Intracerebroventricular Injection of Interleukin-1 Suppresses Peripheral Lymphocyte Function in the Primate

1997 ◽  
Vol 4 (1) ◽  
pp. 12-18 ◽  
Author(s):  
G.M. Sullivan ◽  
S.M. Canfield ◽  
S. Lederman ◽  
E. Xiao ◽  
M. Ferin ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Peripheral Lymphocyte ◽  
Lymphocyte Function ◽  
Intracerebroventricular Injection

Peripheral lymphocyte function in dogs with infection

1983 ◽  
Vol 4 (4) ◽  
pp. 425-431 ◽  
Author(s):  
C.A. Johnson ◽  
R.W. Bull ◽  
R.G. Schirmer
Keyword(s):  
Peripheral Lymphocyte ◽  
Lymphocyte Function

Adhesion molecule expression by the FRTL-5 rat thyroid cell line

1991 ◽  
Vol 130 (3) ◽  
pp. 451-456 ◽  
Author(s):  
N. Tandon ◽  
C. Dinsdale ◽  
T. Tamatani ◽  
M. Miyasaka ◽  
A. P. Weetman
Keyword(s):  
Cell Line ◽  
Adhesion Molecule ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Thyroid Cell ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Thyroid Cells ◽  
Thyroid Cell Line ◽  
Rat Thyroid

ABSTRACT We have examined the expression and function of rat CD54, a homologue of human intercellular adhesion molecule-1 (ICAM-1), by the continuously growing rat thyroid cell line FRTL-5. Approximately 10% of FRTL-5 cells express CD54 under basal conditions and this is not influenced by thyrotrophin. Expression of CD54 is increased by cytokines (γ-interferon, tumour necrosis factor, interleukin-1) and by an activator of C-kinase, phorbol 12-myristate 13-acetate. Blocking ICAM-1 with a monoclonal antibody directed against this molecule significantly (P <0·01) reduced the binding of splenic lymphocytes to FRTL-5 cells but inhibition was consistently greater (P <0·01) in the presence of antibodies against a rat homologue of lymphocyte function-associated antigen-1, the receptor on T cells for ICAM-1. In no case was complete blocking of cluster formation observed. These results show that a pure line of rat thyroid cells can express an ICAM-1 homologue and this is directly enhanced by cytokines. Expression of this homologue is partially responsible for lymphocyte adhesion to thyroid cells, which is likely to be a major event in T cell recognition of thyroid antigens in autoimmune thyroiditis. Journal of Endocrinology (1991) 130, 451–456

Vasculitis in MRL/1pr Mice: Model of Cell-Mediated Autoimmunity

1989 ◽  
Vol 17 (1_part_2) ◽  
pp. 122-128 ◽  
Author(s):  
Carolyn F. Moyer ◽  
Carol L. Reinisch
Keyword(s):  
Inflammatory Cell ◽  
Interleukin 1 ◽  
Function Evaluation ◽  
Lymphocyte Function ◽  
Mice Model ◽  
Experimental Conditions ◽  
Accessory Function ◽  
Accessory Cells ◽  
C3h Mice ◽  
Mononuclear Inflammatory Cell

The destruction of vascular smooth muscle cells (VSMC) in autoimmune arteritis is a poorly understood phenomenon. To approach this problem, VSMC cultures were established. The interaction of these cells (from normal or autoimmune mice) with lymphocytes was then evaluated. Specifically, splenocytes from MRL/1pr or C3H mice were co-cultivated with MRL/1pr or C3H VSMCs. Massive mononuclear inflammatory cell clusters enveloped MRL/1pr VSMCs which culminated in the detachment of MRL/1pr VSMCs from the culture plate. In contrast, the interaction of splenocytes from normal or autoimmune mice did not destroy normal VSMCs. Further investigation indicated that MRL/1pr VSMCs spontaneously expressed both Ia–k and Ia–d, as assessed by fluorescence microscopy and flow cytometry, and released interleukin-1-like factors–-characteristics of accessory cells to T-lymphocyte function. Evaluation of VSMCs accessory function in antigen presentation suggests that these cells may present antigen under specific experimental conditions. As a result of these studies, a novel mechanism of autoimmune vasculitis is proposed. Our hypothesis is that defective biological function of VSMCs from autoimmune mice stimulates a mononuclear inflammatory cell response which culminates in VSMC autodestruction.

scholarly journals Modulatory effect of antibiotics on cytokine production by human monocytes in vitro.

