Monocyte Interleukin-1 Secretion Is Regulated by the Sequential Action of γ-Interferon and Interleukin-2 Involving Monocyte Surface Expression of Interleukin-2 Receptors

1989 ◽  
pp. 299-315 ◽  
Author(s):  
F. Herrmann ◽  
A. Lindemann ◽  
S. A. Cannistra ◽  
M. Brach ◽  
W. Oster ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Interleukin 2 ◽  
Surface Expression ◽  
Sequential Action ◽  
Γ Interferon

Local pathological responses to slow-release recombinant interleukin-1, interleukin-2 and γ-interferon in the mouse and their relevance to chronic inflammatory disease

1989 ◽  
Vol 76 (3) ◽  
pp. 261-263 ◽  
Author(s):  
C. J. Dunn ◽  
M. M. Hardee ◽  
A. J. Gibbons ◽  
N. D. Staite ◽  
K. A. Richard
Keyword(s):  
Slow Release ◽  
Inflammatory Diseases ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Cell Formation ◽  
Chronic Inflammatory Disease ◽  
Tissue Response ◽  
Multinucleate Giant Cell ◽  
Γ Interferon

1. The present study describes the pathological responses to local administration of recombinant cytokines in subcutaneously implanted slow-release ethylene vinyl acetate (EVA) co-polymer in mice. 2. EVA-recombinant human interleukin-1β (104 units) implants induced the formation of chronic granulomatous inflammatory tissue between 4 and 7 days after implantation, characterized by predominant macrophage infiltration, neovascularization and fibrosis which persisted up to 21 days after-implantation. EVA-recombinant human interleukin-1α (104–105 units) implants induced a qualitatively similar but less intense response. 3. In contrast, recombinant human interleukin-2 (102–104 units) implants resulted in early lymphocytic vasculitis (4 days) and the development of a predominantly lymphoid lesion comprised of lymphoblasts and significant mononuclear cell proliferation by 7 days. 4. EVA-recombinant γ-interferon (103–104 units) implants failed to elicit a significant tissue response; with the exception of multinucleate giant cell formation the characteristics of these lesions closely resembled the mild fibrotic responses observed for EVA-bovine serum albumin (0.5–12.5 mg) implants. 5. These observations suggest that continuous endogenous local release of interleukin-1 or interleukin-2 in vivo is sufficient for the development of specific pathological features characterizing chronic immuno-inflammatory diseases.

scholarly journals The Combined Effect of Weaning Stress and Immune Activation during Pig Gestation on Serum Cytokine and Analyte Concentrations

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2274
Author(s):  
Haley E. Rymut ◽  
Laurie A. Rund ◽  
Courtni R. Bolt ◽  
Maria B. Villamil ◽  
Bruce R. Southey ◽  
...  
Keyword(s):  
Immune Activation ◽  
Management Practices ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Blood Chemistry ◽  
Respiratory Syndrome Virus ◽  
Weaning Stress ◽  
And Control ◽  
Metabolic Hormone

Weaning stress can elicit changes in the metabolic, hormone and immune systems of pigs and interact with prolonged disruptions stemming from maternal immune activation (MIA) during gestation. The present study advances the characterization of the combined effects of weaning stress and MIA on blood chemistry, immune and hormone indicators that inform on the health of pigs. Three-week-old female and male offspring of control gilts or gilts infected with the porcine reproductive and respiratory syndrome virus were allocated to weaned or nursed groups. The anion gap and bilirubin profiles suggest that MIA enhances tolerance to the effects of weaning stress. Interleukin 1 beta and interleukin 2 were highest among weaned MIA females, and cortisol was higher among weaned relative to nursed pigs across sexes. Canonical discriminant analysis demonstrated that weaned and nursed pigs have distinct chemistry profiles, whereas MIA and control pigs have distinct cytokine profiles. The results from this study can guide management practices that recognize the effects of the interaction between MIA and weaning stress on the performance and health of pigs.

Failure of FK-506, a new immunosuppressant, to prevent cerebral vasospasm in a canine two-hemorrhage model

1993 ◽  
Vol 79 (5) ◽  
pp. 710-715 ◽  
Author(s):  
Kazuya Nagata ◽  
Tomio Sasaki ◽  
Junichi Iwama ◽  
Takashi Mori ◽  
Shoko Iwamoto ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Muscle Layer ◽  
Treated Group ◽  
Control Group ◽  
Fk 506 ◽  
Content Type

