Parasitic infection, nutrition, and immune response

Parasites differ enormously in their abilities to evade normal host defenses. Intracellular protozoa are capable of surviving and multiplying within phagocytes and other cells whereas most nematodes do not multiply within the host. Both T lymphocyte-mediated immune responses and antibody production are important in limiting parasite invasion and in eliminating them. Of the nonspecific factors, macrophages, natural killer cells, and nonantibody serum factors can cause damage to parasites. Malnutrition impairs immunity, most notably cell-mediated processes. The number of T lymphocytes is reduced and there are significant alterations in T cell subsets. Mucosal antibody response is blunted, complement activity is decreased, and microbicidal capacity of phagocytes is reduced. Such changes in host resistance are important determinants of the final outcome of host-parasite interactions.     

大麻和大麻受体与免疫应答

大麻类物质通过与免疫细胞表面抑制性G蛋白偶联受体CB1和CB2结合 ,调节免疫细胞的功能和细胞因子的产生。大麻受体可根据组织分布不同分为中枢型和外周型两类 ,前者主要分布在脑组织中而后者主要分布在免疫细胞表面。绝大多数大麻类物质具有结合两种类型受体的能力 ,而且内源性大麻可以快速通过血脑屏障 ,提示其可能是神经 免疫轴中的活跃递质。     

Pentastomids and the immune response

Pentastomids are a class of crustacean endoparosites that, as adults, parasitize the respiratory tract of vertebrates. They have evolved some unique strategies for long-term survival in vertebrate lungs which appear to be equally useful in thwarting inflammatory responses in the tissues of intermediate hosts. In this article, John Riley outlines the possible biological roles and immunological relevance of pentastomid excretory/secretory (E/S) products that may be important to parasite survival.     

Tryptophan and the immune response

The immune system continuously modulates the balance between responsiveness to pathogens and tolerance to non-harmful antigens. The mechanisms that mediate tolerance are not well understood, but recent findings have implicated tryptophan catabolism through the kynurenine metabolic pathway as one of many mechanisms involved. The enzymes that break down tryptophan through this pathway are found in numerous cell types, including cells of the immune system. Some of these enzymes are induced by immune activation, including the rate limiting enzyme present in macrophages and dendritic cells, indoleamine 2,3-dioxygenase (IDO). It has recently been found that inhibition of IDO can result in the rejection of allogenic fetuses, suggesting that tryptophan breakdown is necessary for maintaining aspects of immune tolerance. Two theories have been proposed to explain how tryptophan catabolism facilitates tolerance. One theory posits that tryptophan breakdown suppresses T cell proliferation by dramatically reducing the supply of this critical amino acid. The other theory postulates that the downstream metabolites of tryptophan catabolism act to suppress certain immune cells, probably by pro-apoptotic mechanisms. Reconciling these disparate views is crucial to understanding immune-related tryptophan catabolism and the roles it plays in immune tolerance. In this review we examine the issue in detail, and offer additional insight provided by studies with antibodies to quinolinate, a tryptophan catabolite which is also necessary for nicotinamide adenine dinucleotide (NAD +) production. In addition to the immunomodulatory actions of tryptophan catabolites, we discuss the possible involvement of quinolinate as a means of replenishing NAD + in leucocytes, which is depleted by oxidative stress during an immune response.     

Effects of acute temperature or salinity stress on the immune response in sea cucumber, Apostichopus japonicus

Invertebrates are increasingly raised in mariculture, where it is important to monitor immune function and to minimize stresses that could suppress immunity. The activities of phagocytosis, superoxide dismutase (SOD), catalase (CAT), myeloperoxidase (MPO), and lysozyme (LSZ) were measured to evaluate the immune capacities of the sea cucumber, Apostichopus japonicus, to acute temperature changes (from 12 °C to 0 °C, 8 °C, 16 °C, 24 °C, and 32 °C for 72 h) and salinity changes (from 30‰ to 20‰, 25‰, and 35‰ for 72 h) in the laboratory. Phagocytosis was significantly affected by temperature increases in 3 h, and by salinity (25‰ and 35‰) changes in 1 h. SOD activities decreased significantly in 0.5 h to 6 h samples at 24 °C. At 32 °C, SOD activities decreased significantly in 0.5 h and 1 h exposures, and obviously increased for 12 h exposure. CAT activities decreased significantly at 24 °C for 0.5 h exposure, and increased significantly at 32 °C in 3 h to 12 h exposures. Activities of MPO increased significantly at 0 °C in 0.5 h to 6 h exposures and at 8 °C for 1 h. By contrast, activities of MPO decreased significantly in 24 °C and 32 °C treatments. In elevated-temperature treatments, activities of LSZ increased significantly except at 32 °C for 6 h to 12 h exposures. SOD activity was significantly affected by salinity change. CAT activity decreased significantly after only 1 h exposure to salinity of 20‰. Activities of MPO and LSZ showed that A. japonicus tolerates limited salinity stress. High-temperature stress had a much greater effect on the immune capacities of A. japonicus than did low-temperature and salinity stresses.     

