The present experiment was undertaken to validate a probiotic of canine origin for its potential use in dogs. A total of fifteen adult female Labrador dogs were allocated to three equal groups and fed a basal diet without probiotic (control) or with probiotic of either canine (Lactobacillus johnsonii CPN23; cPRO) or dairy (L. acidophilus NCDC 15; dPRO) origin for 9 weeks. The digestibility of most macronutrients remained similar among the groups; however, fibre digestibility was improved (P = 0·034) in dogs receiving cPRO. The faecal fermentative metabolites ammonia (P < 0·05) and lactate (P = 0·094) were altered favourably, indicating a positive influence of both probiotics. Faecal concentrations of acetate, propionate and butyrate were increased (P < 0·01) in both probiotic groups. However, improvements were higher in cPRO v. dPRO. The delayed-type hypersensitivity reaction to intradermal inoculation of phytohaemagglutinin-P was higher (P = 0·053) in cPRO as compared with control. The antibody response to sheep erythrocytes was, however, similar across the three groups. Overall, in dogs, the canine-origin probiotic was superior when compared with the dairy-origin probiotic.

Naturally acquired immunity to the blood-stage of the malaria parasite develops slowly in areas of high endemicity, but is not sterilizing. It manifests as a reduction in parasite density and clinical symptoms. Immunity as a result of blood-stage vaccination has not yet been achieved in humans, although there are many animal models where vaccination has been successful. The development of a blood-stage vaccine has been complicated by a number of factors including limited knowledge of human-parasite interactions and which antigens and immune responses are critical for protection. Opinion is divided as to whether this vaccine should aim to accelerate the acquisition of responses acquired following natural exposure, or whether it should induce a different response. Animal and experimental human models suggest that cell-mediated immune responses can control parasite growth, but these responses can also contribute to significant immunopathology if unregulated. They are largely ignored in most blood-stage malaria vaccine development strategies. Here, we discuss key observations relating to cell-mediated immune responses in the context of experimental human systems and field studies involving naturally exposed individuals and how this may inform the development of a blood-stage malaria vaccine.

Introduction: Significant changes in immune function have been found in mood disorders. Controlled studies in bipolar disorder concerning cell-mediated immunity and thyroid autoimmunity are reviewed, and presented together with preliminary findings from our own ongoing study.

Method: Using Medline and other sources, 14 controlled studies as well as some other relevant studies were found.

Results: Bipolar disorder is associated with an acute phase response and activation of the cell-mediated immune system, and with an increased prevalence of antithyroid autoantibodies.

Conclusion: Changes in immune function, in connection with neuroendocrine changes, may provide new hypotheses for the pathophysiology of mood disorders.

Current development efforts of subunit vaccines against Toxoplasma gondii, the aetiological agent of toxoplasmosis, have been focused mainly on tachyzoite surface antigens (SAGs) such as SAG2, due to their attachment roles in the process of host-cell invasion. In the present study, we aimed to produce poly(lactide-co-glycolide) (PLG) microparticles (MPs) containing recombinant SAG2 (rSAG2) to induce improved immunity against T. gondii. The resulting PLG-encapsulated rSAG2 (PLG-rSAG2) MPs, 2·14–3·63 μm in diameter, showed 74–80% entrapment efficiency and gradually released antigenic rSAG2 protein (88·3% of the total protein load) for a long 33-day period. Peritoneal immunization with PLG-rSAG2 MPs in BALB/c mice resulted in not only sustained (10 weeks) lymphocyte proliferation and IFN-γ production but also an improved protective capacity (87%) against a lethal subcutaneous challenge of 1×104 live tachyzoites of T. gondii (RH strain). In conclusion, the sustained release of rSAG2 protein from PLG-rSAG2 MPs extends Th1 cell-mediated immunity (lymphocyte proliferation and IFN-γ production) and induces improved protection against T. gondii tachyzoite infection in mice.

The Shozu Herpes Zoster (SHEZ) Study was designed to clarify the incidence of and predictive and immunological factors for herpes zoster in a defined community-based Japanese population. As part of this series, a total of 5683 residents aged ⩾50 years received a varicella-zoster virus (VZV) skin test with VZV antigen, and 48 h later, the erythema and oedema were assessed by measuring the longest diameter. The diameters of both the erythema and oedema decreased with the increasing age of the subject. Sixty-three subjects contracted herpes zoster within a year after receiving the VZV skin test. Analysis of the herpes zoster incidence rate vs. the skin test reaction revealed that the shorter the diameter of erythema or oedema, the greater the likelihood of herpes zoster. These results demonstrated that the VZV skin test is an excellent surrogate marker for predicting the risk of herpes zoster.

