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Results for “Immune function”

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At least 1,657 records · Page 92Linked to original sources
PubMed2006

The comparison of changes in behavior, neurochemistry, endocrine, and immune functions after different routes, doses and durations of administrations of IL-1beta in rats.

BACKGROUND: Increased interleukin-1beta (IL-1) in the brain and periphery has been associated with neurodegenerative and psychiatric disorders. However, results from different IL-1 sources, administrating routes, doses and treatment duration were inconsistent and confused. The neuroendocrine-immune mechanism by which IL-1-induced behavioral changes occur is still unclear. METHODS: In the present study, the acute and sub-chronic effects of rat recombinant IL-1, following either intraperitoneal (ip) or intracerebroventricular (icv) injection, were studied on the behavior, corticosterone secretion, peripheral inflammatory responses and brain monoamines. RESULTS: In the open field apparatus, IL-1 (ip) increased locomotor activity but decreased the activity following icv administration. IL-1 had a greater anxiogenic effect in the elevated plus maze after icv than after ip administration. In the Morris water maze spatial memory was only impaired following sub-chronic and icv administration. Both acute and sub-chronic IL-1 increased the serum corticosterone concentration and decreased the release of the anti-inflammatory cytokine IL-10 from whole blood cultures. However, centrally administered IL-1 increased, while peripherally administered decreased, the release of PGE2 from blood cultures. After sub-chronic administration, the noradrenaline concentration was decreased in several limbic regions, while the turnovers of serotonin and dopamine were increased. DISCUSSION: These results suggest that 1) IL-1 effects depended on the dose, route and duration of administration, and 2) IL-1 enhances the responsiveness of rats to stressful environmental stimuli. In addition, the sub-chronic administration of IL-1 induces behavioral, neurotransmitter, hormonal and immune changes that may be causally implicated in the mechanism of some of psychiatric disorders such as depression.

Animals↗
PubMed1993

Glutamine in parenteral solutions enhances intestinal mucosal immune function in rats.

Biliary secretory immunoglobulin A (sIgA) and proportions of IgA+ plasma cells, helper T cells, and suppressor/cytotoxic T cells in intestinal tissue were lower in rats receiving a standard total parenteral nutrition (TPN) solution than in those receiving TPN enriched with glutamine. Parenteral solutions supplemented with glutamine may preserve the ability of intestinal immune tissue to produce sIgA-synthesizing plasma cells following antigenic stimulation.

Animals↗
PubMed2004

Regulation of immune function by calorie restriction and cyclophosphamide treatment in lupus-prone NZB/NZW F1 mice.

We compared the effects of calorie restriction (CR) and cyclophosphamide (CTX) on the progression of lupus nephritis and immunological changes in NZB/NZW F1 mice. Ad libitum (AL)/CTX and CR delayed onset of proteinuria and significantly decreased serum levels of anti-dsDNA, anti-histone, and circulating immune complex antibodies. CTX and CR prevented the increase in and activation of B cells, the decline in CD8(+) T cells, and maintained a higher proportion of naïve CD4(+) and CD8(+) cells. MHC class I antigen and LFA-1 expression on CD8(+) T cells and MHC class II antigen on B cells were also decreased. AL/CTX and CR prevented the increase in production of IL-10 and up-regulated IL-2 production in T cells ex vivo. We concluded that both CR and CTX can delay the onset of autoimmune disease, in part by maintaining higher numbers of naïve T cells and the immune responsiveness of T cells and decreasing the proportion of B cells.

Animals↗
PubMed1979

Studies of immune functions of patients with systemic lupus erythematosus. Complement-dependent immunoglobulin M anti-thymus-derived cell antibodies preferentially inactivate suppressor cells.

