleukin-1 beta (IL-1 beta) and IL-2 gene expression in murine splenic cells. The authors found that 10 ng/ml of LPS in the culture medium induced expression of IL-1 beta but not IL-2, while infection with SFV-A7 did not induce either of these two cytokines. However, when SFV-A7 and LPS were applied together, a synergistic increase of both IL-1 beta and IL-2 was observed. Further experiments showed that addition of SFV-A7 3 h before LPS enhanced, whereas addition of the virus 3 h after the LPS inhibited, IL-1 beta gene expression. These results indicate that an interaction of virus and Gram-negative bacteria can result in an altered cytokine gene expression.
Animals↗
Biological effects of the immunomodulator beta 1-3D polyglucose are strongly potentiated by conjugation to biodegradable microbeads.
It is demonstrated that the biological effects of the immunomodulator beta 1-3D polyglucose, when covalently linked to polymethacrylate or biodegradable albumin microbeads, are strongly potentiated. The potentiation is recorded as an increased protection effect of the conjugates in Escherichia coli sepsis in mice, and as increased IL-1 production by murine macrophages in vitro.
Adjuvants, Immunologic↗
Characterization and cytokine-stimulating activities of acidic heteroglycans from Tremella fuciformis.
Four acidic heteroglycans, T2a-T2d, were isolated from the body of Tremella fuciformis Berk. They contained 1.9%-2.9% of acetyl groups and were composed of mannose (Man), glucuronic acid (GlcA), and small amounts of xylose (Xyl), glucose (Glc), and fucose (Fuc). According to methylation analysis they had a mannan backbone consisting of 3-linked Man, and side chains containing glucosyl, mannosyl, fucosyl, xylosyl, and glucuronic acid residues. The side chains were attached through O-2, O-4, or O-6 in about 40 percent of backbone mannosyl residues. Molecular masses of the four polysaccharides were 410, 250, 34, and 20 kDa, respectively. T2a-T2d induced human monocytes to produce interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF) in vitro. The products of Smith degradation (T2a-S) and lithium degradation (T2a-L) of T2a and the product of deacetylation (T2b-D) of T2b also induced monocytes to secret IL-1 as efficiently as the original polysaccharides, indicating that xylosyl and glucuronic acid residues as well as acetyl groups were not important to promote the cytokine-stimulating activity.
Cells, Cultured↗
Rhythms of immunity.
Rhythms of daily activity are found in all vertebrate species, some of them being diurnal (like humans, dogs, pigeons), others--nocturnal (like mice, rats and bats). Some species undergo very pronounced seasonal changes, as they hibernate in the winter or mate only at the specific seasons. The main regulator (a clock and a calendar) for daily and seasonal rhythms is the periodicity of the external light-darkness, reflected by the periodicity of melatonin secretion from the pineal gland, which is inhibited by light and induced during the darkness. In contrast to melatonin which peaks during the night both in diurnal and noctural species, the cyclicity of other hormones and several immune parameters correlates with the pattern of the animal locomotor activity-resting. The immune parameter that peaks at one time of day for a diurnal species peaks about 12 h later for a nocturnal one. Various immune parameters peak at various time points, anticipating an encounter with pathogens during the period of activity while energetically expensive resolution of the immune response during the resting. Daily and seasonal cyclicity of the immune functions are temporally integrated with other physiologic and behavioral processes and all of them are regulated and coordinated with daily and seasonal changes of an external environment by the neuroendocrine homeostatic system.
Animals↗
Characterisation of acidic heteroglycans from Tremella fuciformis Berk with cytokine stimulating activity.
Four kinds of acidic heteroglycan, T3a-T3d, were isolated from the body of the fungus Tremella fuciformis Berk. The molecular weights of T3a-T3d were 550, 420, 55, and 48 kDa, respectively. Glycosidic linkage analysis showed that they had a mannan backbone consisting of 3-linked Man p, and side chains containing glucosyl, mannosyl, fucosyl, xylosyl, and glucuronic acid residues attached through O-2, O-4, or O-6 of about half of the backbone mannosyl residues. A partial acidic hydrolysate of T3a could be divided into a low-branching region (T3a-1, 2, 3, 4) mainly branched at the 2-position of 3-linked Man p in the mannan backbone, and a high-branching region (T3a-5A) branched at the 2,4- or 2,4,6-positions of 3-linked Man p in the backbone. The low-branching region, which is predominant in the backbone, was substituted with non-reducing terminal Glc pA, Fuc p and short side chains consisting of (1-->6)-linked Glc p and (1-->2)-linked Man p linked through C-2 of the mannan backbone. The high-branching region, which is a minor component of the backbone, was linked with long side chains of (1-->6)-linked Glc p and (1-->4)-linked Glc pA in their branching points. T3a-T3d were able to induce human monocytes to produce interleukin-1, interleukin-6, and tumor necrosis factor in vitro. The different fragments of the acidic hydrolysate of T3a (T3a-1, 2, 3, 4, 5A) also induced monocytes to secret interleukin-6 with high potency, indicating that the activity may be caused by a common structure, (1-->3)-mannan in the four heteroglycans and their fragments. The change of molecular weight had no obvious influence on the activity of the heteroglycans.
