Sympathetic nervous system--immune system interactions in young and old Fischer 344 rats.
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Aging↗
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Presentation of protective antigen to the mouse immune system: immune sequelae.
Protective antigen (PA), the major protective component of the existing vaccine, is a potent immunogen. Protective antigen in alhydrogel induced a high serum IgG titre (> log10 4) in both the C57B16 and Balb/c mouse and the predominant subclass of antibody induced was IgG1, indicating that the response to PA was predominantly Th2 directed. When plasmid DNA encoding PA was used to immunize the Balb/c mouse, a low serum IgG titre was detected (</=log10 1), which was slightly increased by boosting with plasmid DNA. However, when mice immunized with plasmid DNA were later boosted with rPA, a significant and rapid increase in titre (up to threefold) was observed. Priming mice with PA-encoding plasmid DNA may be a mechanism of enhancing and accelerating the immune response to PA.
Animals↗
Trauma: the role of the innate immune system.
Immune dysfunction can provoke (multiple) organ failure in severely injured patients. This dysfunction manifests in two forms, which follow a biphasic pattern. During the first phase, in addition to the injury by trauma, organ damage is caused by the immune system during a systemic inflammatory response. During the second phase the patient is more susceptible for sepsis due to host defence failure (immune paralysis). The pathophysiological model outlined in this review encompasses etiological factors and the contribution of the innate immune system in the end organ damage. The etiological factors can be divided into intrinsic (genetic predisposition and physiological status) and extrinsic components (type of injury or "traumaload" and surgery or "intervention load"). Of all the factors, the intervention load is the only one which, can be altered by the attending emergency physician. Adjustment of the therapeutic approach and choice of the most appropriate treatment strategy can minimize the damage caused by the immune response and prevent the development of immunological paralysis. This review provides a pathophysiological basis for the damage control concept, in which a staged approach of surgery and post-traumatic immunomonitoring have become important aspects of the treatment protocol. The innate immune system is the main objective of immunomonitoring as it has the most prominent role in organ failure after trauma. Polymorphonuclear phagocytes and monocytes are the main effector-cells of the innate immune system in the processes that lead to organ failure. These cells are controlled by cytokines, chemokines, complement factors and specific tissue signals. The contribution of tissue barrier integrity and its interaction with the innate immune system is further evaluated.
Journal Article↗
Ageing and the immune system.
Immune system alterations during ageing are complex and pleiotropic, suggestive of remodelling or altered regulation, rather than simple immune deficiency. The most dramatic changes with age occur within the T cell compartment, the arm of the immune system that protects against pathogens and tumours, consistent with the increased incidence and severity of infection and cancer in the elderly. Indeed, autopsy studies confirm infection as the major cause of death in the very old. Increased serum levels of inflammatory mediators are another hallmark of ageing, suggestive of either regulatory defects or an ongoing attack on sub-clinical neoplastic disease or infection. Qualitative changes in antibody production, including those secreted by the gut mucosal immune compartment, affect responses to foreign antigens as well as to prophylactic vaccines. Innate immunity, the first line of defence that precedes the antigen-specific T and B cell responses, also undergoes changes with age. Some of the immune effects associated with ageing are secondary to overall organismic changes, such as alterations in the viscosity of cell membranes and proteolytic cellular machinery. Evidence suggesting that immune system changes may be involved in some major age-related pathologies, such as atherosclerosis and Alzheimer's disease, will be discussed.
Aging↗
P2 purinoceptors in the immune system.
