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At least 19 recordsLinked to original sources
PubMed2001

Lymphocytes in the bronchoalveolar space reenter the lung tissue by means of the alveolar epithelium, migrate to regional lymph nodes, and subsequently rejoin the systemic immune system.

Lymphocytes in the bronchoalveolar space are routinely obtained and examined in lung diseases such as asthma or sarcoidosis. In a pig model, labeled lymphocytes were found in regional lymph nodes after intrabronchial instillation, indicating that reentry of lymphocytes from the bronchoalveolar space into the body is possible. In the present study, the route and kinetics of the reentry of bronchoalveolar lymphocytes were investigated in a congenic rat model using immunohistochemistry on cryostat and semithin sections and confocal laser scanning microscopy. As early as 15 min after intratracheal instillation lymphocytes were found to leave the bronchoalveolar space by transmigration through alveolar but not bronchial epithelium and were observed in interstitial alveolar tissue. At 6 hr after intratracheal instillation, T and B lymphocytes appeared in the draining lymph nodes of the lung with an increase after 24 and 48 hr. The kinetic pattern clearly differed in nondraining lymph nodes and other organs. After 6 hr, only single cells were found in nondraining lymph nodes, spleen, and blood with a slight increase after 24 hr, and only occasionally were single cells seen in the liver, thymus, or Peyer's patches 24 and 48 hr after instillation. In conclusion, T and B lymphocytes can leave the alveolar space by reentry into the lung tissue through alveolar epithelium. They reach regional lymph nodes by means of lymphatic vessels and are then distributed all over the body to rejoin the systemic immune system. Coming into contact with environmental antigens, these lymphocytes could perform an important function in the lung immune system and might be a target for inhalative therapy.

Animals↗
PubMed1989

Psychoneuroimmunology for the psychoneuroendocrinologist: a review of animal studies of nervous system-immune system interactions.

Evidence for interactions between the nervous and immune systems arises from a number of experimental observations: the behavioral conditioning of immune responses, the effects of stimulation or lesion of brain sites on immune system function, the effects of stressors on immune responses and tumor growth, and physiological and neurochemical changes in the brain during immune responses. The links between the nervous and immune systems probably include glucocorticoids secreted from the adrenal gland, catecholamines and neuropeptides secreted by sympathetic terminals and the adrenal medulla, certain pituitary and gonadal hormones, and polypeptides produced by cells of the immune system. The effect of glucocorticoids is not exclusively immunosuppressive, nor is it adequate to explain all the effects of stress. The effects of opiates on immune function are complex; in vitro, endogenous opiates most often facilitate immune activity, but in vivo, opiates appear to inhibit immune responses and impair tumor rejection. The in vitro effects are rarely prevented by naloxone pretreatment and appear to require the integrity of the C- rather than the N-terminal of beta-endorphin, suggesting a nonopiate character. Infections or the administration of antigens increase circulating concentrations of glucocorticoids and activate cerebral catecholaminergic metabolism, especially in the hypothalamus. These responses suggest that challenges to the immune system are physiologic stressors. Interleukin-1 (IL-1) produced by immune cells may be the mediator of these effects, thus acting as an "immunoneurotransmitter". The cerebral responses suggest that the brain can monitor the progress of immune responses. IL-1 and the glucocorticoids together may form a regulatory feedback mechanism for immune responses.

Animals↗
PubMed1994

Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences.

Psychoneuroimmunology is a relatively new discipline which deals with CNS-immune system interactions. The evidence for such interactions was reviewed, as was the neuroendocrinologic response to stress. Recent evidence indicates that the behavioral, nervous system, and neuroendocrine responses to stress are mediated by hypothalamic CRF, which acts on both the sympathetic nervous system and the HPA axis, resulting in increased levels of corticosteroids, catecholamines, and certain opiates, substances which are generally immunosuppressive. Concentrations of growth hormone and prolactin, which are immunoenhancing, are elevated early during the response to stress but are later suppressed. Although several other neuromediators may also be released with stress, the net effect of a variety of acute stressors is down regulation of the immune system function. In the following minireview, I consider whether stress alters the resistance of the host to infection as well as the immunomodulatory effects of released immune system mediators on the brain.

Animals↗
PubMed2000

Special feature for the Olympics: effects of exercise on the immune system: exercise effects on systemic immunity.

