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Focussing on V 4 with its motif of the “darkest valley” (NIB) the dynamics, theological coherence and background motives of Psalm 23 are laid out. Comparison with the newly edited Ancient Near Eastern prayer Sb19319 from second millennium b.c.e. Susa brings several parallel elements to light. Some theses on Old Testament concepts of death conclude the article.

Im Maximilianmuseum in Augsburg findet im ‚Maximiliansjahr‘ 2019 die Ausstellung „Maximilian I. (1459-1519). Kaiser. Ritter. Bürger zu Augsburg“ statt. Die Ausstellung beherbergt außer hochwertigen Leihgaben auch ein besonderes Highlight: In einer virtuellen Umgebung werden längst abgerissene Stadttore computergestützt nachmodelliert und für die Besucher wieder zugänglich, obwohl die Originale schon lange nicht mehr Teil des Stadtbildes sind. Eines davon war einst eine berühmte Touristenattraktion: Augsburgs ‚Alter Einlass‘, das Nachttor, erbaut 1514 angeblich für Kaiser Maximilian I. Abgerissen wurden die letzten Überreste der großflächigen Anlage 1867. Besonders die komplexen Mechaniken im Inneren des Durchgangs waren weithin berühmt und können nun durch penible wissenschaftliche Recherche und Virtual-Reality-Brillen wieder erfahrbar gemacht werden. Augsburg‘s Maximilianmuseum, which is not only the city’s art-historical museum but also includes the history of the town, will be home to an exhibition themed around Emperor Maximilian Ist in the third quarter of 2019. Within the exhibition there is one very special highlight to be found: Embedded in a virtual-reality-environment, two of the city’s historical gates are getting a computer-based re-modeling and will be opened for visitors, even though the original buildings were torn down many years ago. The larger of those gates, the ‚Alter Einlass‘ of Augsburg, an entrance to the city erected in 1514, was initially built for Emperor Maximilian Ist. The last remains of this complex building were torn down in 1867. Once famous for its hidden mechanics, the famous portal can now be experienced once again through virtual-reality-glasses., MEMO Medieval and Early Modern Material Culture Online; Volume 2019 (4); Seitenzahl: x; ISSN: 2523-2932

Die vorliegende Ausgabe nimmt den 500. Todestag Kaiser Maximilians I. zum Anlass, das Thema „Gedächtnis und Gedenken“ aufzugreifen. In ihr versammeln sich Forschungsbeiträge aus den Bereichen Kunstgeschichte, Bauforschung, Museumswissenschaften, Archäologie und Geschichtswissenschaft, die sich mit der Funktion von Objekten als Medien der Erinnerung in historischen Kontexten auseinandersetzen. Mit Beiträgen von Heidrun Lange-Krach, Christoph Emmendörffer, Christoph Hauptmann, Ilja Sallacz, Chassica Kirchhoff, Nina Stainer, Jochen Vennebusch, Claudia Theune und Iris Winkelbauer. Elisabeth Gruber, Gabriele Schichta: Editorial; Jochen Hermann Vennebusch: „Du, geliebter Leser, erbarme dich zugleich unser“ – Der „Hillinus-Codex“ (Cod. 12) als mehrschichtiges Erinnerungsobjekt; Chassica Kirchhoff: Memories in Steel and Paper: A Spectacular Armor and its Representation In Early Modern Augsburg; Heidrun Lange-Krach, Christoph Emmendörffer, Christoph Hauptmann, Ilja Sallacz: Ein neuer Weg zur Stadtgeschichte – Virtual Reality im Maximilianmuseum; Claudia Theune, Iris Winkelbauer: Erinnerung an Maximilian I. auf Schloss Hanfelden in der Steiermark; Nina Stainer: Der Weg der Zeichnung. Die Handzeichnung als Medium der Kommunikation, Erinnerung und Selbstzeugnis des Bildhauers im 17. Jahrhundert, MEMO Medieval and Early Modern Material Culture Online; Volume 2019 (4); Seitenzahl: x; ISSN: 2523-2932

