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Journal articles on the topic 'IL-10 deficiency'

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Published: 1 April 2023

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1

Asadullah, K., K. Stephanek, M. Leupold, et al. "Relative IL-10 deficiency and effects of IL-10 therapy in psoriasis." Journal of Dermatological Science 16 (March 1998): S30. http://dx.doi.org/10.1016/s0923-1811(98)83173-3.

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2

Wan, Xin, Wen Juan Huang, Wen Chen, et al. "IL-10 Deficiency Increases Renal Ischemia-Reperfusion Injury." Nephron Experimental Nephrology 128, no. 1-2 (2014): 37–45. http://dx.doi.org/10.1159/000366130.

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3

Hennessy, A., H. L. Pilmore, L. A. Simmons, and D. M. Painter. "A Deficiency of Placental IL-10 in Preeclampsia." Journal of Immunology 163, no. 6 (1999): 3491–95. http://dx.doi.org/10.4049/jimmunol.163.6.3491.

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Abstract Accommodation of the fetoplacental unit in human pregnancy requires maternal immune tolerance to this “semiallograft”. Local antiplacental immunity is modified by synthesis of uncommon histocompatibility Ags (e.g., HLA-G), growth factors, and cytokines by the placenta. Placental interleukins have been identified in reproductive tissues, but their roles in adaptive maternal immunity and determining term pregnancy outcomes have not been fully clarified. This study examined the distribution of IL-10 and TNF-α staining in term placentas. Women with proteinuric hypertension (PE, n = 10) were compared with an age-matched group with normal pregnancy (NP, n = 14) and gestational hypertension (GH, n = 6). Using immunohistochemistry of parrafin-fixed tissues, trophoblast cells were identified by cytokeratin 7 and cytokeratin 18 staining. The cytokine binding of villous trophoblast cells was scored depending on the extent of circumferential cytoplasm staining (<25%; intermediate or >75%). The cytokine positive decidual cells were scored as a percentage of total extravillous trophoblast cells. There was a reduction in villous IL-10 immunostaining compared with normal term placenta (PE, 10.2 ± 1.1, mean ± SEM; NP, 14.07 ± 1.16 Mann-Whitney U test; p = 0.02). In these patients, there was an increase in TNF-α immunostaining. Sparse endovascular extravillous trophoblast cells demonstrated nuclear IL-10 staining in 30% of patients with preeclampsia. Serum IL-10 was diminished in women with preeclampsia compared with normal pregnancy. In conclusion, villous trophoblast demonstrated diminished immunostaining of IL-10 in preeclampsia. This abnormality may be associated with heightened maternal antifetal immunity and therefore inadequate placental development in preeclampsia.
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4

Zigmond, Ehud, Biana Bernshtein, Gilgi Friedlander, et al. "Macrophage-Restricted Interleukin-10 Receptor Deficiency, but Not IL-10 Deficiency, Causes Severe Spontaneous Colitis." Immunity 40, no. 5 (2014): 720–33. http://dx.doi.org/10.1016/j.immuni.2014.03.012.

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5

Jones, Steven P., Steven D. Trocha, and David J. Lefer. "Cardioprotective actions of endogenous IL-10 are independent of iNOS." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (2001): H48—H52. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h48.

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Myocardial ischemia-reperfusion (I/R) is a well-known stimulus for acute inflammatory responses that promote cell death and impair pump function. Interleukin-10 (IL-10) is an endogenous, potent anti-inflammatory cytokine. Recently, it has been proposed that IL-10 inhibits inducible nitric oxide synthase (iNOS) activity after myocardial I/R and consequently exerts cardioprotective effects. However, whether this actually occurs remains unclear. To test this hypothesis, we utilized iNOS-deficient (−/−), IL-10 −/−, and IL-10/iNOS −/− mice to examine the potential mechanism of IL-10-mediated cardioprotection after myocardial I/R. Wild-type, iNOS −/−, IL-10 −/−, and IL-10/iNOS −/− mice were subjected to in vivo myocardial ischemia (30 min) and reperfusion (24 h). Deficiency of iNOS alone did not significantly alter the extent of myocardial necrosis compared with wild-type mice. We found that deficiency of IL-10 resulted in a significantly ( P < 0.05) larger infarct size than that in wild-type hearts. Interestingly, deficiency of both IL-10 and iNOS yielded significantly ( P < 0.01) larger myocardial infarct sizes compared with wild-type animals. Histological examination of myocardial tissue samples revealed augmented neutrophil infiltration into the I/R myocardium of IL-10 −/− and IL-10/iNOS −/− mice compared with hearts of wild-type mice. These results demonstrate that 1) deficiency of endogenous IL-10 exacerbates myocardial injury after I/R; 2) the cardioprotective effects of IL-10 are not dependent on the presence or absence of iNOS; and 3) deficiency of IL-10 enhances the infiltration of neutrophils into the myocardium after I/R.
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6