Basidiomycota↗
Macrophage cytotoxicity against murine meth A sarcoma involves nitric oxide-mediated apoptosis.
We have studied the cytotoxic effect of stimulated macrophages on Meth A tumor cells in vitro. When stimulated with interferon-gamma and soluble beta-1,3-D-glucan, macrophages exerted cytotoxicity towards syngeneic Meth A tumor cells. This cytotoxicity was associated with a high level of nitric oxide production. Both cell death and nitric oxide production were significantly inhibited by the addition of aminoguanidine, a specific inhibitor of inducible nitric oxide synthase (iNOS), to the culture medium. The cytotoxic effect was accompanied by internucleosomal cleavage of DNA as shown by electrophoresis and DNA fragmentation assay.
Animals↗
European Commission COST/STD Initiative. Report of the expert panel VI. Concerted efforts in the field of mucosal immunology.
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Animals↗
Characterization and cytokine stimulating activities of heteroglycans from Tremella fuciformis.
Three heteroglycans, T1a, T1b, and T1c, have been isolated from the body of Tremella fuciformis Berk. They are composed of mannose (Man), xylose (Xyl), glucose (Glc), fucose (Fuc), and glucuronic acid (GlcA). According to methylation analysis and partial acidic hydrolysis the main chains of T1a, T1b, and T1c consisted of (1-->3)-linked Man, which was branched at the 2, 4, or 6 positions. The branching points were linked with nonreducing terminal GIcA-residues or (1-->6)-linked glucan-chains. Molecular weights of the three heteroglycans are 53,000, 18,000, and 12,000 D respectively, but they undergo self-aggregation in water. T1a-T1c induce human monocytes to produce interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF) in vitro. Acidic hydrolysate fractions of T1a (T1a-1, 2, 3, 4, 5) with molecular weight from 53,000 to 1,000 D, also induce human monocytes to produce IL-6 as efficient as T1a.
Carbohydrates↗
Nonself as a stressor--inflammation as a stress reaction.
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Inflammation↗
Interferon-gamma inhibits endocytosis of soluble animated beta-1,3-D-glucan and neutral red in mouse peritoneal macrophages.
We previously demonstrated that soluble animated beta-1,3-D-glucan (AG) is internalized after binding to a specific beta-glucan receptor on macrophages. Internalization, but not binding, of AG is reduced when the macrophages are treated with IFN-gamma. Because our data indicated that AG is taken up by macrophages through beta-glucan receptor-mediated endocytosis, we wanted to characterize further the inhibitory effect of IFN-gamma on endocytosis. We compared the internalization of AG and neutral red (NR). NR is internalized by macrophages through fluid-phase endocytosis. AG and NR showed a similar influx/efflux pattern. The initial rate of accumulation was much larger for AG than for NR, however, probably because of the involvement of the beta-glucan receptor in the uptake of AG. Internalized AG was associated with membranes of the endocytic vesicles and formed characteristic rings on confocal laser scanning microscopy (CLSM) images. Both the influx and efflux of AG and NR was inhibited by treatment of macrophages with IFN-gamma. Phorbol myristate acetate (PMA) added to the cell cultures increased the accumulation of AG and NR and reversed the inhibitory effect of IFN-gamma. The effect of PMA was dependent on functionally intact microfilaments and microtubules. CLSM showed that the accumulated AG was localized mostly in small vesicles (size < 2 microns) in IFN-gamma-treated cells, in large and small vesicles in untreated cells, and mostly in large vesicles (size > 2 microns) in PMA-treated cells. In conclusion, IFN-gamma inhibits both the beta-glucan receptor-mediated endocytosis of AG and the fluid-phase endocytosis of NR, probably by inhibiting the formation of large vesicles.
Amination↗
A peptide derived from the amino terminus of endothelial-monocyte-activating polypeptide II modulates mononuclear and polymorphonuclear leukocyte functions, defines an apparently novel cellular interaction site, and induces an acute inflammatory response.
Endothelial-monocyte-activating polypeptide II (EMAP II) is a novel mediator isolated from conditioned medium of methylcholanthrene A-induced tumor cells which modulates properties of endothelial cells, mononuclear phagocytes (MPs), and polymorphonuclear leukocytes (PMNs) in vitro and induces an acute inflammatory response in vivo. A synthetic peptide comprising 15 residues from the N-terminal region (residues 6-20) was shown to induce directional migration of MPs and PMNs, with half-maximal effect at approximately 200-250 pM, whereas a peptide from the C terminus of EMAP II, as well as other irrelevant peptides, were without effect. Modulation of cellular phenotype by EMAP II-derived peptide was suggested by peptide-induced elevation of cytosolic free calcium concentration in fura-2-loaded MPs and PMNs and by stimulation of peroxidase release in PMNs. Consistent with these in vitro data, EMAP II-derived N-terminal peptide-albumin conjugates injected into the mouse footpad elicited inflammatory cell tissue infiltration, whereas albumin alone or EMAP II-derived C-terminal peptide conjugated to albumin incited little response. Binding of 125I-labeled EMAP II-derived peptide (residues 12-20) to MPs was saturable (Kd approximately 200 pM) and was blocked in a dose-dependent manner by the addition of intact EMAP II and unlabeled EMAP II-derived peptides (residues 6-20 and 12-20), whereas interleukin 1, tumor necrosis factor, formyl-methionyl-leucinyl-phenylalanine, or irrelevant peptides were without effect. Cross-linking of 125I-EMAP II-derived peptide (residues 12-20) by disuccinimidyl suberate to human MPs demonstrated a band, approximately 73 kDa, on reduced sodium dodecyl sulfate-polyacrylamide gel electrophoresis. 125I-EMAP II-derived peptide also demonstrated specific binding to human PMNs and murine RAW cells. These data indicate that the N-terminal region of EMAP II defines a biologically active locus of the molecule which interacts with target cells via a potentially novel cellular receptor.