Patients with systemic lupus erythematosus (SLE) produce excessive amounts of autoantibodies. It has also been demonstrated in several systems that such patients have a relative loss of suppressor thymus-derived (T) cells that inhibit the immune response. This loss of suppressor cells has been suggested as one of the causes of the excessive production of antibodies in patients with SLE. In the present report we have tested the hypothesis that anti-T-cell antibodies found in the plasma of some patients with SLE preferentially kill suppressor cells. T cells from normal individuals can be activated by concanavalin A to develop suppressor cell activity. We therefore cultured normal T cells together with concanavalin A in the presence of plasma or plasma fractions from patients with SLE. We found that plasma from patients with active SLE, in which anti-T-cell antibodies were present, inhibited the development of suppressor activity in such cultures. In contrast, plasma from other active patients and patients with inactive SLE, in which no anti-T-cell antibodies could be detected, failed to block the development of such suppressor activity. Absorption of the plasma that contained anti-T-cell antibodies with T cell, but not non-T cells, could eliminate the suppressor-inhibiting activity of the SLE plasma that contained anti-T-cell antibodies. The immunoglobulin (Ig)M, but not the IgG, fraction of the plasma was shown to possess the inhibiting property and complement was found to be necessary for the effect of such anti-T-cell antibodies. We also demonstrated that exposure of normal T cells to such anti-T-cell antibodies and complement did not affect another population of T cells that could proliferate in response to mitogens.Thus, certain patients with SLE have in their plasma an antibody of the IgM class that can selectively eliminate a population of T cells capable of developing suppressor function. The loss of suppressor T cells in patients with SLE may be the result of the effects of such antibody activity in vivo.

Adult↗
PubMed2000

Differential production of prostaglandin E(2) in male and female mice subjected to thermal injury contributes to the gender difference in immune function: possible role for 15-hydroxyprostaglandin dehydrogenase.

We have previously reported a macrophage-mediated gender difference in postburn immunosuppression, which was dependent upon elevated levels of circulating 17beta-estradiol (E(2)) and, in part, interleukin-6. Herein we examined the role of prostaglandin E(2) (PGE(2)), a potent suppressor of cell-mediated immunity. Circulating levels of PGE(2) were significantly elevated in females but not males at 10 days postburn (P < 0.01), and indomethacin treatment fully restored the delayed-type hypersensitivity and splenocyte proliferative responses of thermally injured females. While there was no difference in cyclooxygenase-2 protein expression in the lungs and liver of thermally injured male and female mice, there was a marked decrease in the protein expression of 15-hydroxyprostaglandin dehydrogenase in females. These data demonstrate that PGE(2) is a critical mediator of immunosuppression in thermally injured female mice and that the increase in circulating PGE(2) is derived, in part, from decreased degradation and clearance of PGE(2).

Animals↗
PubMed1983

Effect of nonsteroidal antiinflammatory drugs on immune function.

Nonsteroidal antiinflammatory drugs (NSAID) have been thought to act by inhibiting the production of prostaglandins. Until recently, prostaglandins have been considered to be mainly proinflammatory compounds, responsible for pain, increased blood flow, and edema. It has more lately been realized that prostaglandins, particularly PGE2, have important immunoregulatory properties. Thus NSAID, by inhibiting PGE2 production, modulate immune responses in vitro and in vivo. One or more of these immunomodulating effects of NSAID may play a role in their efficacy as arthritis medications. The purpose of this paper is to review the immunologic role of PGE2 and the immunologic effects of NSAID.

Adult↗
PubMed2003

Alterations of immune functions in barrier disrupted skin by UVB irradiation.

BACKGROUND: While immunologic events elicited by acute barrier disruption or UVB irradiation have been studied in detail, the biological sequel of multiple insults to the skin is not well understood. OBJECTIVE: Since the skin would receive a variety of simultaneous stimuli in daily life, we tested the effects of sequential treatments with barrier disruption and UVB exposure on skin immunity. METHODS: Earlobes of BALB/c mice received tape-stripping and subsequently low-dose UVB exposure. Control mice were treated with either tape-stripping or UVB. The expression of surface markers and cytokine production in Langerhans cells and keratinocytes and the elicitation response of contact hypersensitivity were compared. RESULTS: By flow cytometry, tape-stripping augmented the expression of MHC class II, CD54, CD80, CD86 and CD40 on Langerhans cells, whereas UVB decreased the expression of some of these molecules. Combination of tape-stripping and UVB induced largely intermediate levels between these two. Upon stimulation with L cells expressing CD40L, Langerhans cells from tape-stripped and UVB-irradiated earlobes strongly transcribed mRNA for interleukin-1beta compared to each treatment. In keratinocytes, tape-stripping or UVB slightly upregulated tumor necrosis factor-alpha and interleukin-1alpha production at both mRNA and protein levels, whereas these two treatments synergistically increased the production of these cytokines. The in vitro hapten-presenting ability of Langerhans cells to trinitrophenyl-immune lymph node T cells ranked first in tape-stripping, second in tape-stripping plus UVB and third in UVB, and so did the intensity of elicitation responses in contact hypersensitivity to a hapten, picryl chloride. CONCLUSION: It is suggested that barrier disruption and UVB antagonize with each other in contact hypersensitivity as a reflection of their effects on Langerhans cell antigen-presenting function, but they synergize in cytokine production by both Langerhans cells and keratinocytes.