Summary Dendritic cells (DC) modulate immune responses depending on the nature of the antigens. Receptors capable of discriminating these antigens on the basis of the pathogen-associated molecular patterns (PAMP) belong to the Toll-like receptor (TLR) family. The macrophage-activating lipopeptide 2 kDa (MALP-2), a synthetic lipopeptide derived from Mycoplasma fermentans , signals through TLR-2 and TLR-6. The aim of this study was to examine whether MALP-2 can modulate the functional properties of human monocyte-derived DC. The effects of this treatment were compared to those of the TLR-4 agonist lipopolysaccharide (LPS). To ensure clinical applicability, DC were generated under serum-free conditions. MALP-2 and LPS stimulation induced the expression of CD83 and increased the expressions of CD80, CD86, HLA-ABC and CD40. Furthermore, both substances decreased the endocytotic capacity of DC and induced the release of bioactive TNF-α and IL-10, whereas LPS additionally increased IL-12 release. Pretreatment with both substances boosted the allostimulatory capacity of DC. In a coculture with autologous lymphocytes, either MALP-2 or LPS pretreated DC induced a marked proliferation of lymphocytes, but only DC prestimulated with MALP-2 activated lymphocytes to produce the cytokines IL-4, IL-5 and IFN-γ. No polarisation of lymphocytes into T-helper (Th)1 or Th2 was detected. These data indicate that MALP-2 is a potential candidate to modulate DC for clinical applications.

Pulmonary infections are important causes of morbidity and mortality in immunosuppressed patients after transplantation. After experimental irradiation and syngeneic bone marrow transplantation in mice, macrophages show reduced repopulation in the lung compared with that in other tissues. Macrophages are major microbicidal immune effector cells in host pulmonary defense. Therefore, we examined the role of locally applied cytokines for macrophage repopulation in the lung. An accelerated repopulation of macrophages in the lung was observed after intranasal application of macrophage-colony stimulating factor (M-CSF), but this effect was not enhanced by a combination of M-CSF with interleukin (IL)-3. Local proliferation contributed to this effect. Macrophages in the lung tissue of M-CSF-treated mice displayed greater secretion of IL-6, whereas M-CSF treatment did not enhance the gene expression of other macrophage-specific chemokines. The role of M-CSF treatment was determined in pulmonary murine cytomegalovirus infection using an irradiation/reconstitution model. The M-CSF treatment had no effect on virus load in the lung tissue. However, phosphate-buffered saline-treated mice seemed to develop stronger inflammation after viral infection than M-CSF-treated mice. We conclude that local M-CSF treatment modulates cellular inflammation in the lung during immunosuppression.

In this study, transgenic CD2F1 mouse lines (C-1.1-C-1.11) bearing a transgene encoding the murine growth factor M-CSF under the control of the liver specific alpha-1-antitrypsin gene promoter were generated. Transgenic C-1.4 mice showed elevated expression of transgene-encoded M-CSF in the liver and displayed a 2-3-fold increase of M-CSF plasma levels and of macrophage numbers in the liver as compared with non-transgenic littermates. M-CSF transgenic mice showed increased resistance against sublethal i.v. infections with Listeria monocytogenes as compared with infected non-transgenic mice. To investigate the influence of M-CSF in murine systemic lupus erythematosus (SLE), the M-CSF transgenic mouse line C-1.4 was bred into the genetic background of SLE-prone MRL+/+ mice. The resulting C-1.4/MRL transgenic mice bearing increased endogenous M-CSF levels showed consistently lower levels of anti-ss-DNA autoantibodies as compared with non-transgenic MRL+/+ mice. The life span of the C- 1.4/MRL transgenic mice and the severity of the disease in these mice remained unchanged as compared with their non-transgenic littermates. It is concluded that in addition to M-CSF further factors must be involved in the acceleration of the autoimmune disease in SLE prone MRL/lpr mice.