Immune cells express plasma membrane receptors for extracellular nucleotides. Both G protein-linked metabotropic and channel-forming ionotropic receptors have been described, although no P2 receptor subtype has been cloned from the immune system thus far. Metabotropic receptors have been described in human B but not T lymphocytes; they have not been found in mouse B and T cells. Ionotropic receptors seem to be ubiquitously expressed in the immune system; however, their functional properties, if not their pharmacology, appear to be different in different immune cells. Human T normal and B leukaemic lymphocytes, human macrophages, mouse B and T lymphocytes, mouse microglial and macrophage cells, and rat mast cells express ionotropic receptors that recognize ATP4- as the preferred ligand, are activated by 3'-O-(4-benzoyl)benzoyl ATP and inhibited by oxidized ATP. The pharmacological profile of ionotropic receptors expressed by different immune cells is similar, but their permeability properties may be different: the pore formed by receptors expressed by macrophages, microglial cells and mast cells is typically permeable to charged molecules of molecular mass up to 900 Da; on the contrary, that expressed by lymphocytes has a molecular cut-off of 200-300 Da. The ionotrpic receptor of immune cells is modulated by inflammatory cytokines (e.g. interleukin [IL]-2 and gamma-interferon) and is also modulated during monocyte to macrophage differentiation. Transient stimulation of the ionotropic receptor of macrophages and microglial cells elicits IL-1 beta release. Sustained activation leads to cell death, either by necrosis or apoptosis, depending on the given cell type.
Animals↗
Pulmonary clearance of Pseudomonas aeruginosa in neutropenic mice. Effects of systemic immunization.
Systemic immunization with killed Pseudomonas improves pulmonary clearance of these bacteria in normal mice. To test the effects of active systemic immunization on early pulmonary clearance of Pseudomonas in neutropenic mice, Balb/c mice were intraperitoneally immunized with 10(8) Pseudomonas or injected with saline twice weekly for 2 wk. Ten days after the last immunization, immunized and control mice received tail vein injections with either nitrogen mustard or saline daily for 3 days. Two days after the last nitrogen mustard injection, mice were intrabronchially challenged with 10(6) or 10(4) live Pseudomonas and clearance was assessed 4 h later. With the higher inoculum, immunization (neutrophil-replete and neutropenic mice) augmented pulmonary clearance. The improvement in clearance with the higher inoculum was associated with a marked increase in bronchoalveolar lavage anti-Pseudomonas IgG. However, bacteria grew in the lungs of all neutropenic mice. Immunization did not alter pulmonary clearance of the lower inoculum of Pseudomonas, and bacterial growth occurred in the neutropenic mice. Gentamicin was administered to mice 2 h after intrabronchial challenge with 10(6) Pseudomonas to determine whether its effects were additive to immunization. Gentamicin improved pulmonary clearance effected by immunization only in the neutrophil-replete mice; immunization provided no additional benefit to gentamicin in the neutropenic mice. These data show that both neutrophils and immunization contribute to Pseudomonas clearance. Immunization improves pulmonary clearance of Pseudomonas in neutropenic mice with a sufficiently high inoculum, but bacterial growth still occurs. Gentamicin treatment is effective in eliminating bacteria in this model and immunization has no additional benefit.
Agranulocytosis↗
Systemic immunity.
Systemic acquired resistance (SAR) provides enhanced, long-lasting systemic immunity to secondary infection by a range of biotrophic, hemibiotrophic and necrotrophic pathogens that have diverse modes of infection. Considerable effort has focussed on the conserved central positive regulator of SAR, NON-EXPRESSOR OF PATHOGENESIS-RELATED1 (NPR1), and its control by changes in cellular redox potential. Recently, genetic and genomic approaches have highlighted a critical role for nucleocytoplasmic communication and protein secretion in establishing effective systemic immunity. Identification of the mobile signals and the mechanisms by which they are perceived in distal tissues remains challenging, but emerging evidence suggests that signal translocation uses lipid-derived (possibly jasmonate-based) signals and lipid-binding chaperones. Furthermore, the demonstration that autophagy interdicts and inactivates a systemic cell death signal adds further complexity to elucidating how mobile signals are decoded and transduced for effective immunity.
Gene Expression Regulation, Plant↗
Psychoneuroimmunology: interactions between central nervous system and immune system.
Psychoneuroimmunology, a rapidly developing field, has to do with the complex bidirectional interactions between the central nervous system and the immune system. Neuroendocrine influences modulate immune function, and there is feedback from the immune system to the brain. CNS-immune interaction appears to play a role in psychosocial influences on immunologically resisted and mediated diseases. With the growing evidence now at hand, over 30 "postulates" can be proposed for specific implications of CNS-immune interaction.
Animals↗
In vitro effect of biogenic amines on the hormone content of immune cells of the peritoneal fluid and thymus. Is there a hormonal network inside the immune system?
