Search

A captive harbour porpoise (Phocoena phocoena) was monitored for 80 consecutive days, 10 days before attachment of a satellite dive recorder and a VHF-radio tag, 30 days during attachment and 40 days after removal of the transmitters. Dive data recorded by the satellite transmitter was collected during the attachment. Daily food intake was measured and each week the porpoise was taken out of the water for a physical examination. Behavioural observations logged on the handheld computer showed an immediate effect of the tagging in time spent resting at the surface (logging), which was four to six times higher on the day of attachment. Digital video recordings showed a significant increase in the mean duration of rolls at the surface immediately after attachment. The mean duration of dives was shorter before attachment than both after the tagging and after removal of the transmitters. Furthermore the frequency of surfacings farthest away from where the porpoise was taken out of the pool for tagging, was highest the first five days following the tagging. Dive data from the satellite tag showed a semidiurnal diving pattern, with increased mean dive depth in the first 24 hours after attachment. The heart rate was fairly constant during the tagging, but the mean heart rate increased significantly from 161 beats per minute (bpm) to 180 bpm after the first hole in the dorsal fin was made. The body weight of the porpoise increased up to the time of tagging (16 May 2000), after which it decreased until six days prior to release (28 July 2000); this was probably due to the seasonal trend in blubber thickness of harbour porpoises rather than an effect from the tagging. After one month of attachment, a reaction occurred around the frontal pinhole and the transmitters were removed. This reaction was probably due to drag from two tags and seaweed attached to the tags during the last part of the attachment period. After the tags were removed epithelia closed the pinholes after two days.

It has been more than 15 years since the identification of individual interleukin-27 (IL-27) and IL-27 receptor components. The last decade has seen the description of the signaling pathways engaged by IL-27 and an appreciation has emerged that this cytokine can modulate the intensity and duration of many classes of T cell responses. The goal of this article is to provide an overview of the immunobiology of IL-27 and to review advances in understanding the functions of individual IL-27 and IL-27 receptor sub-units and the role of IL-27 in dictating the balance between protective and pathological immunity. Additionally, this cytokine has been proposed as a therapy to modify inflammatory conditions or promote anti-tumor responses and situations where experimental and clinical data sets implicate IL-27 in the outcome of disease are highlighted.

To set safety criteria for levels of sounds produced during pile driving for offshore wind parks, temporary hearing threshold shifts sTTSsd were studied in a harbor porpoise and two harbor seals. A psychoacoustic behavioral technique was used to quantify TTS and hearing recovery in the animals exposed to underwater sounds swhite noise in a 1/1-octave band around 4 kHzd. Hearing thresholds were determined once a day for a narrow-band frequency swept sine wave s3.9–4.1 kHzd before and after exposure to the fatiguing noise, which was offered at two sound pressure levels s131 and 119 dB re 1 μPa for the porpoise and 151 and 139 dB re 1 μPa for the sealsd each at four durations s15, 30, 60, and 120 mind. Recovery was quantified by measuring hearing thresholds at 4, 8, 12, and 48 min after the noise exposure. The results show that TTS in harbor porpoises occurred at a sound exposure level threshold approximately 20 dB below the threshold for which TTS occurred in harbor seals.

We have demonstrated the existence of human cytokine synthesis inhibitory factor (CSIF) [interleukin 10 (IL-10)]. cDNA clones encoding human IL-10 (hIL-10) were isolated from a tetanus toxin-specific human T-cell clone. Like mouse IL-10, hIL-10 exhibits strong DNA and amino acid sequence homology to an open reading frame in the Epstein-Barr virus, BCRFI. hIL-10 and the BCRFI product inhibit cytokine synthesis by activated human peripheral blood mononuclear cells and by a mouse Th1 clone. Both hIL-10 and mouse IL-10 sustain the viability of a mouse mast cell line in culture, but BCRFI lacks comparable activity in this assay, suggesting that BCRFI may have conserved only a subset of hIL-10 activities.

Interleukin 10 (IL-10) and viral IL-10 (v-IL-10) strongly reduced antigen-specific proliferation of human T cells and CD4+ T cells clones when monocytes were used as antigen-presenting cells. In contrast, IL-10 and v-IL-10 did not affect the proliferative responses to antigens presented by autologous Epstein-Barr virus-lymphoblastoid cell line (EBV-LCL). Inhibition of antigen-specific T cell responses was associated with downregulation of constitutive, as well as interferon gamma-or IL-4-induced, class II MHC expression on monocytes by IL-10 and v-IL-10, resulting in the reduction in antigen-presenting capacity of these cells. In contrast, IL-10 and v-IL-10 had no effect on class II major histocompatibility complex (MHC) expression on EBV-LCL. The reduced antigen-presenting capacity of monocytes correlated with a decreased capacity to mobilize intracellular Ca2+ in the responder T cell clones. The diminished antigen-presenting capacities of monocytes were not due to inhibitory effects of IL-10 and v-IL-10 on antigen processing, since the proliferative T cell responses to antigenic peptides, which did not require processing, were equally well inhibited. Futhermore, the inhibitory effects of IL-10 and v-IL-10 on antigen-specific proliferative T cell responses could not be neutralized by exogenous IL-2 or IL-4. Although IL-10 and v-IL-10 suppressed IL-1-alpha, IL-1-beta, tumor necrosis factor alpha (TNF-alpha), and IL-6 production by monocytes, it was excluded that these cytokines played a role in antigen-specific T cell proliferation, since normal antigen-specific responses were observed in the presence of neutralizing anti-IL-1, -IL-6, and -TNF-alpha mAbs. Furthermore, addition of saturating concentrations of IL-1-alpha, IL-1-beta, IL-6, and TNF-alpha to the cultures had no effect on the reduced proliferative T cell responses in the presence of IL-10, or v-IL-10. Collectively, our data indicate that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.

Human rIL-4 was studied for its capacity to induce lymphokine-activated killer (LAK) cell activity. In contrast to IL-2, IL-4 was not able to induce LAK cell activity in cell cultures derived from peripheral blood. IL-4 added simultaneously with IL-2 to such cultures suppressed IL-2-induced LAK cell activity measured against Daudi and the melanoma cell line MEWO in a dose-dependent way. IL-4 also inhibited the induction of LAK cell activity in CD2+, CD3-, CD4-, CD8- cells, suggesting that IL-4 acts directly on LAK precursor cells. IL-4 added 24 h after the addition of IL-2 failed to inhibit the generation of LAK cell activity. Cytotoxic activity of various types of NK cell clones was not affected after incubation in IL-4 for 3 days, indicating that IL-4 does not affect the activity of already committed killer cells. No significant differences were observed in the percentages of Tac+, NKH-1+ and CD16+ cells after culturing PBL in IL-2, IL-4 or combinations of IL-2 and IL-4 for 3 days. IL-4 also inhibited the activation of non-specific cytotoxic activity in MLC, as measured against K-562 and MEWO cells. In contrast, the Ag-specific CTL activity against the stimulator cells was augmented by IL-4. Collectively, these data indicate that IL-4 prevents the activation of LAK cell precursors by IL-2, but does not inhibit the generation of Ag-specific CTL.