Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections by gram-negative bacteria are one of the major causes of death in newborns. Bacterial clearance is deficient in septic neonates, which seems to increase their susceptibility to infections. In this study, we observed a significant improvement in clearance of Klebsiella pneumoniae in newborn wistar rats inoculated by intraperitoneal via with 800 mg k soybean phosphatidylcholine (PC), compared to the control group injected with PBS (p 0.05). The overall survival rate was improved (p 0.05) and the white blood cell counts showed a greater leukocytosis and neutrophilia during the peak of bacteremia in the PC treated animals. Circulating levels of interleukin-6 were greater in the PC group, which developed an intense splenic hematopoiesis of the granulocyte (p 0.05) and megakariocyte series (p 0.01). No significant changes were observed in bone marrow granulocyte deposits in both study groups. The improvement in survival rate, the changes in leukocyte counts and the splenic hematopoiesis may be associated with the increased production of IL-6. These results suggest that IL-6 plays a role in the protection mechanism induced by PC in this experimental model of newborn septicemia. PC seems to be an immunomodulator of the acute response to gram-negative bacterial infection.
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PMID:[Phosphatidylcholine induces an increase in the production of interleukin-6 and improves survival of rats with neonatal sepsis caused by Klebsiella pneumoniae]. 749 35

Interleukin-6 (IL-6) is a pleiotropic cytokine that enhances the maturation of megakaryocytes. In mice, in vivo treatment with IL-6 results in elevated platelet counts both in untreated animals and after myelosuppressive therapy. In this study, we assessed the effect of continuous infusion of IL-6 in sublethally irradiated (7 Gy) mice on peripheral blood cell counts and progenitor cells in bone marrow and spleen. Female Swiss mice were treated by continuous infusion with 1 or 10 micrograms IL-6 per day for 7 or 14 days. Continuous infusion of IL-6 for 7 days resulted in elevated levels of circulating IL-6 (mean: 1872 pg/mL vs. 100 pg/mL for phosphate-buffered saline [PBS]-treated controls) and in an accelerated reconstitution of platelets starting at day 12 after irradiation. In IL-6-treated animals, the 50% pretreatment platelet count was reached on day 15 vs. day 21 for irradiated controls receiving no IL-6. Treatment with IL-6 for 14 days resulted in a further increase in platelet counts, exceeding the pretreatment counts. The number of colony-forming units-megakaryocyte (CFU-Mk) was significantly elevated from day 6 to 18 in the spleen but not in bone marrow. To assess the contribution of extramedullary megakaryocytopoiesis in the spleen to IL-6-induced platelet recovery, IL-6 was also administered to splenectomized mice. The stimulatory effect of IL-6 on platelet recovery was preserved in these animals, indicating that megakaryocytopoiesis in the spleen did not contribute to the accelerated recovery of platelets. The neutrophil counts were elevated during IL-6 treatment and became similar to controls after cessation of therapy, whereas the numbers of colony-forming units-granulocyte/macrophage (CFU-GM) in the bone marrow were elevated from day 9 to 24 in all animals treated with 10 micrograms IL-6 per day. In conclusion, continuous infusion of IL-6 stimulates platelet recovery after irradiation without increasing the number of CFU-Mk and conversely stimulates the proliferation of myeloid progenitor cells without an effect on neutrophil reconstitution.
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PMID:Continuous infusion of interleukin-6 in sublethally irradiated mice accelerates platelet reconstitution and the recovery of myeloid but not of megakaryocytic progenitor cells in bone marrow. 824 64