Immune cells contain different hormones and hormone-like molecules, such as insulin, endorphin, triiodothyronine (T3) histamine, serotonin. In earlier in vitro experiments insulin down-regulated histamine, serotonin and T3 content of thymus cells. Now we studied the effect of biogenic amines on the endorphin, T3, serotonin and histamine content of rat peritoneal and thymic cells. Cells were obtained from male rats of 100g body weight. 100 ng/ml serotonin or 300 ng/ml histamine was added for 30 min. After that the cells were prepared for flow cytometric analysis with antibodies to endorphin, T3, histamine and serotonin as primary antibodies and anti-rabbit IgG as secondary antibody. Finishing the measurements the cells were also studied by confocal microscopy. T3 concentration (binding of anti-T3 antibody) increased in peritoneal mast cells after serotonin treatment and in the monocyte-macrophage-granulocyte group after histamine treatment. Thymocytes' T3 content radically decreased after both treatments. Serotonin and histamine treatment also radically reduced the amine content of each other. Endorphin level was resistant to hormonal treatments. The results call attention to a possible hormonal network inside the immune system in which hormones produced by the immune cells themselves can influence each other.
Animals↗
Stress-induced suppression of the cellular immune reactions: on the neuroendocrine control of the immune system.
Immune competence is considered as a state of equilibrium between humoral and cellular immunity. This notion fits well with the functionally antagonistic cytokine profiles in cell groups of CD4(+)-helper cells as described by Mosmann and Coffman. The Th-1 cells release mainly IL-2, IL-12 and IFN gamma and thereby stimulate the cellular immune reactions. Conversely, the Th-2 cells produce predominantly IL-4, IL-6 and IL-10, thus enhancing humoral immune reactions. Recently, it has been shown that the lymphokine profiles in Th-2 are linked to changes of the humoral balance between cortisol and dehydroepiandrosterone. These studies show that there exist states of equilibrium between T- and B-cell-mediated immune reactions, which may selectively be altered to the disadvantage of the T-cellular immunity by a stress-induced enhancement of cortisol release. In an attempt to restitute stress-induced immunosuppression, a dampening of the cortisol release hormone in the hypothalamus should, therefore, be of primary importance.
Animals↗
Receptor-mediated interaction between the sympathetic nervous system and immune system in inflammation.
The sympathetic nervous system plays a central role in establishing communication between the central nervous system and the immune system during inflammation. Inflammation activates the sympathetic nervous system, which causes release of the transmitters of the sympathetic nervous system in the periphery. The transmitters of the sympathetic nervous system are the catecholamines noradrenaline and adrenaline and the purines ATP, adenosine, and inosine. Once these transmitters are released, they stimulate both presynaptic receptors on nerve terminals and post-synaptic receptors on immune cells. The receptors that are sensitive to catecholamines are termed adrenoceptors, whereas the receptors that bind purines are called purinoceptors. Stimulation of the presynaptic receptors exerts an autoregulatory effect on the release of transmitters. Ligation of the postsynaptic receptors on inflammatory cells modulates the inflammatory activities of these cells. The present review summarizes some of the most important aspects of the current state of knowledge about the interactions between the sympathetic nervous system and the immune system during inflammation with a special emphasis on the role of adreno and purinoceptors.
Animals↗
[How are psychological processes, the neuroendocrine system and immune system integrated?].
This short overview shows that there are bidirectional interactions between the central nervous system (CNS) and the immune system and deals with their anatomical and physiological correlates. Moreover, a number of immunological findings related to exogenous stress, depressive disorders and schizophrenias are discussed. An attempt is made to cautiously interpret the data presented and to demonstrate that the field of psychoneuroimmunology provides plenty of rewarding challenges for future research.
Antibody Formation↗
The brain and the immune system: an intact immune system is essential for the manifestation of withdrawal in opiate addicted rats.
Gamma irradiation (500 rad) is often used to suppress the immune system in mice, rats and man. Recently, it was shown that irradiation prior to chronic morphine treatment, dramatically reduces the severity of naloxone-precipitated withdrawal in morphine-dependent animals. In the present study adoptive transfer of 2-6 x 10(8) splenocytes to irradiated rats prior to chronic morphine treatment restored the severity of all withdrawal signs precipitated by naloxone. In contrast, adoptive transfer of fractionated splenocyte subpopulations only partially restored withdrawal severity; and transfer of irradiated splenocytes, red blood cells or diluted numbers of normal splenocytes did not have any observed restorative effect. These findings suggest that specific cellular activities or factors derived from lymphoid cells are required for the expression of opiate withdrawal.