✓ In order to clarify the possible role of immunological reaction in the pathogenesis of cerebral vasospasm, the authors examined the prophylactic effect of the immunosuppressant agents FK-506 and cyclosporin A on chronic vasospasm in a canine two-hemorrhage model. While a mean constriction of the basilar artery to 81.0% ± 4.0% (± standard error of the mean) occurred on Day 2 and to 63.8% ± 3.5% on Day 7 in the untreated group, constriction to 77.9% ± 3.4% on Day 2 and 62.8% ± 3.0% on Day 7 was demonstrated in the FK-506-treated group (difference not significant). This tendency was also noted in the cyclosporin A-treated group, with basilar artery constriction to 81.8% ± 3.7% and 56.3% ± 2.7%, respectively (difference not significant). The histological changes of the basilar artery, including corrugation of the elastic lamina, detachment of endothelial cells, and vacuolar formation in the smooth-muscle layer were not different in the two treated groups and the one control group. Since these immunosuppressant agents are known to inhibit the release of interleukin-2 (IL-2), the level of IL-2 was examined in the cerebrospinal fluid of patients with cerebral vasospasm. While interleukin-1 gradually increased in level as time passed, the level of IL-2 was consistently low during the course of the study, indicating less participation of IL-2 in the pathogenesis of cerebral vasospasm. This clinical observation matched the experimental results. The authors conclude that cell-mediated immunoreaction, initiated mainly by IL-2, plays little role in the pathogenesis of cerebral vasospasm.

scholarly journals Maturation of acute T-lymphoblastic leukemia cells after CD2 ligation and subsequent treatment with interleukin-2

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1182-1192 ◽  
Author(s):  
F Mentz ◽  
F Ouaaz ◽  
A Michel ◽  
C Blanc ◽  
P Herve ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Phosphorylation ◽  
Lymphoblastic Leukemia ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Subsequent Treatment ◽  
Leukemic Cells ◽  
Cell Phenotype ◽  
Cell Functions

Abstract In this study, we have investigated the ability of various cytokines to induce the maturation of acute lymphoblastic leukemia (T-ALL) cells with early T-cell phenotype. Leukemic blasts from 17 untreated T-ALL patients were assayed for their ability to acquire mature T-cell markers, CD3/T-cell receptor (TCR) in particular, after incubation with one or a combination of recombinant human interleukin-1 (IL-1), IL-2, IL-4, IL-7, and CD2-specific monoclonal antibody (MoAb). IL-7 or IL-2 induced the proliferation of some leukemic cells, whereas sequential cell treatment with CD2-MoAb and then IL-2 promoted CD3/TCR expression on nearly all CD2+ cells (15 of 16), except for 1 T-ALL that developed into CD3-CD16+CD56+ cells. Differentiation of T-ALL cells was also evidenced through the downregulation of CD34 precursor cell antigen, the generation of CD4+ and CD8+ cells from CD4+ CD8+ precursors, and the acquisition of mature T-cell functions. CD2 ligation induced a progressive increase of surface expression of IL-2 receptor alpha (IL- 2R alpha) and IL-2R beta and an accelerated in vitro death of leukemic cells. The ligation of IL-2R by IL-2 rescued T-ALL cells from death and promoted their progression toward more mature cells expressing extracellular CD3/TCR alpha beta complexes. Intracellular analysis indicates that TCR alpha transcription and membrane translocation of both TCR alpha and TCR beta were promoted in these conditions. Analysis of intracellular signals transduced during T-ALL differentiation indicated that CD2-ligation induced Ca2+ influx and that the ligation of CD2 and IL-2R induced distinct tyrosine phosphorylation patterns. The addition of inhibitors of tyrosine phosphorylation abolished T-ALL cell differentiation, which suggests the involvement of tyrosine kinases in this phenomenon. Together, we showed the constant maturation of leukemic early T cells after stimulation of surface CD2 and the high- affinity IL-2R.

scholarly journals Production of cytokines by bone marrow cells obtained from patients with multiple myeloma

Blood ◽  
1989 ◽  
Vol 74 (4) ◽  
pp. 1266-1273 ◽  
Author(s):  
A Lichtenstein ◽  
J Berenson ◽  
D Norman ◽  
MP Chang ◽  
A Carlile
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
In Vitro Production ◽  
Osteolytic Bone Disease ◽  
Vitro Production ◽  
Necrosis Factor

Abstract Previous work with continuously cultured multiple myeloma lines suggested that cytokine production by tumor cells may mediate some of the medical complications of this disease. To further investigate this issue, we assayed freshly obtained bone marrow (BM) cells from myeloma patients for the in vitro production of cytokines and the presence of cytokine RNA. Production of cytokine protein was assessed by bioassays with the aid of specific neutralizing anticytokine antibodies. These assays detected interleukin-1 (IL-1) and tumor necrosis factor (TNF) secretion by myeloma BM cells, which was significantly greater than secretion from similarly processed BM cells of control individuals. In contrast, lymphotoxin and interleukin-2 (IL-2) production could not be detected. The levels of IL-1 and TNF produced in vitro peaked at 24 hours of culture and correlated with stage and the presence (or absence) of extensive osteolytic bone disease. Northern blot analysis demonstrated the presence of IL-1 beta and TNF RNA in uncultured myeloma BM cells but no detectable IL-1 alpha or lymphotoxin RNA. In addition, the amount of cytokine RNA correlated with protein production, being significantly greater in patients' BM cells than in control marrow. These data suggest a role for IL-1 beta and/or TNF in the pathophysiology of multiple myeloma and argue against a role for lymphotoxin or IL-2.

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