Gunnett, Carol A., Donald D. Heistad, Daniel J. Berg, and Frank M. Faraci. "IL-10 deficiency increases superoxide and endothelial dysfunction during inflammation." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (2000): H1555—H1562. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1555.

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Little is known about the role of interleukin-10 (IL-10), an anti-inflammatory cytokine, in blood vessels. We used IL-10-deficient mice (IL-10 −/−) to examine the hypothesis that IL-10 protects endothelial function after lipopolysaccharide (LPS) treatment. The responses of carotid arteries were studied in vitro 6 h after injection of a relatively low dose of LPS (10 μg ip). In IL-10 −/− mice, the maximum relaxation to ACh (3 μM) was 56 ± 6% (means ± SE) after LPS injection and 84 ± 4% after vehicle injection ( P < 0.05). Thus endothelium-dependent relaxation was impaired in carotid arteries from IL-10 −/− mice after LPS injection. In contrast, this dose of LPS did not alter relaxation to ACh in vessels from wild-type (IL-10 +/+) mice. Relaxation to nitroprusside and papaverine was similar in arteries from both IL-10 −/− and IL-10 +/+ mice after vehicle or LPS injection. Because inflammation is associated with increased levels of reactive oxygen species, we also tested the hypothesis that superoxide contributes to the impairment of endothelial function by LPS in the absence of IL-10. Results using confocal microscopy and hydroethidine indicated that levels of superoxide are elevated in carotid arteries from IL-10 −/− mice compared with IL-10 +/+ mice after LPS injection. The impaired relaxation of arteries from IL-10 −/− mice after LPS injection was restored to normal by polyethylene glycol-suspended superoxide dismutase (50 U/ml) or allopurinol (1 mM), an inhibitor of xanthine oxidase. These data provide direct evidence that IL-10 protects endothelial function after an acute inflammatory stimulus by limiting local increases in superoxide. The source of superoxide in this model may be xanthine oxidase.
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7

Wang, B., L. Zhuang, H. Fujisawa, and D. N. Sauder. "Effect of IL-10 deficiency on the migration of epidermal Langerhans cells in IL-10 null mice." Journal of Dermatological Science 16 (March 1998): S90. http://dx.doi.org/10.1016/s0923-1811(98)83537-8.

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8

Zhang, Guag-Xian, Fang Zhou, Bogoljub Ciric, et al. "Ability of LPS to regulate expression of tolerance-related molecules on dendritic cells is blocked by IL-10 deficiency (48.18)." Journal of Immunology 188, no. 1_Supplement (2012): 48.18. http://dx.doi.org/10.4049/jimmunol.188.supp.48.18.

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Abstract Interleukin-10 (IL-10) is an anti-inflammatory cytokine that plays an important role in regulating the local inflammatory immune response, but regulatory mechanisms of this cytokine have not been fully elucidated. Here we demonstrate that IL-10 deficiency renders LPS treatment ineffective in regulating expression of CD40, CD80, CD86, B7-H2 and B7-DC on dendritic cells (DCs) and blocks up-regulation of IL-27. This inability to respond to LPS was found in both IL-10-/- bone marrow-derived and splenic DCs. Compared to wild type DCs, IL-10-/- DCs expressed similar levels of TLR4 and CD14, but produced less LPS binding protein (LBP). The deficiency in LBP production may explain the failure of IL-10-/- DCs to respond normally to LPS. Moreover, lack of IL-10 modulated the proportions of CD11c+CD8+ and CD11c+B220+ DCs, which play an important role in local inflammatory responses and tolerance. IL-10 deficiency also blocked expression of galectin-1, CD205 and CD103, which are necessary for central and peripheral tolerance. While they did not respond to LPS, IL-10-/- DCs produced increased levels of IL-6 and CCL4 after TNF-α treatment. Together, our results demonstrate that IL-10 deficiency affects the immune functions of DCs, which may contribute to the increased severity of autoimmune diseases seen in IL-10-/- mice.
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9

Pérez-de Puig, Isabel, Francesc Miró, Angélica Salas-Perdomo, et al. "IL-10 Deficiency Exacerbates the Brain Inflammatory Response to Permanent Ischemia without Preventing Resolution of the Lesion." Journal of Cerebral Blood Flow & Metabolism 33, no. 12 (2013): 1955–66. http://dx.doi.org/10.1038/jcbfm.2013.155.

