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Immunol Lett. 2002 Dec 3;84(3):211-6.
Effect of chondroitin sulfate on murine splenocytes sensitized with ovalbumin.

Sakai S, Akiyama H, Harikai N, Toyoda H, Toida T, Maitani T, Imanari T.

Graduate School of Pharmaceutical Sciences, Chiba University, 1-33, Yayoi-cho, Inage-ku, Chiba 263-8522, Japan.

Chondroitin sulfate (CS) is a glycosaminoglycan that is widely present in animals organisms, and it has anti-inflammatory and chondroprotective properties. To examine the effects of CS on the immune system, splenocytes obtained from ovalbumin (OVA)-sensitized BALB/c mice were challenged with OVA in the presence of CS, and cytokine levels in the medium of the cultured cells were measured. CS induced secretion of Th1-type cytokines (IFN-gamma, IL-2, and IL-12) by OVA-sensitized splenocytes but suppressed secretion of Th2-type cytokines (IL-5 and IL-10). Flow cytometric assay showed a significantly higher percentage of helper T cells (CD4(+)CD8(-) cells) among the splenocytes cultured with OVA and CS than with OVA alone. Analysis of the IFN-gamma mRNA level of the splenocytes by the real-time quantitative RT-PCR technique revealed higher levels in the splenocytes cultured with OVA and CS than in the splenocytes cultured with OVA alone. This is the first demonstration that CS inhibits antigen-induced IgE production through induction of cytokine secretion by Th1 cells, and this finding suggests a potential use of CS in preventing IgE-mediated allergy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12413739&dopt=Abstract

Vet Microbiol. 2002 Dec 20;90(1-4):367-82.
Fundamentals of host immune response against Brucella abortus: what the mouse model has revealed about control of infection.

Baldwin CL, Parent M.

Paige Laboratory, Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA. cbaldwiasci.umass.edu

The studies reviewed here evaluated the role cellular immune system components play in control of brucellosis by conducting comparative studies with brucella-resistant C57BL/10 or C57BL/6 mice and susceptible BALB/c mice. We have shown by both in vitro and in vivo studies that activation of macrophages with interferon-gamma (IFN-gamma) is an important factor for control of infection with B. abortus in the mouse model and that the mechanism of anti-brucella activity largely involved reactive oxygen intermediates. Differences in control of the organism by resistant and susceptible mice was not related to inherent differences in the ability of their macrophages to control infection either with or without IFN-gamma activation nor was it attributable to NK cells since we found no role for them in control of brucellosis in either mouse strain. However, relative resistance to brucellosis did correlate with increased production of IFN-gamma by CD4 T cells during the first weeks after infection while IL-10 contributed to susceptibility in BALB/c mice. Moreover, by 3 weeks post-infection splenocytes from the susceptible BALB/c mice failed to produce IFN-gamma and relied on TNF-alpha as well as CD8 T cells to control infection until the end of the plateau phase around 6 weeks post-infection when IFN-gamma production resumed and clearance began. In contrast, IFN-gamma was crucial for control throughout the infection in the more resistant C57BL/6 mice and the mice died in its absence by 6 weeks post-infection compared to 12 weeks for the more susceptible mice that relied on additional mechanisms of control. In contrast to the IFN-gamma knock-out mice, both beta2 microglobulin knock-out C57BL/6 mice, which do not express conventional MHC class I molecules and thus cannot present antigen to CD8 T cells, or perforin knock-out C57BL/6 mice, which have no T cell cytotoxic activity, controlled and cleared the infection as well as normal C57BL/6 mice. The hiatus of IFN-gamma production in BALB/c mice correlated with very high levels of total IL-12 and it was postulated that the lack of IFN-gamma was a consequence of p40 homodimer blocking activity. However, reduction of p40 IL-12 in vivo through administration of indomethacin reduced the infection without a concomitant measurable increase in IFN-gamma. Current studies are aimed at elucidating the mechanism of the IFN-gamma hiatus. 2002 Elsevier Science B.V.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12414157&dopt=Abstract

Clin Diagn Lab Immunol. 2002 Nov;9(6):1165-8.
Phagocytosis and killing of bacteria by professional phagocytes and dendritic cells.