Converging data from different disciplines indicate that central nervous system processes are capable of influencing immune responses. This paper concentrates on recent studies documenting behaviorally conditioned suppression and enhancement of immunity. Exposing rats or mice to a conditioned stimulus previously paired with an immunomodulating agent results in alterations in humoral and cell-mediated immune responses to antigenic stimuli, and unreinforced reexposures to the conditioned stimuli result in extinction of the conditioned response. Although the magnitude of such conditioning effects has not been large, the phenomenon has been independently verified under a variety of experimental conditions. The biological impact of conditioned alterations in immune function is illustrated by studies in which conditioning operations were applied in the pharmacotherapy of autoimmune disease in New Zealand mice. In conditioned animals, substituting conditioned stimuli for active drugs delays the onset of autoimmune disease relative to nonconditioned animals using a dose of immunosuppressive drug that, by itself, is ineffective in modifying the progression of disease. The hypothesis that such conditioning effects are mediated by elevations in adrenocortical steroid levels receives no support from available data. Despite its capacity for self-regulation, it appears that the immune system is integrated with other psychophysiological processes and subject to modulation by the brain.

The objective of this investigation was to determine the influence of flaxseed oil on responses representative of primary humoral and cell-mediated adaptive immune competence in immunosenescent mice. Male and female C57BL/6J mice, 85 weeks old, were randomized between two complete purified diets differing only in oil source (cold-pressed safflower or flaxseed). After 8 weeks, humoral competence was assessed in six mice per group as the serum haemagglutinin titre to sheep red blood cells (SRBC) and cell-mediated competence was assessed, in an additional six mice per group, as the delayed hypersensitivity response to SRBC. A zero-time control group (88 weeks old) and a young adult positive control group (12 weeks old) were each tested similarly (six per immune response), revealing age-related depression in both antibody and cell-mediated competence at 88 weeks of age. After the 8-week experimental period, the antibody response of the two test groups of geriatric mice remained below the young adult level (P=0·04) and the cell-mediated response of the saffloweroil group also continued to exhibit age-related depression (20% of young adult level, P=0·0002). By contrast, the anti-SRBC delayedhypersensitivity response of the flaxseed group no longer differed from the response of the young adults but exceeded that of the safflower and zero-time control senescent groups (P=0·0002). Depression in primary cell-mediated competence, the most outstanding aspect of immunosenescence, can be addressed by means of a dietary source of 18:3n-3 without longer-chain PUFA.

The relationships between haematozoan parasites, cell-mediated immune response, territory features and colour morph were investigated in tawny owls Strix aluco, in the Park of Monza in Milan, northern Italy. Rufous and grey birds were found to differ significantly in their blood parasite loads, particularly during the breeding season, when rufous birds hosted more parasites than grey birds. The increase in parasitaemia of rufous owl was not, however, owing to the breeding status of sampled individuals. Although body condition was similar between the two colour morphs, immune response was higher in grey than in rufous owls for the same level of parasites. Moreover, parasites seemed to influence breeding of rufous birds negatively, because only individuals with no or few parasites reproduced. Both these results suggested a higher susceptibility to parasites of rufous owls. Nevertheless, a habitat effect existed because parasite loads increased significantly with woodland extent and tree-density within owl territories, and rufous birds defended more wooded territories than grey ones. Thus, the differential parasitaemia between colour morphs in tawny owls may be the result of both a differential exposure to flying vectors depending on habitat selection and a differential colour-based susceptibility of individuals.

Breast cancer is a complex disease. Its aetiology is multifactorial, its period of development can span decades, and its clinical course is highly variable. Evaluation of the role of the immune response in either the development or control of breast cancer is also complex. Nevertheless, there is substantial information that in this disease, the immune response is not a host defence reaction and may even serve to facilitate cancer development. This evidence comes from a variety of sources including clinical–pathological investigations in women that show a correlation between the intensity of lymphocytic infiltration into the tumour mass with poor prognosis, studies in breast cancer patients that demonstrate a similar correlation between delayed hypersensitivity reactivity or in vitro assays of immune reactivity to tumour cell membranes or non-specific antigens and poor prognosis, and analyses of cancer incidence in chronically immunosuppressed, kidney transplant recipients who develop an unexpectedly low incidence of breast cancer. The overall conclusions from these human studies are corroborated by observations in mouse mammary tumour models that also demonstrate immune enhancement of breast cell proliferation in vitro and of breast cancer development in vivo. Potential mechanisms for these effects include production, by inflammatory cell infiltrates, of direct or indirect modulators of breast cell growth, e.g. cytokines, peptide or steroid hormones, enzymes involved in steroid metabolism, as well as of antibodies to growth factors or their receptors. These immune facilitatory mechanisms must be overcome if immune-based therapies are to be applied successfully in breast cancer.