Herein, we report a technically simple method for isolation and culture of human follicular melanocytes based on explant cultures of epilated hair follicles. This technique does not require any surgical intervention and allows the isolation and cultivation of follicular melanocytes from a comparatively small amount of raw material. Generally, 30-60 human anagen hair follicles have been plucked from the scalp of healthy donors and cultivated under low oxygen pressure (5%). After a short period of time cells of various types were growing out from the outer root sheath (ORS) of the hair follicles. Under the selected culture conditions, most of the cells other than melanocytes have been eliminated and a nearly 100% pure population of melanocytes has been achieved, as confirmed by immunohistochemical analyses for melanocyte-specific markers, for example, Tyrosinase-1, S-100 and premelanosomal antigens. These melanocytes derived from the ORS were proliferating for up to 2 months.

Pulmonary macrophages play a crucial role in the defense of inhaled pathogens. We characterized functional properties of alveolar (AM) and interstitial (IM) macrophages from rats. AM exhibited a pronounced microbicidal capacity as shown by an elevated production of reactive oxygen intermediates (ROI), nitric oxide (NO), tumor necrosis factor (TNF)-alpha, and tumor cytotoxicity when compared with IM. In contrast, IM were superior to AM regarding mechanisms mainly involved in the induction and maintenance of specific immune reactions (major histocompatibility complex [MHC] class II expression, interleukin [IL]-1 and IL-6). In this line, we were interested in whether the microbicidal potential of AM could be augmented by treating Lewis rats with rat recombinant interferon (IFN)-gamma (5 x 10(2) to 1 x 10(5) U/animal) intratracheally, avoiding infection of interstitial lung macrophages or other organ-associated macrophages. The pulmonary cytokine application resulted in an activation of AM when macrophages from IFN-treated animals were compared with control macrophages from saline-treated rats 18 h after the treatment: (1) mediator release (ROI, NO, TNF-alpha, IL-6), (2) tumoricidal activity; (3) dose-dependent increase of MHC class II expression. The local immunomodulation enhanced the resistance of normal and immunosuppressed rats against respiratory infections with Listeria monocytogenes. Taken together, local activation of lung macrophages is a feasible therapeutic strategy against pulmonary infections.

In previous studies we have demonstrated that 50 Hz, 100 μT magnetic field (MF) exposure of female Sprague-Dawley rats for 13 weeks significantly enhances the development and growth of mammary tumors in a breast cancer model. The present study was designed to test the hypothesis that, at least in part, the tumor (co)promoting effect of MF exposure is due to MF effects on the immune surveillance system, which is of critical importance in protecting an organism against the development and growth of tumors. For this purpose, female Sprague-Dawley rats of the same age as in the mammary tumor experiments were continuously exposed for different periods (2, 4, 8, and 13 weeks) to a 50 Hz, 100 μT MF. Control groups were sham-exposed simultaneously. Following the different exposure periods, splenic lymphocytes were cultured and the proliferative responses to the T-cell-selective mitogen concanavalin A (Con A) and the B-cell-selective pokeweed mitogen (PWM) were determined. Furthermore, the production of interleukin-1 (IL-1) was determined in the splenocyte cultures. The mitogenic responsiveness of T cells was markedly enhanced after 2 weeks of MF exposure, suggesting a co-mitogenic action of MF. A significant, but less marked increase in T-cell mitogenesis was seen after 4 weeks of MF exposure, whereas no difference from sham controls was determined after 8 weeks, indicating adaptation or tolerance to this effect of MF exposure. Following 13 weeks of MF exposure, a significant decrease in the mitogenic responsiveness of lymphocytes to Con A was obtained. This triphasic alteration in T-cell function (i.e., activation, tolerance, and suppression) during prolonged MF exposure resembles alterations observed during chronic administration of mild stressors, substantiating the hypothesis that cells respond to MF in the same way as they do to other environmental stresses. In contrast to T cells, the mitogenic responsiveness of B cells and IL-1 production of PWM-stimulated cells were not altered during MF exposure. The data demonstrate that MF in vivo exposure of female rats induces complex effects on the mitogenic responsiveness of T cells, which may lead to impaired immune surveillance after long-term exposure. Bioelectromagnetics 19:259–270, 1998. © 1998 Wiley-Liss, Inc.