1996 ◽  
Vol 40 (6) ◽  
pp. 1366-1370 ◽  
Author(s):  
K Morikawa ◽  
H Watabe ◽  
M Araake ◽  
S Morikawa
Keyword(s):  
Antimicrobial Agents ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Immunomodulatory Activity ◽  
Lymphocyte Function ◽  
Dependent Manner ◽  
Human Monocytes ◽  
Concentration Dependent Manner ◽  
Cytokine Synthesis

Some antimicrobial agents have been reported to modify the host immune and inflammatory responses both in vivo and in vitro. Fosfomycin (FOM) and clarithromycin (CAM) have immunomodulatory activity on human lymphocyte function. In the present study, we examined the effects of FOM and CAM on cytokine synthesis by lipopolysaccharide (LPS)-stimulated human monocytes in comparison with that of dexamethasone in vitro. The three drugs demonstrated positive or negative effects on the synthesis of various cytokines by LPS-primed monocytes. They suppressed the synthesis of tumor necrosis factor alpha, interleukin 1 alpha (IL-1 alpha), IL-1 beta, the IL-1 receptor antagonist, and granulocyte-macrophage colony-stimulating factor in a concentration-dependent manner at concentrations between 1.6 and 40 micrograms/ml. On the contrary, the drugs showed different actions on the synthesis of IL-6 and IL-10. Namely, FOM enhanced both IL-6 and IL-10 synthesis, CAM enhanced only IL-10 synthesis, but dexamethasone deeply suppressed the synthesis of both cytokines. These data indicate that antibacterial agents may modify acute-phase inflammatory responses through their effects on cytokine synthesis by monocytes.

Lipocortin 1 fragment modifies pyrogenic actions of cytokines in rats

1990 ◽  
Vol 259 (2) ◽  
pp. R266-R269 ◽  
Author(s):  
F. Carey ◽  
R. Forder ◽  
M. D. Edge ◽  
A. R. Greene ◽  
M. A. Horan ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Interleukin 1 ◽  
Physiological Role ◽  
Polyclonal Antiserum ◽  
Intracerebroventricular Injection ◽  
Interleukin 1 Beta ◽  
Recombinant Fragment ◽  
Central Effects ◽  
Colonic Temperature ◽  
Dose Dependent

Lipocortins form a group of proteins that have been proposed as mediators of the anti-inflammatory actions of glucocorticoids. Intracerebroventricular injection of a recombinant fragment of lipocortin 1 (NH2-terminal 1-188) caused dose-dependent (0.4-1.2 micrograms) reductions in the acute increases in colonic temperature and oxygen consumption, which occurred in response to central injections of recombinant interleukin 1 beta and gamma-interferon in conscious rats. In contrast the lipocortin fragment did not affect the response to prostaglandin E2, and its activity was prevented by heat treatment or by pretreatment of animals with polyclonal antiserum raised to the fragment. Central injection of antiserum significantly enhanced the thermogenic responses to interleukin 1 beta in rats treated with dexamethasone without affecting the responses in normal animals. These results support a physiological role for lipocortin in the central effects of glucocorticoids.

Interleukin-1 induces changes in sleep, brain temperature, and serotonergic metabolism

1997 ◽  
Vol 272 (2) ◽  
pp. R601-R606 ◽  
Author(s):  
C. Gemma ◽  
L. Imeri ◽  
M. G. de Simoni ◽  
M. Mancia
Keyword(s):  
Time Course ◽  
Preoptic Area ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Secondary Effect ◽  
Intracerebroventricular Injection ◽  
Early Increase ◽  
Cortical Temperature ◽  
Freely Moving

Simultaneous recordings of sleep-wake activity and of serotonergic metabolism in the medial preoptic area were performed in freely moving rats after the intracerebroventricular injection of interleukin-1 (IL-1) at dark onset. IL-1 (2.5 ng) induced a biphasic increase in slow-wave sleep and an early increase in serotonergic metabolism starting 30 min postinjection. Phasic, state-specific changes (which have been described in spontaneous sleep) were superimposed on this tonic, overall increase in serotonergic metabolism. IL-1 (25 ng) induced an increase in wakefulness and a delayed increase in serotonergic metabolism, which started 120 min postinjection. This suggests that the time course of the serotonergic activation could play a role in mediating IL-1 effects on sleep. Both doses of IL-1 induced a similar and significant increase in brain cortical temperature, suggesting that IL-1 effects on sleep are not a secondary effect of the increase in cortical temperature and that the serotonergic system is not involved in IL-1-induced fever.

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