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Stroke induces inflammation that can aggravate brain damage. This work examines whether interleukin-10 (IL-10) deficiency exacerbates inflammation and worsens the outcome of permanent middle cerebral artery occlusion (pMCAO). Expression of IL-10 and IL-10 receptor (IL-10R) increased after ischemia. From day 4, reactive astrocytes showed strong IL-10R immunoreactivity. Interleukin-10 knockout (IL-10 KO) mice kept in conventional housing showed more mortality after pMCAO than the wild type (WT). This effect was associated with the presence of signs of colitis in the IL-10 KO mice, suggesting that ongoing systemic inflammation was a confounding factor. In a pathogen-free environment, IL-10 deficiency slightly increased infarct volume and neurologic deficits. Induction of proinflammatory molecules in the IL-10 KO brain was similar to that in the WT 6 hours after ischemia, but was higher at day 4, while differences decreased at day 7. Deficiency of IL-10 promoted the presence of more mature phagocytic cells in the ischemic tissue, and enhanced the expression of M2 markers and the T-cell inhibitory molecule CTLA-4. These findings agree with a role of IL-10 in attenuating local inflammatory reactions, but do not support an essential function of IL-10 in lesion resolution. Upregulation of alternative immunosuppressive molecules after brain ischemia can compensate, at least in part, the absence of IL-10.
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10

Marco, Roberto Di, Ming Xiang, Paola Zaccone, et al. "Concanavalin A-induced Hepatitis in Mice is Prevented by Interleukin (IL)-10 and Exacerbated by Endogenous IL-10 Deficiency." Autoimmunity 31, no. 2 (1999): 75–83. http://dx.doi.org/10.3109/08916939908994050.

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11

Thaxton, Jessica E., Roberto Romero, and Surendra Sharma. "TLR9 Activation Coupled to IL-10 Deficiency Induces Adverse Pregnancy Outcomes." Journal of Immunology 183, no. 2 (2009): 1144–54. http://dx.doi.org/10.4049/jimmunol.0900788.

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12

Bristol, Ian J., Mark A. Farmer, Yingzi Cong, et al. "Heritable Susceptibility for Colitis in Mice Induced by IL-10 Deficiency." Inflammatory Bowel Diseases 6, no. 4 (2000): 290–302. http://dx.doi.org/10.1097/00054725-200011000-00006.

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13

Bristol, Ian J., Mark A. Farmer, Yingzi Cong, et al. "Heritable susceptibility for colitis in mice induced by IL-10 deficiency." Inflammatory Bowel Diseases 6, no. 4 (2000): 290–302. http://dx.doi.org/10.1002/ibd.3780060407.

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14

Li, Qing-Ya, Zhi-Zhong Guo, Jian Liang, et al. "Interleukin-10 Genotype Correlated to Deficiency Syndrome in Hepatitis B Cirrhosis." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/298925.

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Traditional Chinese medicine (TCM) syndrome is an important basis for TCM diagnosis and treatment. As Child-Pugh classification as well as compensation and decompensation phase in liver cirrhosis, it is also an underlying clinical classification. In this paper, we investigated the correlation between single nucleotide polymorphisms (SNPs) of Interleukin-10 (IL-10) and TCM syndromes in patients with hepatitis B cirrhosis (HBC). Samples were obtained from 343 HBC patients in China. Three SNPs of IL-10 (−592A/C, −819C/T, and −1082A/G) were detected with polymerase chain-reaction-ligase detection reaction (PCR-LDR). The result showed the SNP-819C/T was significantly correlated with Deficiency syndrome (P=0.031), but none of the 3 loci showed correlation either with Child-Pugh classification and phase in HBC patients. The logistic regression analysis showed that the Excess syndrome was associated with dizzy and spider nevus, and the Deficiency syndrome was associated with dry eyes, aversion to cold, IL-10-819C/T loci, and IL-10-1082A/G loci. The odds ratio (OR) value at IL-10-819C/T was 4.022. The research results suggested that IL-10-819C/T locus (TC plus CC genotype) is probably a risk factor in the occurrence of Deficiency syndrome in HBC patients.
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15

Landuyt, Ashley E., Barbara J. Klocke, Lennard W. Duck, et al. "ICOS ligand and IL-10 synergize to promote host–microbiota mutualism." Proceedings of the National Academy of Sciences 118, no. 13 (2021): e2018278118. http://dx.doi.org/10.1073/pnas.2018278118.