Inflammatory cytokines play a key role in the myocardial injury produced by viral myocarditis. Although interleukin-6 (IL-6) reportedly possesses antiviral properties, its effect in viral myocarditis is unclear. To investigate the role of IL-6 in viral myocarditis induced by encephalomyocarditis virus (EMCV) in mice, we evaluated (1) the survival rate following IL-6 administration, (2) the viral titer in the heart, (3) viral replication in the heart by in situ hybridization, (4) histopathological changes using immunohistochemical staining, (5) neutralizing antibody against EMCV, (6) circulating interferon and tumor necrosis factor-alpha (TNF-alpha), (7) viral suppression in vitro by IL-6, and (8) natural killer (NK)-cell activity. Eight-week-old C3H/HeJ mice were injected intraperitoneally with EMCV (day 0) and were also injected subcutaneously twice daily for 4 consecutive days with 10 micrograms/0.1 mL of human IL-6 on day -4 (group A), day 0 (group B), or day +4 (group D) for 4 days. As a control, 0.1 mL PBS instead of IL-6 was injected on day 0 for 4 days (group C). Certain mice were killed on day 4. The myocardial virus titers, viral replication in situ, and NK-cell activity in the spleen were determined. Decreased viral titer and viral replication in the heart reduced the titer of circulating TNF-alpha, and lower NK-cell activity was observed in group B versus group C (control group). The titer of neutralizing antibodies against EMCV was significantly (P < .05) increased in group B compared with group C. The remaining mice were killed on days 10 and 30 after infection. The ratio of heart weight (HW) to body weight (BW) and myocardial injury in group B were reduced versus group C on days 10 and 30. The HW of group B on day 30 did not differ from the normal control group. The ratio of splenic weight to BW and the ratio of thymic weight to BW of group B increased on day 10, with expanded follicles observed in the spleen and enlargement of the medulla observed in the thymus. Immunohistochemical study revealed an increased percentage of macrophages in the heart and spleen of group B. In summary, IL-6 reduces myocardial damage in mice with viral myocarditis. Modification of immune responses together with reduction in viral replication appears to be the mechanism of the IL-6 effect. Although IL-6 is likely important in the process of viral antigen presentation, early activation of immune responses and attenuation of viral replication appear most significant, as reflected in the limited time window during which IL-6 is effective in myocarditis.
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PMID:Modification of viral myocarditis in mice by interleukin-6. 862 Jun 5

The effect of interleukin-6 (IL-6) secreted by a human atrial myxoma in vitro was investigated in C3H female mice with acute viral myocarditis. A culture medium containing IL-6 (100 ng/ml) and IL-8 (250 ng/ml), was prepared; viral myocarditis was induced by exposure to the encephalomyocarditis virus. Mice were assigned to four groups: 1) intraperitoneal (i.p.) injection of supernatant with IL-6 and IL-8 (0.2 ml/mice) given simultaneously with virus, 500 pfu for 4 days (Group 1); 2) i.p. injection of supernatant with IL-6 starting on Day 4 for 4 days in the same manner (Group 2); 3) i.p. injection of culture medium simultaneously with the virus (Group 3); and 4) i.p. injection of PBS in the same manner (Group 4). Uninfected control mice were administered medium only (Group 5) or supernatant with IL-6 and IL-8 (Group 6) for 4 days without virus. The survival rate on Day 14 in Group 1 was 90% significantly (p < 0.01) prolonged. The ratio of heart weight-to-day weight in the Group 1 was significantly (p < 0.01) lower. Histopathological examination revealed that cardiac necrosis and cellular infiltration in Group 1 was reduced compared with Group 3. Moreover, the radio of spleen weight/body weight in Group 1 was significantly (p < 0.01) higher than that of Group 3 and of Group 4. To confirm the effect of IL-6 or IL-8, mice were treated with recombinant IL-6 to IL-8 simultaneously with virus for 4 days. IL-6 treated mice survived significantly compared with IL-8 treated mice and untreated mice. The viral titer on day 4 of IL-6 treated mice was significantly lower than IL-8 treated or untreated mice. Thus, IL-6 derived from human myxoma improved the survival of murime viral myocarditis and reduced myocardial necrosis when the myxoma-derived IL-6 was administered simultaneously with the virus, due to eliciting cellular immunity in the spleen.
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PMID:Interleukin-6 secreted from human myxoma reduces murine viral myocarditis. 863 94