Heavy exertion has acute and chronic influences on systemic immunity. In the resting state, the immune systems of athletes and non-athletes are more similar than disparate with the exception of NK cell activity, which tends to be elevated in athletes. Many components of the immune system exhibit adverse change after prolonged, heavy exertion. These immune changes occur in several compartments of the immune system and body (e.g. the skin, upper respiratory tract mucosal tissue, lung, blood and muscle). Although still open to interpretation, most exercise immunologists believe that during this 'open window' of impaired immunity (which may last between 3 and 72 h, depending on the immune measure) viruses and bacteria may gain a foothold, increasing the risk of subclinical and clinical infection. The infection risk may be amplified when other factors related to immune function are present, including exposure to novel pathogens during travel, lack of sleep, severe mental stress, malnutrition or weight loss.

Cytokines↗
PubMed1988

Nervous system-immune system interactions: an overview.

Links between the nervous and immune systems are suggested by the behavioural conditioning of immunosuppression, the effects of brain lesions and stress on immune responses, and physiological and chemical changes in the brain during immune responses. These links probably include glucocorticoids secreted from the adrenal gland, catecholamines and neuropeptides secreted by sympathetic terminals and the adrenal medulla, certain pituitary hormones, and polypeptides produced by cells of the immune system. The effect of glucocorticoids is not exclusively immunosuppressive, nor is it adequate to explain all the effects of stress. In vitro endogenous opiates facilitate lymphocyte proliferation and natural killer (NK) cell activity, but in vivo opiates appear to inhibit immune responses and impair tumour rejection. Increases of circulating glucocorticoids after infection and an apparent activation of cerebral catecholaminergic cells indicate that challenges to the immune system are interpreted physiologically as stressors. Moreover, they suggest that the brain may be able to monitor the progress of immune responses. Certain protein factors produced by the thymus gland (thymosins) may be able to counter stress-induced deficits in immunological responses.

Animals↗
PubMed2002

F4 receptor-independent priming of the systemic immune system of pigs by low oral doses of F4 fimbriae.

Oral administration of F4 fimbriae of Escherichia coli induces intestinal mucosal immune responses in F4 receptor-positive (F4R(+)) pigs, but not in F4R(-) pigs. We examined whether F4 fimbriae in F4R(-) animals behave like a food antigen and can induce oral tolerance. Therefore, F4R(+) and F4R(-) pigs were fed 2mg of F4 and challenged i.m. to evaluate the effect of oral F4 on the systemic immune system. As control antigen, two different oral doses (2 and 600 mg) of OVA were used. Thirty days after the i.m. OVA challenge, the OVA-specific serum IgG titre in 600 mg-fed pigs was lower than that in non-fed animals, indicating that tolerance was induced. Conversely, in the 2mg-fed pigs a rapid increase of OVA-specific IgG with higher titres than those in non-fed pigs was seen following challenge, indicating a priming of the systemic immune system. A similar priming was seen in both F4-fed F4R(-) and F4R(+) pigs. Upon challenge, non-fed pigs displayed a primary immune response with a slow increase of F4-specific serum IgG, whereas F4-fed F4R(-) and F4R(+) pigs showed secondary responses with a rapid increase of serum IgG. This was expected in F4R(+) pigs, as in these animals oral F4 induces F4-specific antibody-secreting cells in the spleen, suggesting a priming of the systemic immune system. However, also the F4-fed F4R(-) pigs displayed a secondary response, despite the failure to detect a response upon oral F4 administration. These findings suggest that the F4 antigen, at a dose of 2 mg, behaves like a common food antigen in F4R(-) pigs, namely it induces a systemic priming.

Animals↗
PubMed1987

Salmonella typhimurium aroA mutants as carriers of the Escherichia coli heat-labile enterotoxin B subunit to the murine secretory and systemic immune systems.