Nagl M, Kacani L, Mullauer B, Lemberger EM, Stoiber H, Sprinzl GM, Schennach H, Dierich MP.

Department of Otorhinolaryngology, Leopold-Franzens-University of Innsbruck Innsbruck, Austria. m.nagibk.ac.at

Dendritic cells (DC) represent a class of professional antigen-presenting cells whose primary function is to alert the immune system, not to clear invading microorganisms. The objective of our study was to compare the abilities of polymorphonuclear neutrophilic leukocytes (PMN), monocytes, monocyte-derived macrophages (MDM), monocyte-derived immature DC (imDC), and mature DC (maDC) to ingest and destroy Staphylococcus aureus and Escherichia coli. Acridine orange staining and fluorescence microscopy demonstrated that MDM, followed by monocytes, imDC, and PMN, internalized bacteria well but that maDC exhibited less pronounced phagocytic activity. PMN, monocytes, and MDM exhibited a much higher capacity to kill ingested bacteria than both imDC and maDC. In summary, these data are in agreement with the generally accepted idea that different types of leukocytes fulfill specialized tasks in antigen presentation and killing of pathogens.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12414745&dopt=Abstract

J Virol. 2002 Dec;76(23):12259-64.
Processing and degradation of exogenous prion protein by CD11c(+) myeloid dendritic cells in vitro.

Luhr KM, Wallin RP, Ljunggren HG, Low P, Taraboulos A, Kristensson K.

Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden.

The immune system plays an important role in facilitating the spread of prion infections from the periphery to the central nervous system. CD11c(+) myeloid dendritic cells (DC) could, due to their subepithelial location and their migratory capacity, be early targets for prion infection and contribute to the spread of infection. In order to analyze mechanisms by which these cells may affect prion propagation, we studied in vitro the effect of exposing such DC to scrapie-infected GT1-1 cells, which produce the scrapie prion protein PrP(Sc). In this system, the DC efficiently engulfed the infected GT1-1 cells. Unexpectedly, PrP(Sc), which is generally resistant to protease digestion, was processed and rapidly degraded. Based on this observation we speculate that CD11c(+) DC may play a dual role in prion infections: on one hand they may facilitate neuroinvasion by transfer of the infectious agent as suggested from in vivo studies, but on the other hand they may protect against the infection by causing an efficient degradation of PrP(Sc). Thus, the migrating and highly proteolytic CD11c(+) myeloid DC may affect the balance between propagation and clearance of PrP(Sc) in the organism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12414965&dopt=Abstract

Onkologie. 2002 Oct;25(5):456-64.
Dendritic cells as adjuvants in antitumor immune therapy.

Felzmann T, Gadner H, Holter W.

Forschungsinstitut fur krebskranke Kinder, Wien, Austria. felzmancri.univie.ac.at

While there has been considerable progress in the development of techniques to identify tumor-associated antigens, the traditional methods for delivering these antigens in the context of a tumor vaccine are, in many cases, crude and inadequate. Most adjuvants that are in principle available for such a vaccine have been discovered empirically and their mechanism of immune-stimulatory action is poorly understood. In addition, preclinical studies suggest that most of the conventional adjuvants often fail to elicit activation of both the humoral and the cellular arm of the immune system. Among other reasons, these findings have led to the application of dendritic cells (DCs) as adjuvants. In such experiments DCs were pulsed in vitro with tumor antigens which, upon in vivo application, caused tumor rejection in experimental mouse tumor systems, and such preparations indeed increased antitumor immunity in cancer patients. Recent advances in the understanding of the function of DCs and their first clinical applications in antitumor immune therapy are described. 2002 S. Karger GmbH, Freiburg

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12415201&dopt=Abstract

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