Activation of autoreactive T-lymphocytes by cultured syngeneic glomerular mesangial cells. The capacity of intrinsic, glomerular mesangial cells (MC) to cause an autoreactive response of syngeneic lymphocytes in vitro are presented. Initial experiments demonstrated the MHC class II dependent capacity of MC to present exogenous antigen to sensitized lymph node lymphocytes (LN) and to activate naive, allogeneic LN in the absence of a nominal antigen. However, the most striking finding of the present investigation was that mouse MC (C57BL/6 or DBA/2) augmented a significant activation of naive, syngeneic lymphocytes. The extent of the proliferative lymphocyte response was comparable to that observed after stimulation with allogeneic MC. Moreover, during syngeneic coculture substantial amounts of interferon bioactivity were generated. Equipotent concentrations of rm IFN-γ were sufficient to induce class II MHC expression of mouse MC. In control experiments the macrophage cell line, IC-21 (C57BL/6), or freshly prepared DBA/2 mouse peritoneal macrophages did not elicit a syngeneic LN response. Using MC, which had not been pretreated, the MC-specific LN stimulation occurred after prolonged periods of coculture. The stimulation index (S.I.) was 9.77 after 144 hours compared with LN controls (S.I. = 1). However, a 48 hour pretreatment of MC with either rm IFN-γ alone or in combination with rh TNF-α and/or the continuous presence of rm IL-1α during coculture periods from 72 to 144 hours substantially enhanced the proliferative LN response. Analysis of non-adherent LN by flow cytometry (FACS) after 96 or 120 hours coculture with MC revealed an increased ratio of Thy1.2 + to B220 + cells with a predominant rise of L3T4 + T-helper cells compared to Lyt2 + cytotoxic T-cells. Furthermore, immune fluorescence microscopy showed that a fraction of Thy 1.2 + lymphoblasts adhered to MC. FACS analysis of these adherent LN after detachment demonstrated that in comparison to cocultures with untreated MC, cocultures of LN with IFN-γ/TNF-α pre-treated MC resulted in a 24.4% increase of Thy1.2 + cells, with 89% of these being L3T4 + T-helper lymphocytes. In conclusion, autoreactivity of preferentially T-helper cells to cocultured glomerular MC was shown, which may represent a useful model of T-lymphocyte dependent glomerulonephritis.

Flow cytometric analyses were performed to study intracellular single-cell calcium transients ([Ca2+]i) in suspended human neutrophils during the initial phase of N-formyl peptide stimulation. Thereby, two neutrophil populations became apparent. Early maximally Ca2+-responding (high fluorescence) neutrophils and not-yet Ca2+-responding (low fluorescence) neutrophils, but no neutrophils with intermediate levels of [Ca2+]i, were detected. Within 7 s the number of low fluorescence neutrophils decreased and the number of high fluorescence neutrophils increased maximally. This suggests that [Ca2+]i transients occurred abruptly in individual neutrophils within a time interval below 1 s. At lower N-formyl peptide concentrations the lag times of individual neutrophils and the interval time of maximal activation of the [Ca2+]i-responding neutrophil population increased, however the percentage of [Ca2+]i-responding cells decreased. Surprisingly, no influence of the N-formyl peptide concentration on the [Ca2+]i-induced fluorescence signal of the individual cell was observed: it was always in an almost maximal range or not responding. In parallel, binding studies performed with fluorescein-labeled N-formyl peptide revealed that the heterogeneity of [Ca2+]i-responding cells cannot be explained by different receptor occupancy. In summary, this study demonstrates that [Ca2+]i transients induced by N-formyl peptides in suspended individual human neutrophils occur very rapidly in an almost “all-or-none manner” and that the mean increasing fluorescence signal of a calcium indicator within a whole neutrophil population results from varying lag times of the individual cells, rather than from the mean simultaneous progress of many cells. © 1993 Wiley-Liss, Inc.