The SCIDhu PBL model of human Ig production was modified by using human interleukin-6 (hIL-6) secreting tumors for continuous hIL-6 production, in vivo. On day one, SCID mice were injected subcutaneously with 200 microliters PBS (control mice), 10(4) SP2/0-Ag14 cells (IL-6+ mice) or 10(4) hIL-6 secreting SP2/0-hIL6.17 cells (IL-6- mice). The mice were reconstituted with human PBMC on day two and immunized with 100 micrograms of tetanus toxoid (TT) on days two and fifteen. Serum hIL-6 concentrations in IL-6+ mice ranged between 2.9 and 38.1 ng/ml by days 26-33. IL-6+ mice had enlarged spleens and lymph nodes (LN). Flow cytometry and histology showed that SCIDhu PBL mouse spleen, LN and peritoneal exudate cells (PEC) contained mostly murine myeloid lineage cells. In addition, many more human B cells, T cells and IL-2R(+)-activated lymphocytes were present in spleen, LN and PEC of IL-6+ mice. Despite enhanced lymphocyte engraftment and activation, by day 14 IL-6+ mice produced up to 6-fold less TT-specific IgG relative to total IgG than either control group. TT-specific and total Ig sera concentrations were equivalent in all three groups on days 26-33. Our results suggest that sustained circulating hIL-6 enhanced human delayed-type hypersensitivity (DTH)-like inflammatory responses with consequential inhibition of TT-specific IgG production in SCIDhu PBL mice.
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PMID:Human IL-6 enhances human lymphocyte engraftment and activation but not human antibody production in SCIDhu PBL mice. 956 65

The concentration of interleukin-6 (IL-6), alpha1-acid glycoprotein (alpha1-AG), and corticosterone (CORT) was investigated chronologically (0 h to 14 d) in the sera of 2-wk-old specific-pathogen-free chicks inoculated with Escherichia coli lipopolysaccharide (LPS). In the LPS group the IL-6 level was elevated from 1 h to 2 d and was the highest at 3 h. From 4 to 14 d the IL-6 level was low in the LPS group. In the PBS group, IL-6 was not detected except a mild increase from 1 h to 6 h. In the LPS group, the alpha1-AG level increased from 6 h to 4 d, and the peak was 2 d. In the PBS group the alpha1-AG level was always low. The CORT level in the LPS group was higher than that of PBS group at 1 h. This study suggests that E. coli LPS may elevate serum IL-6 and CORT, and that IL-6 and CORT may increase the alpha1-AG level in the chicks.
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PMID:Serum levels of interleukin-6, alpha1-acid glycoprotein, and corticosterone in two-week-old chickens inoculated with Escherichia coli lipopolysaccharide. 962 44

We investigated the heterogeneity of the humoral immune responses to whole cells and lipopolysaccharide (LPS) of Actinobacillus actinomycetemcomitans serotype b and production of cytokines in inbred strains of mice. Nine such strains were tested: A/J (H-2(a)), C57BL/6 (H-2(b)), BALB/c (H-2(d)), DBA/2 (H-2(d)), B10.BR (H-2(k)), C3H/He (H-2(k)), C3H/HeJ (H-2(k)), DBA/1 (H-2(q)) and B10.S (H-2(s)). Mice were immunized intraperitoneally with whole cells of A. actinomycetemcomitans ATCC 43718 (serotype b) in phosphate buffered saline (PBS; pH 7.2) emulsified with an equal volume of Freund's incomplete adjuvant. Serum immunoglobulin G (IgG), immunoglobulin A (IgA) and immunoglobulin M (IgM) levels against A. actinomycetemcomitans were measured by an ELISA system. ELISA analysis, using LPS fractions from serotype a, b or c strains of A. actinomycetemcomitans as the coating antigens, revealed that mice strains C3H/He, C3H/HeJ, B10.BR and B10.S had an extremely high-IgM response against serotype b LPS. High-IgM titer sera contain also elevated levels of IgA antibodies to the antigen. To compare the cytokine production among inbred mice, the amounts of interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-6 (IL-6) released from mouse splenocytes were measured using ELISA systems specific for these cytokines. A. actinomycetemcomitans serotype b LPS stimulation induced IL-6 release from murine splenocytes of all tested strains. However, IL-4 and IL-5 were detected only in high-IgM/IgA responders to A. actinomycetemcomitans serotype b LPS, not in low-IgM/IgA responders. Thus, we found a relationship between the humoral immune response to LPS of A. actinomycetemcomitans serotype b and production of type 2 cytokines by splenocytes.
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PMID:Heterogeneity in the immune response to serotype b LPS of Actinobacillus actinomycetemcomitans in inbred strains of mice. 1076 9