Animals↗
[Development of the immune system].
Immune protection in vertebrates is provided by a dual system: the cellular immune response, mediated by T lymphocytes and the humoral immune response, mediated by B lymphocytes. These lymphocytes develop immunocompetence in the primary lymphoid organs: thymus, for the T lymphocytes and bursa of Fabricius (in birds), on its equivalent (in mammals), for B lymphocytes. The crucial period during which thymus and bursa influence the immunological development is the embryonic and early postnatal life. Hemopoietic stem cells home to these primary lymphoid organs during well-defined periods of colonization. Under the influence of thymic and bursal microenvironments, they become oriented respectively toward the T or B cell differentiation pathway. They acquire various membrane antigens and an antigen receptor. T lymphocytes also learn to recognize self-antigens (antigens encoded by the Major Histocompatibility Complex). T and B lymphocytes then colonize respectively T-dependent and B-dependent areas of secondary lymphoid organs where they become functional. Some immune deficiencies result from a defect in development which can affect selectively T or B lymphocytes or both systems in case of severe combined immunodeficiency disorders.
Animals↗
Virus-associated immunopathology: animal models and implications for human disease. 1. Effects of viruses on the immune system, immune-complex diseases, and antibody-mediated immunologic injury.
The tissue damage caused by virus infection has been traditionally explained by the ability of viruses to multiply in cells and thereby injure or destroy them. Recent evidence suggests, however, that lesions may also be caused by the host's immune response to viral antigens and that the immune system itself may be perturbed by some viruses. This memorandum reviews recent developments in viral immunopathology, with special reference to animal model systems, and indicates the possible relevance of the new concepts and techniques for certain diseases of man. Certain viruses, notably the leukaemia viruses and some of those causing persistent infections, depress the host's ability to mount an antibody response to antigens, while other viruses may enhance the antibody response. Cell-mediated immunity may also be depressed. Another immunopathological manifestation of virus infection is immune-complex disease. When viruses or their antigens persist in the circulation they combine with specific antibody, and the resulting complexes lodge in various sites, especially the kidney. Further combination with complement leads to the release of tissue-damaging substances. A third condition associated with virus infection is antibody-mediated immunologic injury. Both oncogenic and non-oncogenic viruses frequently induce new antigens on the surface of the cells they invade. When antibody attaches to these antigens in the presence of complement, the cells are destroyed.
Animals↗
[Neuroimmunomodulation. The bi- and unilateral correlations between the nervous system and the immune system].
The nervous system-immune system relationships, namely the modulatory effects of the former upon the latter and vice versa, have been considered both in physiological and pathological conditions. The nervous system communicates with the immune system in two biochemical ways, by means of neurohormones and neurotransmitters, using anatomical and functional pathways related to the pituitary system (the manifold endocrine axes between hypophysis and peripheral endocrine glands) and autonomic system (especially the orthosympathetic one, and to much lesser extent the parasympathetic system). The immune system is able to modulate some nervous functions via cytokines, peptidic molecules produced by immunocytes, that can also be secreted in certain conditions by neural cells, such as astrocytes, microgliocytes and even neurons. The knowledge of physiology of the neuroimmunomodulation and related pathological changes may be very useful for understanding the pathogenesis and the pathophysiology of neuroimmunological diseases, and for their diagnosis and treatment.
Animals↗
[Intestine-associated immune system. Local immune response--systemic tolerance].
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Cell Movement↗
Receptor-mediated local fine-tuning by noradrenergic innervation of neuroendocrine and immune systems.
Immune responses can be modulated by noradrenergic input at (1) hypothalamic (CRF and ACTH release), (2) immune cell (cytokine production), and (3) adrenal cortex (glucocorticoid production) level. Elucitating the basic mechanisms responsible for immunological responses and diseases may be helpful in developing therapeutic approaches for many disorders, such as autoimmune diseases.
Adrenal Cortex↗