Amino Acid Sequence↗
A novel immunomodulator soluble aminated beta-1,3-D-glucan: binding characteristics to mouse peritoneal macrophages.
We have previously reported that soluble aminated beta-1,3-D-glucan (AG), a potent immunomodulator, specifically inhibited binding and internalization of AG-coated microbeads (GDM) in mouse peritoneal macrophages. The present study was undertaken to determine parameters of AG binding to macrophages. For this purpose, AG was conjugated with tyraminyl cellobiose (TC), which can be radioiodinated. With this method the immunomodulator was labelled with a very high specific radioactivity, allowing sensitive measurements of binding. Maximal binding capacity was 0.33 micrograms [125I]TC-AG/10(6) cells. Binding was inhibited by TC-AG and AG, but not by mannose and mannan, showing that the receptor different from the mannose receptor was involved. Binding was reversible, with an initial association rate of 120 cpm/min, and a much faster initial dissociation rate of 680 cpm/min. Bound [125I]TC-AG was internalized. These findings suggest that both AG and GDM are bound and internalized via the same beta-glucan receptor in mouse peritoneal macrophages.
Adjuvants, Immunologic↗
Aminated beta-1,3-D-polyglucose activates salmon pronephros macrophages in vitro.
Salmon pronephros macrophages were stimulated in vitro using a novel immunomodulator, aminated beta-1,3-D-polyglucose. Activation of these cells was judged by the measurement of superoxide anion formation, pinocytotic activity, acid phosphatase activity and morphological criteria. Stimulated macrophages showed increased superoxide anion formation compared with unstimulated control cells as measured by reduction of Nitroblue tetrazoleum, and an increased level of acid phosphatase activity. Furthermore, stimulated macrophages showed increased pinocytotic activity and a significant increase in cell diameter and spreading.
Acid Phosphatase↗
IFN-gamma inhibits internalization of soluble aminated beta-1,3-D-glucan by macrophages and thereby down-regulates the glucan induced release of TNF-alpha and IL-1 beta.
We have previously shown that soluble animated beta-1,3-D-glucan (AG) and glucan-derivatized microbeads (GDM) bind to the specific beta-glucan receptor on mouse peritoneal macrophages. Phagocytosis of GDM by macrophages is mediated through the beta-glucan receptor. IFN-gamma which increases macrophage phagocytic capacity, also increased the phagocytosis of GDM. In the present study we show that IFN-gamma inhibits internalization of AG in macrophages in a dose- and time-dependent manner. The inhibitory effect of IFN-gamma was neutralized by treatment of the macrophages with cycloheximide. These results were confirmed by confocal laser scanning microscopy which showed that IFN-gamma treated cells incorporated less fluorescein-labelled AG than did untreated cells. IFN-gamma did not change the macrophage-binding capacity for AG showing that the inhibitory effect of IFN-gamma is not caused by decreased number of beta-glucan receptors on the cells. The stimulatory effect of AG on IL-1 beta and TNF-alpha release from macrophages was reduced by pretreatment of the cells with IFN-gamma. We conclude that the uptake of AG and GDM in macrophages, both mediated through the beta-glucan receptor, are differently regulated by IFN-gamma. The reduced internalization of AG after IFN-gamma treatment of macrophages, is probably responsible for the down-regulation of IL-1 and TNF-alpha secretion.
Animals↗
The biology of macrophages: II. Inflammation and tumors.
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Animals↗
Cytokines and PGE2 modulate the phagocytic function of the beta-glucan receptor in macrophages.
Under serum-free conditions the beta-glucan receptor of mouse macrophages mediates phagocytosis of beta-1,3-D-glucan-coated microbeads (diameter 2 microns). IFN-gamma increases the phagocytic function of the beta-glucan receptor in a dose-dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN-gamma to the cells. The effect disappears within 24 h. The effect of IFN-gamma may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis. IL-1 also increases the phagocytic function of the beta-glucan receptor giving a dose-dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL-1 to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the beta-glucan receptor, but TNF together with IL-1 prolongs the effect of IL-1. PGE2 reduces the phagocytic function of the beta-glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time-course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells.
Animals↗