Herein, we report a technically simple method for isolation and culture of human follicular melanocytes based on explant cultures of epilated hair follicles. This technique does not require any surgical intervention and allows the isolation and cultivation of follicular melanocytes from a comparatively small amount of raw material. Generally, 30-60 human anagen hair follicles have been plucked from the scalp of healthy donors and cultivated under low oxygen pressure (5%). After a short period of time cells of various types were growing out from the outer root sheath (ORS) of the hair follicles. Under the selected culture conditions, most of the cells other than melanocytes have been eliminated and a nearly 100% pure population of melanocytes has been achieved, as confirmed by immunohistochemical analyses for melanocyte-specific markers, for example, Tyrosinase-1, S-100 and premelanosomal antigens. These melanocytes derived from the ORS were proliferating for up to 2 months.

Mouse macrophage precursor cells with natural killer (NK) like activity, derived from in vitro culture of light-fraction-bone marrow cells in the presence of colony-stimulating factor 1 (CSF-1) and low dose IL-2, were incubated with high dose (1000 U/ml) IL-2. After 3 days of incubation, cells had developed from NK like (killing Yac-1 but not P815) into LAK-like (killing both YAC-1 and P815) effector cells. Morphological studies revealed that LAK activity occurred at the time when macrophage precursors with NK like activity containing few cytoplasmic granules had further differentiated into cells with abundant azurophilic granules in their cytoplasma. Proliferation of macrophage-precursor derived NK/LAK-like cells was dependent on the presence of colony-stimulating factor, generation of cytoplasmic granules was induced by IL-2 in a dose dependent way. Flow cytometric analysis showed that macrophage precursor-derived LAK effectors were positive for NK 1.1 but almost negative for F4/80. When the same starting cell population was cultured in the presence of 200 U/ml Interferon gamma (IFN gamma), proliferation was completely stopped and within 3-4 days all cells differentiated into mature macrophages expressing F4/80. In context with our previous data, we describe here a continuum of development from agranular macrophage precursors to granular cells with NK-like activity and further to cells with LAK activity under the influence of CSF-1 as growth factor and IL-2 as granule- and cytotoxicity-inducing factor.

Purified polysaccharides from cell cultures of the plant Echinacea purpurea were investigated for their ability to enhance phagocytes' activities regarding nonspecific immunity in vitro and in vivo. Macrophages (M phi) from different organ origin could be activated to produce IL-1, TNF alpha and IL-6, to produce elevated amounts of reactive oxygen intermediates and to inhibit growth of Candida albicans in vitro. Furthermore, in vivo the substances could induce increased proliferation of phagocytes in spleen and bone marrow and migration of granulocytes to the peripheral blood. These effects indeed resulted in excellent protection of mice against the consequences of lethal infections with one predominantly M phi dependent and one predominantly granulocyte dependent pathogen, Listeria monocytogenes and C. albicans, respectively. Specific immune responses to sheep red blood cells (antibody production) and to listeria (DTH) were not affected by the polysaccharides. The possibility of clinical use is discussed.

In a search for novel immunostimulating substances we detected that culture supernatants of the gram-positive phytopathogenic bacterium, Rhodococcus fascians , were able to induce cytokine release (TNF α ) from mouse peritoneal macrophages. Monoclonal antibodies were generated against the active principle, and were employed for its isolation and partial characterization as a high molecular (MW>100 kDa) glycoprotein. In addition, methods practicable for its biotechnological preparation and several ELISA variants for its determination were developed.