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Genome-wide association studies have identified ICOSLG, which encodes the inducible costimulator ligand (ICOSLG or ICOSL) as a susceptibility locus for inflammatory bowel disease. ICOSL has been implicated in the enhancement of pattern recognition receptor signaling in dendritic cells, induction of IL-10 production by CD4 T cells, and the generation of high-affinity antibodies to specific antigens—all of which can potentially explain its involvement in gastrointestinal inflammation. Here, we show that murine ICOSL deficiency results in significant enrichment of IL-10–producing CD4 T cells particularly in the proximal large intestine. Transient depletion of IL-10–producing cells from adult ICOSL-deficient mice induced severe colonic inflammation that was prevented when mice were first treated with metronidazole. ICOSL-deficient mice displayed reduced IgA and IgG antibodies in the colon mucus and impaired serum antibody recognition of microbial antigens, including flagellins derived from mucus-associated bacteria of the Lachnospiraceae family. Confirming the synergy between ICOSL and IL-10, ICOSL deficiency coupled with CD4-specific deletion of the Il10 gene resulted in juvenile onset colitis that was impeded when pups were fostered by ICOSL-sufficient dams. In this setting, we found that both maternally acquired and host-derived antibodies contribute to the life anti-commensal antibody repertoire that mediates this protection in early life. Collectively, our findings reveal a partnership between ICOSL-dependent anti-commensal antibodies and IL-10 in adaptive immune regulation of the microbiota in the large intestine. Furthermore, we identify ICOSL deficiency as an effective platform for exploring the functions of anti-commensal antibodies in host–microbiota mutualism.
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16

Rong, Heng-Mo, Xiao-Jun Qian, Chao Zhang, Ting Li, and Zhao-Hui Tong. "IL-17 Inversely Correlated with IL-10 via the STAT3 Gene in Pneumocystis-Infected Mice." Mediators of Inflammation 2019 (September 10, 2019): 1–12. http://dx.doi.org/10.1155/2019/6750861.

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Background. Pneumocystis pneumonia (PCP) remains a common opportunistic infection in immunosuppressed individuals. Current studies showed that multiple immune cells and cytokines took part in the host defense against Pneumocystis (PC). However, the roles of IL-17 and IL-10 in the development of PCP have not been elucidated. Methods. IL-10 and IL-17 levels in serum from PCP mice were detected via ELISA. The percentages of B10 cells, IL-10+ macrophages, and IL-10+ T cells in the lung from IL-17–/– PCP mice and Th17 cells and IL-17+γδT cells in IL-10–/– PCP mice were examined via flow cytometry. Also, antibody neutralization examination was also performed to elucidate the relationship of IL-17 and IL-10 in the PCP model. Results. We noted the increase of IL-17 and IL-10 levels in serum from mice infected with Pneumocystis. Furthermore, deficiency of IL-17 or IL-10 could lead to the delayed clearance of Pneumocystis and more severed lung damage. Our data also demonstrated that IL-17 deficiency enhanced the serum IL-10 level and the percentages of B10 cells, IL-10+ macrophages, and IL-10+ T cells in the lung from PCP mice. Interestingly, we also noted an increase of the IL-17 level in serum and Th17 cell and IL-17+γδT cell percentages in the lung from IL-10–/– PCP mice. Using antibody neutralization experiments, we found that the STAT3 gene might play a critical role in the interplay of IL-17 and IL-10 in PCP. Conclusion. Taken together, our results demonstrated that IL-17 and IL-10 could play the protective roles in the progression of PCP and the inverse correlation of them might be mediated by STAT3.
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17

Roers, Axel, Lisa Siewe, Elke Strittmatter, et al. "T Cell–specific Inactivation of the Interleukin 10 Gene in Mice Results in Enhanced T Cell Responses but Normal Innate Responses to Lipopolysaccharide or Skin Irritation." Journal of Experimental Medicine 200, no. 10 (2004): 1289–97. http://dx.doi.org/10.1084/jem.20041789.