Chaperonins and the immune response

Chaperonins are a major target of the immune response to bacteria. Infection, or immunization, with bacteria induces a strong antibody response to chaperonins, and the same proteins also provide a focus for activation of T lymphocyte subsets--including CD4, CD8 and gamma-delta T cells. The high degree of sequence conservation between prokaryotic and eukaryotic chaperonins makes them candidate antigens for models of autoimmunity based on molecular mimicry, and it is possible that the immune response to chaperonins has both protective and pathogenic potential. The interactions between chaperonins and the immune response are reviewed in this article, primarily from the perspective of intracellular bacterial infection.     

Interplay between thermal and immune ecology: effect of environmental temperature on insect immune response and energetic costs after an immune challenge

Although the study of thermoregulation in insects has shown that infected animals tend to prefer higher temperatures than healthy individuals, the immune response and energetic consequences of this preference remain unknown. We examined the effect of environmental temperature and the energetic costs associated to the activation of the immune response of Tenebrio molitor larvae following a lipopolysaccharide (LPS) challenge. We measured the effect of temperature on immune parameters including phenoloxidase (PO) activity and antibacterial responses. Further as proximal and distal costs of the immune response we determined the standard metabolic rate (SMR) and the loss of body mass (m_b), respectively. Immune response was stronger at 30 °C than was at 10 or 20 °C. While SMR at 10 and 20 °C did not differ between immune treatments, at 30 °C SMR of LPS-treated larvae was almost 25–60% higher than SMR of PBS-treated and naïve larvae. In addition, the loss in m_b was 1.9 and 4.2 times higher in LPS-treated larvae than in PBS-treated and naïve controls. The immune responses exhibited a positive correlation with temperature and both, SMR and m_b change, were sensitive to environmental temperature. These data suggest a significant effect of environmental temperature on the immune response and on the energetic costs of immunity.     

Predation risk, host immune response, and parasitism

Predation risk may affect the allocation priorities of limitingresources by potential prey. Investment in immune function shouldreceive reduced priority, when hosts are exposed to predatorsbecause of the costs of immune function. We tested this hypothesisby randomly exposing adult house sparrows, Passer domesticus,to either a cat, Felis catus, or a rabbit, Oryctolagus cuniculus,for 6 h while assessing their ability to raise a T-cell–mediatedimmune response to a challenge with phytohemagglutinin. Sparrowsexposed to a cat had a significant reduction of, on average,18% and 36% in T-cell response in two different experimentscompared with sparrows that were exposed to a rabbit. In a fieldexperiment with a barn owl, Tyto alba, or a rock dove, Columbalivia, placed next to a nest-box during laying, we found a meanreduction in T-cell–mediated immune response of 20%. Inmales, the reduction in cell-mediated immune response owingto cat exposure increased with increasing size of the badge,which is a secondary sexual character, but only during the breedingseason. In a third experiment, house sparrows were either exposedto a barn own, T. alba, or a rock dove, C. livia, and developmentof malarial infections was recorded during the following 6 weeks.Individual sparrows exposed to a predator had a higher prevalenceand intensity of Haemoproteus malarial infection than did controlindividuals. Therefore, exposure to predators reduced theirability of hosts to cope with parasitism mediated through effectson immune function.     

Tumor stress, cell death and the ensuing immune response

A cornucopia of physiological and pathological circumstances including anticancer chemotherapy and radiotherapy can induce cell death. However, the immunological consequences of tumor cell demise have remained largely elusive. The paradigm opposing 'apoptosis versus necrosis' as to their respective immunogenicity does not currently hold to predict long-term immunity. Moreover, the notion that tumor cells may be 'stressed' before death to be recognized by immune cells deserves to be underlined. 'Eat-me', 'danger' and 'killing' signals released by stressed tumor under the pressure of cytotoxic compounds may serve as links between the chemotherapy-elicited response of tumor cells and subsequent immune responses. This review will summarize the state-of-the-art of cancer immunity and describe how tumor cell death dictates the links between innate and acquired immunity.     

Dermatophytosis of the scalp: Incidence,immune response,and epidemiology

Tinea capitis remains a common infection among the pediatric population of North America. The gray patch Microsporum audouinii infections of the 1950's have been supplanted by the black dot ringworm of Trichophyton tonsurans. The clinical presentation of T. tonsurans infection is quite variable and may be related to specific host T-lymphocyte response. This dermatophytosis is most frequently incurred from contact with an infected child either directly or via a variety of fomites. Current studies indicate that an asymptomatic adult carrier state may also exist which could contribute to the morbidity of this mycosis.Part of a DissertationPresented as a part of the Everett S. Beneke Symposium in Mycology, May 27, 1988.