Integration of neuro-endocrine immune responses in defense of mucosal surfaces.
ABSTRACT Neuro-endocrine immunology, a field arising from curiosity about the mind-body connection, is evolving rapidly. From intriguing, but seemingly unexplainable observations with human infections and disease, experimental systems have been developed that provide a solid scientific basis for new understanding. There have been major efforts to understand influences of the nervous system on immune and inflammatory responses, e.g., innervation of the immune system, molecular communication pathways, and complex phenomena such as conditioning of immune responses and mechanisms of host defenses. In turn, the immune system communicates with the neuro-endocrine systems. Imbalances in the neuro-endocrine-immunologic circuitry are relevant in host defenses and in injury and repair. Examples of these themes in neuro-endocrine-immunology arise in several host-parasite models of neurogenic inflammation, immediate hypersensitivity responses, and granuloma formation. The hypothalamic-pituitary-adrenal axis and the cervical sympathetic trunk-submandibular gland axis provide important models to enhance understanding of this poorly known component of the host-parasite relationship.
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ABSTRACT: C57BL/6 mice infected with Trypanosoma cruzi, the causal agent of Chagas' disease, develop severe thymocyte depletion paralleled by an inflammatory syndrome mediated by tumor necrosis factor-alpha (TNF-alpha). The exacerbated inflammatory reaction induces the activation of hypothalamus-pituitary-adrenal (HPA) axis with the consequent release of corticosterone (CT) into the circulation as a protective response. Thymocyte apoptosis has been related to a rise in TNF-alpha and CT levels, and both mediators are increased in T. cruzi-infected C57BL/6 mice. The depletion of immature CD4(+)CD8(+) thymocytes by apoptosis following infection with the parasite was still present in mice defective in both types of TNF-receptors (double knockout). However, thymic atrophy was prevented by adrenalectomy combined with RU486 administration, demonstrating that this is a CT-driven phenomenon. Our results put emphasis on the importance of an appropriated immuno-endocrine balance during T. cruzi infection and show that functional deviations in the immuno-endocrine equilibrium have profound effects on the thymus and disease outcome.Brain Behavior and Immunity 11/2007; 21(7):890-900. · 5.61 Impact Factor
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ABSTRACT: Limited attention has been given to the role mast cells may play in periodontal diseases. Mast cells are indeed found abundantly below and within several types of mucosal epithelia. On the basis of their proteinase content, mast cells are divided into connective tissue (CT) and mucosal phenotypes. The CT phenotype contains both tryptase and chymase (MC(TC)), while the mucosal phenotype contains only tryptase (MC(T)). The in vivo significance of different mast cell phenotypes has not yet been fully established. Mast cells are able to phagocytose, process and present antigens as effectively as macrophages. Recently mast cells were found in high numbers in chronically inflamed gingival tissue taken from patients with chronic marginal periodontitis (CMP). The number of mast cells was found to be even higher in HIV(+) patients with CMP. Furthermore, mast cells also express strongly matrix metalloproteinases (MMPs), which are key enzymes in degradation of gingival extracellular matrix. Mast cells may release preformed cytokines directing local innate and adaptive immune responses. The present review will focus on possible roles for mast cells in periodontal diseases. We certainly feel that this is a key cell in inflamed periodontal tissue and its role in periodontitis needs to be revisited.Journal Of Clinical Periodontology 07/2004; 31(6):413-9. · 3.69 Impact Factor