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Interleukin (IL)-10 is a regulator of inflammatory responses and is secreted by a variety of different cell types including T cells. T regulatory cells have been shown to suppress immune responses by IL-10–dependent, but also IL-10–independent, mechanisms. Herein, we address the role of T cell–derived IL-10 in mice with an inactivation of the IL-10 gene restricted to T cells generated by Cre/loxP-mediated targeting of the IL-10 gene. Splenocytes from this T cell–specific mutant secrete increased amounts of proinflammatory cytokines after activation in vitro compared with show enhanced contact hypersensitivity reactions, and succumb to severe immunopathology upon infection with Toxoplasma gondii. Despite intact IL-10 genes in other cell types, the dysregulation of T cell responses observed in the T cell–specific IL-10 mutant closely resembles the phenotype in complete IL-10 deficiency. However, in contrast to complete IL-10 deficiency, sensitivity to endotoxic shock and irritant responses of the skin are not enhanced in the T cell–specific IL-10 mutant. Our data highlight the importance of T cell–derived IL-10 in the regulation of T cell responses and demonstrate that endotoxic shock and the irritant response of the skin are controlled by IL-10 from other cell types.
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18

Neven, Benedicte, Emilie Mamessier, Julie Bruneau, et al. "A Mendelian Predisposition to B Cell Lymphoma Caused by IL-10R2 Deficiency." Blood 120, no. 21 (2012): 5092. http://dx.doi.org/10.1182/blood.v120.21.5092.5092.

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Abstract Abstract 5092 Background The fact that monogenic interleukin (IL)-10 and IL-10 receptor deficiencies cause very early-onset, severe inflammatory bowel disease demonstrates the IL-10 pathway's crucial role in preventing microbiota-driven gut inflammation. However, no other severe complications of IL-10/IL-10R deficiencies have been reported to date. Methods A cohort of six patients with IL-10/IL-10R deficiency was retrospectively surveyed for phenotypic expression. The identification of a number of cases of lymphoma prompted an in-depth characterization of available biopsy material, with immunohistochemical staining, cytogenetic studies and gene expression profiling. Results Four patients (all with a complete IL-10R2 deficiency) had developed B cell non-Hodgkin's lymphoma between the ages of 5 and 6 years. Cytogenetic and IgH clonality analyses suggested that one of the patients developed at least 3 distinct lymphomas. The patients' tumors had the characteristics of diffuse large B cell lymphomas and contained monoclonal, Epstein-Barr-virus-negative germinal center B cells. Nuclear expression of the NF-κB factor c-REL was detected in all of the six lymphomas tested. Conclusions IL-10R deficiency is associated with a high risk of developing a B cell lymphoma with an unusual phenotype. Our results highlight an unexpected role of the IL-10R pathway in the control of lymphomagenesis. Disclosures: No relevant conflicts of interest to declare.
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19

Pini, Maria, Melissa E. Gove, Raja Fayad, Robert J. Cabay, and Giamila Fantuzzi. "Adiponectin deficiency does not affect development and progression of spontaneous colitis in IL-10 knockout mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 2 (2009): G382—G387. http://dx.doi.org/10.1152/ajpgi.90593.2008.

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The goal of this study was to investigate the role of the adipokine adiponectin (APN) in development of spontaneous colitis in IL-10 knockout (KO) mice. To this aim, we generated double IL-10 APN KO mice and compared their disease development to that of single IL-10 KO mice. Both IL-10 KO and double IL-10 APN KO mice spontaneously developed colitis of comparable severity. No significant differences in inflammatory infiltrate or crypt elongation were observed in colonic tissue obtained from IL-10 KO and double IL-10 APN KO mice at either 12 or 20 wk of age. A comparable increase in circulating levels of serum amyloid A and IFN-γ was observed in IL-10 KO and double IL-10 APN KO mice as disease progressed. In vitro stimulation of lymphocytes from mesenteric lymph nodes with anti-CD3 and anti-CD28 induced a significantly higher production of IL-17 and TNF-α in IL-10 KO and double IL-10 APN KO mice compared with their healthy littermates. No significant differences in cytokine production from lymphocytes or colonic mRNA expression of cytokines were observed between IL-10 KO and double IL-10 APN KO mice. Both IL-10 KO and double IL-10 APN KO mice had a similar decrease in body weight and bone mass compared with their respective healthy littermates. Finally, APN deficiency did not lead to development of insulin resistance, either in APN KO or double IL-10 APN KO mice. In conclusion, lack of APN does not play a significant role in the pathogenesis of spontaneous colonic inflammation in the IL-10 KO model.
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20

Lukic, Miodrag L., Hui-Rong Jiang, Zakeya Al Rasebi, et al. "Galectin-3 deficiency reduces the severity of experimental autoimmune encephalomyelitis (99.5)." Journal of Immunology 182, no. 1_Supplement (2009): 99.5. http://dx.doi.org/10.4049/jimmunol.182.supp.99.5.