Animals↗
PubMedDate not supplied

Impact of polychlorinated biphenyls (PCBs) on the immune function of fish: age as a variable in determining adverse outcome.

Polychlorinated biphenyls (PCBs) are a major contaminant of global extent in water resources and aquatic biota. Due to its high lipid solubility, PCBs fail to be degraded and, therefore, continue to bioaccumulate throughout the environment and food chain. To determine the impact of PCBs on the immune system of aged and juvenile Japanese medaka (Oryzias latipes), fish were injected with the coplanar PCB congener 126 and examined after 3 and 14 days. PCB 126 produced oxidative stress in both age groups of fish 14 days post-injection; however, juvenile medaka appeared more susceptible than aged fish. Humoral immunity, as determined by antibody forming cell (AFC) numbers, was significantly depressed for up to 14 days post-injection in both age groups. These results demonstrate the sensitivity of the fish immune response for predicting PCB-induced immunotoxicity and identify age as a variable in determining adverse outcome.

Age Factors↗
PubMed2002

Immune function of the decoy receptor osteoprotegerin.

Osteoprotegerin (OPG) is a member of the tumor necrosis factor receptor (TNFR) superfamily. OPG has an important function as a protector of bone, demonstrated by the fact that OPG(-/-) mice have severe osteoporosis. OPG acts as a decoy receptor, binding to RANK ligand (RANKL), thus preventing the interaction between receptor activator of NF-kappaB (RANK) and RANKL. This interaction is required for the development of functionally active osteoclasts. Osteoclasts are cells of the monocytic lineage that are responsible for bone resportion. Furthermore, as well as being an important player in the regulation of bone metabolism, OPG also has a role in the regulation of the immune response. Dendritic cells (DCs) express RANK and T cells express RANKL. The ligation of RANK by RANKL can activate both T cells and DCs. Furthermore, both B cells and DCs secrete OPG, and this secretion is regulated by the CD40 receptor. OPG(-/-) mice have B-cell developmental defects. Also, DCs isolated from OPG(-/-) mice more efficiently present antigen in vitro and secrete elevated amounts of inflammatory cytokines when stimulated with bacterial products, or soluble RANKL in vitro. Taken together, this suggests that OPG plays an important role in the immune response regulating the interactions between T cells and DCs.

Animals↗
PubMed1989

Transgenic HLA-DR alpha faithfully reconstitutes IE-controlled immune functions and induces cross-tolerance to E alpha in E alpha 0 mutant mice.

We have constructed transgenic mice that express the human class II MHC molecule HLA-DR alpha on a genetic background in which the equivalent endogenous gene, H-2 IE alpha, is not expressed. In these mice, DR alpha complemented the E beta chain such that tissue-specific expression of an interspecies hybrid DR alpha-E beta heterodimer was obtained. Despite 25% amino acid differences between DR alpha and E alpha, immune responsiveness to IE-controlled antigens, clonal deletion of IE-reactive T cells, and alloantigenicity were quantitatively and qualitatively indistinguishable in IE-positive mice and in mice that had integrated at least four copies of the transgene. These results demonstrate a remarkable degree of structural, regulatory, and functional conservation. They also suggest that tolerance induction involves only discrete portions of MHC molecules.

Animals↗
PubMed2003

Antigen-specific immune function after hematopoietic stem cell transplantation.

Hematopoietic stem cell recipients are characterized by an immunodeficiency of varying severity and duration. The present review focuses on the antigen-specific function of recipients with the hypothesis that the acquisition of antigen-specific function is predictive of the recipient's capacity to resist lethal infection with environmental pathogens.

Antigens↗