Therapy of selected human malignancies with interferon-alpha is widely accepted but often complicated by the emergence of interferon-alpha resistance. Interferon is a pleiotropic cytokine with antiproliferative, antitumour, antiviral and immunmodulatory effect; it signals through the Jak-STAT signal transduction pathway where signal transducer and activator of transcription 1 plays an important role. Here we report both, a lack of signal transducer and activator of transcription induction in interferon-alpha resistant renal cell carcinoma cells and signal transducer and activator of transcription 1 reinduction of phorbol 12-myristate 13-acetate-stimulated peripheral blood mononuclear cells supernatant. Preliminary experiments on the identification of the molecules that reinducing signal transducers and activators of transcription 1 indicate that interferon-gamma may be the responsible candidate cytokine, but several others may be involved as well. This work provides the basis for therapeutic strategies directed at the molecular modulation of interferon-alpha resistance in human neoplasms.

Pulmonary macrophages play a crucial role in the defense of inhaled pathogens. We characterized functional properties of alveolar (AM) and interstitial (IM) macrophages from rats. AM exhibited a pronounced microbicidal capacity as shown by an elevated production of reactive oxygen intermediates (ROI), nitric oxide (NO), tumor necrosis factor (TNF)-, and tumor cytotoxicity when compared with IM. In contrast, IM were superior to AM regarding mechanisms mainly involved in the induction and maintenance of specific immune reactions (major histocompatibility complex [MHC] class II expression, interleukin [IL]-1 and IL-6). In this line, we were interested in whether the microbicidal potential of AM could be augmented by treating Lewis rats with rat recombinant interferon (IFN)- (5 × 102 to 1 × 105 U/animal) intratracheally, avoiding infection of interstitial lung macrophages or other organ-associated macrophages. The pulmonary cytokine application resulted in an activation of AM when macrophages from IFN-treated animals were compared with control macrophages from saline-treated rats 18 h after the treatment: (1) mediator release (ROI, NO, TNF-, IL-6), (2) tumoricidal activity; (3) dose-dependent increase of MHC class II expression. The local immunomodulation enhanced the resistance of normal and immunosuppressed rats against respiratory infections with Listeria monocytogenes. Taken together, local activation of lung macrophages is a feasible therapeutic strategy against pulmonary infections.

Chemical-induced carcinogenesis has been in the focus of toxicological research for many decades. However, the mechanisms leading to tumor formation are only understood with certain substances. The intake of potential carcinogens by inhalation is a major route of exposure. Chemical-induced lung tumors are the final manifestation of a multistep pathway, resulting in an imbalance between cell proliferation and cell death by apoptosis. The impact of certain confounding factors e.g. extent of inflammatory response, type of genotoxic event, antagonizing principles and genetic background are discussed in this article. Finally, methods to assess the inflammatory potential of chemicals are referred to.

The immune response against Leischmania donovani infection has been investigated in one resistant mouse strain (C3H/HeJ) and three susceptible mouse strains (C57BL/6, BALB/c, and B10D2/n). In order to correlate the strain-specific course of infection with the individual T cell response phenotype, the ex vivo cytokine secretion patterns of splenic lymphocytes were assessed by ELISA (interferon-gamma [IFN-gamma], interleukin-4 [IL-4], IL-10) or by bioassay (IL-2). The strain-dependent differences in the course of infection correlated closely with the potency of T cells to produce IFN-gamma. C3H/HeJ mice produced high amounts of IFN-gamma before and during the infection, whereas susceptible mice produced low amounts of IFN-gamma earla during L. donovani infection. However, C57BL/6 mice, which recovered from the infection rapidly after the acute stage, developed marked IFN-gamma response within the first 30 days of infection. In contrast, in BALB/c and B10D2/n mice, the IFN-gamma production diminished during the acute stage, and this was associated with a delay in recovery and with subsequent switching into the chronic stage. Interestingly, CD8+ T cells contributed significantly to IFN-gamma production during this phase. In contrast to IFN-gamma, the levels of IL-4 in response to antigen or mitogen ex vivo were always very low. Moreover, neutralization of endogenous IL-4 in vivo by treatment with soluble murine IL-4 receptor did not result in significant decreases in the parasite burdens in spleen and liver butdi cause a decrease in the serum IgE level of L. donovani-infected BALB/c mice. These results confirm that in visceral leishmaniasis a Th1-dominated immune response is protective against the L. donovani parasites and, furthermore, that the capacity to produce IFN-gamma rather than the presence of IL-4 determines the efficacy of the immune response in susceptible mice. The data show that CD8+ Tcells represent an important source of IFN-gamma during L. donovani infection in susceptible mice, implying a role for this cell type in healing and development of protective immunity.