We investigated the ability of Salmonella typhimurium vaccines to deliver heterologous antigens to the systemic and secretory immune systems of the mouse, while retaining their immunogenicity against salmonellosis. S. typhimurium SL3261, an avirulent aroA mutant, or SL3261 carrying plasmid pBRD026, a pBR322 derivative encoding the gene for Escherichia coli LT-B were used to immunize BALB/c mice orally. Both immunizing strains invaded the mononuclear phagocyte system of the mice, grew slowly until approximately day 14 post-infection, and then were rapidly cleared. No salmonellae were detected in livers, spleens, mesenteric lymph nodes or Peyer's patches by day 42. Mice immunized with either strain and challenged orally with the virulent parent strain, SL1344, several weeks after clearing the immunizing organism, were protected against the lethal S. typhimurium infection. Mice infected with SL3261 (pBRD026) developed substantial levels of IgG and IgA anti-LT-B antibodies 14 days post-infection in both serum and gut samples. The sera neutralized the effects of LT in an in vitro Vero cell assay. Thus, aroA mutants of S. typhimurium can deliver a heterologous antigen from a different enteric pathogen to the murine systemic and secretory immune systems without altering their efficacy against salmonellosis.

Animals↗
PubMed2006

In vivo effects of ELF MFs on collagen synthesis, free radical processes, natural antioxidant system, respiratory burst system, immune system activities, and electrolytes in the skin, plasma, spleen, lung, kidney, and brain tissues.

In this study, the results related with the effects of 50 Hz, 0.2 mT-3 mT MFs exposures on collagen synthesis, epilepsy, electrolytes, lipid peroxidation (MDA), Nitric Oxide (NOx), respiratory burst system (MPO), antioxidant defense system (GSH), and immune system (NK cell activity) in spleen, skin, lung, kidney, brain, and plasma tissues performed at Gazi Biophysics Department are reviewed. Our studies indicate that ELF MFs had effects on the tissues examined.

Animals↗
PubMedDate not supplied

Nervous system-immune system communication.

This essay is based on the premise that certain individuals may have a biologically determined propensity to respond to infection that is manifested by the development of disease such as chronic fatigue syndrome; the sequence of events that leads to this response involves the immune system. Biochemical pathways between the immune and nervous systems are reviewed, and the role of various products in the systemic circulation, including interleukin-1, pituitary hormone, and catecholamines, is highlighted. This premise could be tested by measuring levels of these substances in carefully selected patients and controls.

Animals↗
PubMed2003

The war between the malaria parasite and the immune system: immunity, immunoregulation and immunopathology.

Throughout history malaria has proved to be a significant threat to human health. Between 300 and 500 million clinical cases occur each year worldwide, approximately 2 million of which are fatal, primarily in children. The vast majority of malaria-related deaths are due to infection with Plasmodium falciparum; P. vivax causes severe febrile illness but is rarely fatal. Following repeated exposure to infection, people living in malaria endemic areas gradually acquire mechanisms to limit the inflammatory response to the parasite that causes the acute febrile symptoms (clinical immunity) as well as mechanisms to kill parasites or inhibit parasite replication (antiparasite immunity). Children, who have yet to develop protective immune mechanisms are thus at greater risk of clinical malaria, severe disease and death than adults. However, two epidemiological observations indicate that this is, perhaps, an oversimplified model. Firstly, cerebral malaria - a common manifestation of severe malaria - typically occurs in children who have already acquired a significant degree of antimalarial immunity, as evidenced by lower mean parasite densities and resistance to severe anaemia. One potential explanation is that cerebral malaria is, in part, an immune-mediated disease in which immunological priming occurs during first infection, eventually leading to immunopathology on re-infection. Secondly, among travelers from nonendemic areas, severe malaria is more common - and death rates are higher - in adults than in children. If severe malaria is an immune-mediated disease, what might be priming the immune system of adults from nonendemic areas to cause immunopathology during their first malaria infection, and how do adults from endemic areas avoid severe immunopathology? In this review we consider the role of innate and adaptive immune responses in terms of (i) protection from clinical malaria (ii) their potential role in immunopathology and (iii) the subsequent development of clinical immunity. We conclude by proposing a model of antimalarial immunity which integrates both the immunological and epidemiological data collected to date.

Adult↗
PubMed1993

[The mucosa-associated immune system--immune defense in the gastrointestinal tract].

The intestinal immune system has to protect the mucosa against microbial and toxic agents. This is achieved by elimination of potential antigens, which are inhibited to adhere and to invade the mucosa. Thus, induction of inflammatory processes is prevented. Elimination of antigens is mediated by the secretion and transport of IgA (and especially IgA2) to the lumen of the gut. There, IgA is the most efficient part of the so-called "mucosa block". The composition of mononuclear cells in the lamina propria exhibits the preference of a memory T cell type that is able to provide help for B cells. If IgA-mediated immune response proves not to be sufficient, IgG-mediated inflammatory processes are induced within the mucosa. The role of cytotoxic T cells and, moreover, the biological function of intraepithelial lymphocytes are still controversial.