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Abstract Galectin-3 (Gal-3) is a member of β-galactoside-binding lectin family and plays an important role in inflammatory. However, the precise role of Gal-3 in autoimmune diseases remains obscure. We have investigated the functional role of Gal-3 in experimental autoimmune encephalomyelititis (EAE) following immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. Gal-3 deficient (Gal-3-/-) mice developed significantly milder EAE and markedly reduced leukocyte infiltration in the CNS compared with similarly treated wild-type (WT) mice. Gal-3-/- mice also contained fewer monocytes and macrophages but more apoptotic cells in the CNS than did WT mice. Following Ag stimulation in vitro, lymph node cells from the immunized Gal-3-/- mice produced less IL-17 and IFN-γ than did those of the WT mice. In contrast, Gal-3-/- mice produced more serum IL-10, IL-5 and IL-13 and contained higher frequency of Foxp3+ regulatory T cells in the CNS than did the WT mice. Furthermore, bone marrow-derived dendritic cells from Gal-3-/- mice produced more IL-10 in response to LPS or bacterial lipoprotein than did WT marrow-derived dendritic cells. Moreover, Gal-3-/- dendritic cells induced AG-specific T cells to produce more IL-10, IL-5 and IL-12, but less IL-17 than did WT dendritic cells. Taken together, our data demonstrate that Gal-3 plays an important disease-exacerbating role in EAE through its multifunctions roles in preventing cell apoptosis and increasing IL-17 and IFN-γ synthesis, but decreasing IL-10 production.
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Lazarus, John J., Michelle J. Meadows, Robert E. Lintner, and R. Mark Wooten. "IL-10 Deficiency Promotes IncreasedBorrelia burgdorferiClearance Predominantly through Enhanced Innate Immune Responses." Journal of Immunology 177, no. 10 (2006): 7076–85. http://dx.doi.org/10.4049/jimmunol.177.10.7076.

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22

WHARY, M., B. SHEPPARD, J. CLINE, S. XU, and J. FOX. "IL-10 deficiency reduces Helicobacter pylori gastric colonization in C57BL/6 mice." Gastroenterology 120, no. 5 (2001): A99—A100. http://dx.doi.org/10.1016/s0016-5085(01)80488-1.

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23

Whary, Mark T., Barbara J. Sheppard, Jennifer Cline, Sandy Xu, and James G. Fox. "IL-10 deficiency reduces Helicobacter pylori gastric colonization in C57BL/6 mice." Gastroenterology 120, no. 5 (2001): A99—A100. http://dx.doi.org/10.1016/s0016-5085(08)80488-x.

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24

Sato, Yuichirou, Seiichi Takahashi, Yoshitaka Kinouchi, et al. "IL-10 deficiency leads to somatic mutations in a model of IBD." Carcinogenesis 27, no. 5 (2006): 1068–73. http://dx.doi.org/10.1093/carcin/bgi327.

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Hoffmann, Dirk, Johanna Sens, Sebastian Brennig, et al. "Genetic Correction of IL-10RB Deficiency Reconstitutes Anti-Inflammatory Regulation in iPSC-Derived Macrophages." Journal of Personalized Medicine 11, no. 3 (2021): 221. http://dx.doi.org/10.3390/jpm11030221.