Circulating alveolar macrophages and Type-Il-cells of the lung represent important cells of the respiratory tract with immunomodulatory activities. Alveolar macrophages are the first effector cells of the immune system in the lung to defend bacterial or viral infections. Macrophages influence several cell compartments via direct cell-cell interactions or by secreted products as there are different cytokines or chemokines. Type-ll-pneumocytes are the primary producer ot Surfactant. Additionally, these cells are able to interact with the immune system by secretion of Interleukin-1 (IL-1) and the expression of adhesion molecules as ICAM-1. Our group was interested in the influence of an infection with Respiratory syncytial virus (RSV) on the functions of alveolar macrophages and Typell-cells alone and the interactions between these two cell types. Using in vitro-cultures, it is difficult to examine the influence of one cell compartment of the lung on the other, for this purpose, we established a coculture system using human alveolar macrophages collected from bronchoalveolar lavage and the human cell line A549, representing the characteristics of Type-Il-cells, producing Surfactant, IL-1 and several chemokines i.e. Interleukin-8 (IL-8) and MCP-1. Alveolar macrophages were plated into a 24- well microtiterplate and A549 cells into a tissue culture insert which were placed into the well. To establish the coculture system the movement of the investigated cells through the membrane of the insert was measured to ensure, that no mixing of the cells during the culture occured. We could show, that a pore size of the membrane of 0.45 pm was necessary to inhibit a movement of the cells through the membrane. The cells were infected with RSV either the alveolar macrophages or the A549 cells and after 24 hours, we measured the virus concentration in the culture supernatant. Further, cell culture supernatants were collected at different time points and the concentrations of MCP-1, IL-8 and IL-1 were detected. Infected alveolar macrophages and A549 cells showed an increased secretion of IL-8 in comparison to not infected cells, whereas in the supernatant of cocultured infected alveolar macrophages and A549 cells the strongest increase in the concentration of IL-8 could be demonstrated. The coculture system described is a useful tool to determine interaction between cell compartments without cell-cell-interaction in different situations as there are i.e. infectious diseases.

The use of extracts of Echinacea angustifolia and E. purpurea by the American Indians and later in the Traditional medicine of Europe against wounds, burns, swellings of the lymph glands (mumps), measles and various infections has initiated a thorough chemical and pharmacological search for the active components of the drugs. Since the weak antimicrobial activity found for the extract and the isolated caffeic acid derivative echinacoside, isolated from the root of Echinacea angustifolia, could not explain the therapeutic efficacy of the drug, in vitro and in vivo immunological investigations were started. They resulted in the isolation of several low and high molecular weight compounds such as caffeic acid derivatives, poly-acetylenes, alkylamides, and polysaccharides (see chapter by R. Bauer, this volume). Among them the 2,3–O dicaffeoyl tartaric acid (cichoric acid) and the polysaccharides, a 4–O–methylglucuronoarabinoxylan (EPS-XG) (MW ≅ 35 kDa) and an acidic arabinorhamnogalactan (EPS-AG) (MW ≅ 50 kDa) turned out to be the most active compounds in several in vitro and in vivo immunological assays [1, 2] (Fig. 1). The expensive isolation procedure of the polysaccharides in a pure form and the difficulty of obtaining them with reproducible activity prompted one of us to produce them from tissue cultures of Echinacea purpurea leaves. From the growth medium two homogeneous polysaccharides, i.e. a neutral fucogalactoxyloglucan (MW ≅ 25 kDa) and an acidic arabinogalactan (MW ≅ 75 kDa) could be isolated [3] (Fig. 2a, b).