Animals↗
PubMedDate not supplied

[Prevalence of CD56 /NCAM molecule in nervous system immune system and endocrine glands--accidental coincidence?].

The authors presented advances in the research on isoform of neural cell adhesion molecule CD56/NCAM, which appears to raise interest not only in biology, but also in clinical medicine. Molecular aspects of its synthesis have been presented and universal features of this protein have been underlined. It appears to play an important role in body homeostasis and especially in the interactions between neural, immune and endocrine systems. In relation to the immune system there are data suggesting significance of local protective and regulatory mechanisms in the liver linked to so called NKT (CD56+) cells. Main sites of prevalence of CD56/NCAM have been indicated both in physiology and pathology, especially in malignancy. CD56/NCAM incidence is common in tumors of neuroectodermal and endocrine origin. Besides it may be expressed on cells of several hemopoetic neoplasms originated both, from lymphoid and myeloid lineage. Moreover, the attention was paid to CD56/ NCAM expression in atypical sites as for example on epithelia of bile ducts in children with extrahepatic biliary atresia and on cells of pancreatic ducts in the course of chronic pancreatitis.

Adrenal Glands↗
PubMed1988

The central nervous system--immune system relationship.

Research investigating the pathogenesis of schizophrenia has demonstrated that cellular immune reactions, such as those that occur in known autoimmune diseases, may participate in producing alterations of the central nervous system. Furthermore, epidemiologic studies of immune-mediated diseases have suggested that activation of the central nervous system by stressful stimuli may be capable of influencing the function of the immune system. In support of that interaction, research using animal models of stress has provided valuable information as to the effect of stress on basic immune function and susceptibility to infectious disease. Possible hormonal and direct mechanisms of the central nervous system-immune system interaction have been proposed.

Autoimmune Diseases↗
PubMed2004

Evidence for systemic immune system alterations in sporadic amyotrophic lateral sclerosis (sALS).

Sporadic amyotrophic lateral sclerosis (sALS) is a progressive neuroinflammatory disease of spinal cord motor neurons of unclear etiology. Blood from 38 patients with sALS, 28 aged-match controls, and 25 Alzheimer's disease (AD) patients were evaluated and activated monocyte/macrophages were observed in all patients with sALS and AD; the degree of activation was directly related to the rate of sALS disease progression. Other parameters of T-cell activation and immune globulin levels showed similar disease associated changes. These data are consistent with a disease model previously suggested for AD, wherein systemic immunologic activation plays an active role in sALS.

Adult↗
PubMed2001

Sendai virus fusion protein mediates simultaneous induction of MHC class I/II-dependent mucosal and systemic immune responses via the nasopharyngeal-associated lymphoreticular tissue immune system.

Nasal administration of Ags using a novel hybrid Ag delivery vehicle composed of envelope glycoproteins of Sendai virus on the surface of liposome membranes (fusogenic liposome) efficiently delivered Ags to Ag-sampling M cells in nasopharyngeal-associated lymphoreticular tissue. Additionally, fusogenic liposomes also effectively delivered the Ags into epithelial cells and macrophages in nasopharyngeal-associated lymphoreticular tissue and nasal passages. In vitro Ag presentation assays clearly showed that fusogenic liposomes effectively presented encapsulated Ags via the MHC class II-dependent pathway of epithelial cells as well as macrophages. Fusogenic liposomes also have an adjuvant activity against mucosal epithelial cells to enhance MHC class II expression. According to these high delivery and adjuvant activities of fusogenic liposomes, nasal immunization with OVA-encapsulated fusogenic liposomes induced high levels of OVA-specific CD4(+) Th1 and Th2 cell responses. Furthermore, Ag-specific CTL responses and Ab productions were also elicited at both mucosal and systemic sites by nasal immunization with Ag-encapsulated fusogenic liposomes. These results indicate that fusogenic liposome is a versatile and effective system for the stimulation of Ag-specific immune responses at both mucosal and systemic compartments.

Administration, Intranasal↗