Proinflammatory cytokines play an important role in the mediation of inflammation and trauma. They could be useful for the determination of vitality and wound age. In the present study, 144 human skin wounds due to sharp force were investigated. The material was collected during operations (N=96) and postmortem examinations (N=48). The wound age varied from several seconds or minutes to 9 days. Control skin was available in each individual. The tissue specimens were homogenized and extracted in a solution of PBS and protease inhibitors. Interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) were measured by quantitative ELISA analysis. Statistical evaluation was performed by the t-test using the quotients of levels (wound sample/control skin). In surgical specimens the cytokine levels revealed a clear tendency to increase with wound age. IL-1beta in early skin wounds (</=30 min) and TNF-alpha after a wound age of 1-2 h demonstrated statistically significant changes in comparison with control skin (P<0.05). In autopsy samples with severe traumatization excessive elevation of cytokine levels was observed: IL-1beta, IL-6 and TNF-alpha showed significant increases (P<0.001-0.05) in stab and incised wounds with very short survival times of less than 5 min, but not in possibly supravital injuries. Elevated IL-6 levels persisted in older wounds (>24 h, P<0.05). The quantitative analysis of proinflammatory cytokines in wound extracts can contribute to the determination of vitality and wound age, in particular in the very early post-traumatic interval (classic stab wounds).
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PMID:Quantitative analysis of proinflammatory cytokines (IL-1beta, IL-6, TNF-alpha) in human skin wounds. 1097 34

Interleukin-6 (IL-6) regulates essential physiological functions such as acute phase reaction, immune response and hematopoiesis. We here studied possible protective effects of IL-6 on skin damage caused by 7,12-dimethylbenz[a]anthracene (DMBA) by using IL-6 null mice. The mice were topically applied with a single dose of DMBA (500 microg /mouse) on the dorsal skin. Osmotic pumps filled with recombinant human IL-6 (rhIL-6) were implanted subcutaneously on the ventral side of the mice. Control mice received PBS instead of rhIL-6 by the pump. Severe skin damage was observed in IL-6-null mice, whereas only epidermal hyperplasia was observed in the wild-type mice. Recombinant hIL-6 treatment to DMBA-treated IL-6-null mice suppressed the occurrence of the skin damage, indicating.
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PMID:Interleukin-6 protects skin lesion caused by 7,12-dimethylbenz[a]anthracene. 1273 34

A mastitis model in rats, induced by Staphylococcus aureus infection, was established and the protective effect of CpG-DNA on this model was determined. A S. aureus suspension containing 2 x 10(3) CFU.mL(-1) (SL group), 2 x 10(5) CFU.mL(-1) (SH group) or 100 microL PBS (CON group) was inoculated into the mammary glands of rats 72 h after parturition. The rats were euthanized at 24 h post-infection. The histopathologic changes in mammary tissue from SL were mild, whereas the structural changes of the mammary gland from SH were severe and polymorphonuclear leukocytes (PMNs) accumulated in mammary alveoli. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and N-acetyl-beta-d-Glucosaminidase (NAGase) in mammary tissue from SH were significantly increased, however, those from SL were not significantly changed. Therefore, 2 x 10(5) CFU.mL(-1) was selected to test the potential protective effect of CpG-DNA on mammary glands. CpG-DNA (200 microg) or PBS (100 microL) controls were intramuscularly injected right after parturition of rats. At 72 h post-partum, 2 x 10(5) CFU.mL(-1)of S. aureus (100 microL) were inoculated into the mammary gland of all rats and at pre-infection (0 h), 8, 16, 24, 48 and 72 h after inoculation six rats were euthanatized. CpG-DNA induced more rapid migration of PMNs from blood to mammary tissue at the initial stage of infection, stimulated the secretion of IL-6 and TNF-alpha at different time points, reduced viable S. aureus in mammary tissue and decreased the activity of NAGase. CpG-DNA also promoted the expression of its specific receptor TLR-9 mRNA in mammary tissue. In conclusion, CpG-DNA protected against S. aureus mastitis in a rat model.
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PMID:Protective effect of CpG-DNA against mastitis induced by Staphylococcus aureus infection in a rat model. 1732 66


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