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Patient material from rare diseases such as very early-onset inflammatory bowel disease (VEO-IBD) is often limited. The use of patient-derived induced pluripotent stem cells (iPSCs) for disease modeling is a promising approach to investigate disease pathomechanisms and therapeutic strategies. We successfully developed VEO-IBD patient-derived iPSC lines harboring a mutation in the IL-10 receptor β-chain (IL-10RB) associated with defective IL-10 signaling. To characterize the disease phenotype, healthy control and VEO-IBD iPSCs were differentiated into macrophages. IL-10 stimulation induced characteristic signal transducer and activator of transcription 3 (STAT3) and suppressor of cytokine signaling 3 (SOCS3) downstream signaling and anti-inflammatory regulation of lipopolysaccharide (LPS)-mediated cytokine secretion in healthy control iPSC-derived macrophages. In contrast, IL-10 stimulation of macrophages derived from patient iPSCs did not result in STAT3 phosphorylation and subsequent SOCS3 expression, recapitulating the phenotype of cells from patients with IL-10RB deficiency. In line with this, LPS-induced cytokine secretion (e.g., IL-6 and tumor necrosis factor-α (TNF-α)) could not be downregulated by exogenous IL-10 stimulation in VEO-IBD iPSC-derived macrophages. Correction of the IL-10RB defect via lentiviral gene therapy or genome editing in the adeno-associated virus integration site 1 (AAVS1) safe harbor locus led to reconstitution of the anti-inflammatory response. Corrected cells showed IL-10RB expression, IL-10-inducible phosphorylation of STAT3, and subsequent SOCS3 expression. Furthermore, LPS-mediated TNF-α secretion could be modulated by IL-10 stimulation in gene-edited VEO-IBD iPSC-derived macrophages. Our established disease models provide the opportunity to identify and validate new curative molecular therapies and to investigate phenotypes and consequences of additional individual IL-10 signaling pathway-dependent VEO-IBD mutations.
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Gaistruk, N. A., L. G. Dubas, A. N. Gaistruk, A. V. Melnik, and O. L. Liovkina. "Pathogenetic role of vitamin D deficiency and immune-inflammatory disorders in development of fetal distress in pregnant women with chronic hydramnion." Likarska sprava, no. 3-4 (June 30, 2020): 14–20. http://dx.doi.org/10.31640/jvd.3-4.2020(3).

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The role of vitamin D deficiency and immune-inflammatory disorders in the mechanisms of development of fetal distress in pregnant women with chronic polyhydramnios remains unexplored. Objective: to evaluate the role of vitamin D deficiency and associated immune inflammatory disorders in the development of fetal distress in pregnant women with chronic polyhydramnios. Materials and methods. Surveyed 30 women with a physiological course of pregnancy and 90 pregnant women with chronic polyhydramnios. In the serum, the level of the metabolite of vitamin D – 25(OH)D and the cytokines IL-10 and IL-6 were determined by enzyme immunoassay using standard kits. Statistical processing of the obtained results was performed using standard methods using the «MS Excel» and «Statistica SPSS 10.0 for Windows» application package. The results of the research. In pregnant women with chronic polyhydramnios, there is a significant decrease of the metabolite of vitamin D – 25(OH)D level by 21 % in the serum, a decrease of the level of the anti-inflammatory cytokine IL-10 by 26.4 % and an increase of the concentration of pro-inflammatory IL-6 by 17 % compared to women with physiological course of pregnancy. The occurrence of fetal distress against the background of chronic polyhydramnios is accompanied by a intensification of vitamin D deficiency and immune-inflammatory disorders: levels 25(OH)D and IL-10, respectively, by 18.5 % and 17.5 % less, and IL-6 by 13.3 %, than in women with chronic polyhydramnios without fetal distress. The expressiveness of immune disorders in the organism of pregnant women with chronic polyhydramnios is determined by the level of vitamin D in the organism. Thus, in women with a deficiency of 25(OH)D in the serum, a significant decrease in the IL-10 concentration by 47.8 % and a significant increase in the IL-6 level by 34.6 % were recorded in comparison with the indicators in women with vitamin D deficiency. Conclusions. Vitamin D deficiency and associated immune-inflammatory disorders play an important role in the development of fetal distress in pregnant women with chronic polyhydramnios.
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Bai, Xue-Feng, Jin-Qing Liu, Joseph Carl, Jr., et al. "Enhanced T cell proliferation, Th17 differentiation and unaltered IL-10 production lead to marginally enhanced development of experimental autoimmune encephalomyelitis in EBI3-deficient mice (114.12)." Journal of Immunology 186, no. 1_Supplement (2011): 114.12. http://dx.doi.org/10.4049/jimmunol.186.supp.114.12.

