Food-web comparisons between two shallow vegetated habitat types in the Baltic Sea.

Coastal vegetated habitats maintain highly diverse communities, where the contribution of macrophyte production is significant for macroinvertebrate primary consumers. In the brackish-waters of the Baltic Sea, the taxonomical diversity of different macrophytes includes both marine and limnic species. To study the basal food-web differences of two key vegetated habitat types, either dominated by a perennial brown macroalgae (Fucus vesiculosus) or by angiosperm plants, 13C and 15N compositions of different primary producers and macroinvertebrate consumers were examined, and their diets were estimated by Bayesian mixing models. Carbon isotope diversity of primary producers was high especially in the hard-bottom Fucus-dominated habitats, which was also reflected in a larger consumer isotope niche. However, consumer isotope niche among sites was similar within the same habitat type. Our models indicated that the perennial macrophyte dietary median contribution was about 25% for deposit feeders and omnivores in both habitat types, while epigrazers preferred filamentous algae (30-60%). The niche positions of the abundant clams L. balthica, M. arenaria and C. glaucum differed between the two habitats, but they showed only small (<10% units) differences in their macrophyte dietary contributions. The isotopic compositions of the dominating primary producer assemblage reflected significantly in the isotope niche structure of the associated primary consumers.

Macroalgae fuels coastal soft-sediment macrofauna: A triple-isotope approach across spatial scales.

Shallow coastal zones may provide cross-habitat nutrient subsidies for benthic communities offshore, as macrophyte matter can drift to deeper sediments. To study the relative importance of carbon and nutrient flows derived from different primary food sources in a coastal ecosystem, the diets of clam Macoma balthica, polychaete Marenzelleria spp. and mussel Mytilus trossulus were examined across environmental gradients in the northern Baltic Sea using a triple-isotope approach (i.e. 13C, 15N and 34S) and Bayesian mixing models (MixSIAR). Our results suggest that in shallow habitats, production from Fucus vesiculosus is the primary energy source for M. balthica. The proportion of macroalgae-derived matter in the diet of M. balthica and Marenzelleria spp. decreased following a depth gradient. Our models for M. trossulus indicate that the pelagic POM dominates its diet. Our results indicate a trophic connectivity between shallow macrophyte-dominated and deeper habitats, which receive significant amounts of nutrient subsidies from shallower areas.

IL-4-deficient Balb/c mice resist infection with Leishmania major.

Mice with a genetically engineered deficiency for either IL-4 or IFN-gamma R1 (single mutants), and IL-4/IFN-gamma R1 (double mutants) on the Balb/c and 129Sv background were used to study the course of infection with Leishmania major. In contrast to genetically resistant 129Sv wildtype mice, IL-4/IFN-gamma R1 double mutant mice developed fetal disease with parasite dissemination to visceral organs similar to mice lacking IFN-gamma R1 only. Balb/c mice, which are exquisitely susceptible to L. major, were rendered resistant to infection by disruption of the IL-4 gene. As compared to homozygous IL-4+/- mice, heterozygous IL-4+/- mice, heterozygous IL-4+/- animals consistently developed smaller lesions with less ulceration and necrosis, indicating the likelihood of gene-dosage effects. This implicates that the magnitude of the IL-4 response determines the severity of disease. CD4+ T cells of IL-4-deficient mice showed impaired Th2 cell development, as assessed by quantitative RT-PCR of characteristic cytokines. Development of resistance is not explained by default Th1 development, because this was observed only at very late stages of infection. Moreover, the induction of inflammatory cytokines (e.g., IL-1 alpha, IL-1 beta, TNF-alpha, IL-12) together with iNOS in the lesion and draining lymph nodes was not altered in the absence of IL-4.

Protective effect of leflunomide on the natural course of Leishmania major-induced disease in genetically susceptible BALB/c mice.

Leflunomide has been reported as an immunomodulating agent which acts on a variety of cells including T- and B-lymphocytes. CD4+ T-lymphocytes are essential for the type of disease that develops after infection with the protozoan parasite Leishmania major. A variety of immunological interventions has been shown to modulate disease development. Therefore, the effect of leflunomide on the development of parasite-induced lesions and the ensuing immune response was investigated in genetically susceptible BALB/c mice. Oral feeding for 7 to 10 days of leflunomide (30 mg/kg per day) beginning 2 days prior to or at the day of infection led to the development of a stable resistant phenotype, i.e. to long-lasting (> 13 months) regression of the lesions and clinical cure. Starting leflunomide treatment 3 days after infection was ineffective. The main bioactive metabolite, 1726 B, did not inhibit viability or growth of L. major promastigotes and amastigotes in vitro. Quantitative analysis of CD4+ and CD8+ cells in spleens and lymph nodes of parasite-infected animals treated with leflunomide for 5 days showed no significant effect. In vitro, 1726 B dose-dependently inhibited growth of stimulated T-cells, which could not be restored by saturating amounts of exogenous IL-2 and IL-4. No effect was observed on the killing function of activated macrophages. Taken together, the data indicate that leflunomide is a potent prophylactic agent to prevent an otherwise lethal infection of BALB/c mice.

Mechanisms of mouse spleen dendritic cell function in the generation of influenza-specific, cytolytic T lymphocytes.

We have evaluated the capacity of dendritic cells to function as antigen-presenting cells (APCs) for influenza and have examined their mechanism of action. Virus-pulsed dendritic cells were 100 times more efficient than bulk spleen cells in stimulating cytotoxic T lymphocyte (CTL) formation. The induction of CTLs required neither exogenous lymphokines nor APCs in the responding T cell population. Infectious virus entered dendritic cells through intracellular acidic vacuoles and directed the synthesis of several viral proteins. If ultraviolet (UV)-inactivated or bromelain-treated viruses were used, viral protein synthesis could not be detected, and there was poor induction of CTLs. This indicated that dendritic cells were not capable of processing noninfectious virus onto major histocompatibility complex (MHC) class I molecules. However, UV-inactivated and bromelain-treated viruses were presented efficiently to class II-restricted CD4+ T cells. The CD4+ T cells crossreacted with different strains of influenza and markedly amplified CTL formation. Cell lines that lacked MHC class II, and consequently the capacity to stimulate CD4+ T cells, failed to induce CTLs unless helper lymphokines were added. Similarly, dendritic cells pulsed with the MHC class I-restricted nucleoprotein 147-155 peptide were poor stimulators in the absence of exogenous helper factors. We conclude that the function of dendritic cells as APCs for the generation of virus-specific CTLs in vitro depends measurably upon: (a) charging class I molecules with peptides derived from endogenously synthesized viral antigens, and (b) stimulating a strong CD4+ helper T cell response.