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Abstract Epstein-Barr virus-induced gene 3 (EBI3) encoded protein can form heterodimers with IL-27P28 and IL-12P35 to form IL-27 and IL-35. IL-27 and IL-35 may influence autoimmunity through inhibiting Th17 differentiation, and facilitating the inhibitory roles of Foxp3+ Treg cells, repectively. In this study we have evaluated the development of experimental autoimmune encephalomyelitis (EAE) in EBI3-deficient mice that lack both IL-27 and IL-35. We found that MOG peptide immunization resulted in marginally enhanced EAE development in EBI3-deficient C57BL6 and 2D2 TCR transgenic mice. EBI3-deficiency resulted in significantly increased proliferation and Th17 differentiation of MOG-specific CD4 T cells in the peripheral lymphoid organs and in the central nervous system (CNS). However, IL-10 production was not affected or even enhanced in the peripheral lymphoid organs or the CNS of EBI3-deficient mice. Treg cells from EBI3-deficient 2D2 mice had reduced capacity of inhibiting proliferation of 2D2 T cells. Taken together, we have found that EBI3-deficiency results in marginally enhanced EAE severity, which is associated with enhanced T cell proliferation and Th17 differentiation. However, the relatively milder EAE enhancement and lack of impact on IL-10 production by EBI3-deficiency suggest that alternative signaling pathways (presumably IL27P28-related) can partially compensate for EBI3-deficiency in EBI3-/- mice.
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Balto, Khaled, Hajime Sasaki, and Philip Stashenko. "Interleukin-6 Deficiency Increases Inflammatory Bone Destruction." Infection and Immunity 69, no. 2 (2001): 744–50. http://dx.doi.org/10.1128/iai.69.2.744-750.2001.

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ABSTRACT Periapical bone destruction occurs as a consequence of pulpal infection. In previous studies, we showed that interleukin-1 (IL-1) is the primary stimulator of bone destruction in this model. IL-6 is a pleiotropic cytokine that is induced in these infections and has both pro- and anti-inflammatory activities. In the present study, we determined the role of IL-6 in regulating IL-1 expression and bone resorption. The first molars of IL-6 knockouts (IL-6−/−) and wild-type mice were subjected to surgical pulp exposure and infection with a mixture of four common pulpal pathogens, includingPrevotella intermedia, Fusobacterium nucleatum,Peptostreptococcus micros, and Streptococcus intermedius. Mice were killed after 21 days, and bone destruction and cytokine expression were determined. Surprisingly, bone destruction was significantly increased in IL-6−/− mice versus that in wild-type mice (by 30%; P < 0.001). In a second experiment, the effects of chronic (IL-6−/−) IL-6 deficiency and short-term IL-6 deficiency induced by in vivo antibody neutralization were determined. Both IL-6−/− (30%;P < 0.001) and anti-IL-6 antibody-treated mice (40%;P < 0.05) exhibited increased periapical bone resorption, compared to wild-type controls. The increased bone resorption in IL-6-deficient animals correlated with increases in osteoclast numbers, as well as with elevated expression of bone-resorptive cytokines IL-1α and IL-1β, in periapical lesions and with decreased expression of the anti-inflammatory cytokine IL-10. These data demonstrate that endogenous IL-6 expression has significant anti-inflammatory effects in modulating infection-stimulated bone destruction in vivo.
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Yahia, Ramadan, Shereen M. Mohammed, Manal M. Hassanien, Shabaan H. Ahmed, and Helal F. Hetta. "Vitamin D as a Key Player in Modulating Rheumatoid Arthritis-derived Immune Response." Journal of Pure and Applied Microbiology 14, no. 4 (2020): 2453–65. http://dx.doi.org/10.22207/jpam.14.4.23.

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Rheumatoid arthritis (RA) is a systemic inflammatory disease with chronic nature of joints related to autoimmunity. Vitamin D was found to modulate cell growth, function of immune cells and anti-inflammatory action. The aims of that study were to investigate serum level of vitamin D and some cytokines and to identify the correlation between vitamin D and these cytokines in RA. Totally 40 RA patients without vitamin D supplement were involved in this study. Serum level of vitamin D, interleukin-6 (IL-6), IL-10, IL-35, C-reactive protein (CRP) and tumor necrosis factor α (TNF-α), all of them were measure in all patients by enzyme-linked immunosorbent assay (ELISA). Patients were classified according to Vitamin D levels into two groups; RA patients with Vit. D deficiency (n=25) and RA patients with Vit. D sufficiency (n=15). IL-6 was lower significantly (P = 0.03) in RA patients with Vit. D sufficiency than RA patients with Vit. D deficiency. IL-10 and IL-35 were higher significantly (P = 0.0234, P = 0.0356 respectively) in RA patients with Vit. D sufficiency than RA patients with Vit. D deficiency. Vit. D was significantly positively correlated with both IL-10 (r = 0.4516, P = 0.0034) and IL-35 (r = 0.3424, P = 0.0329) and negatively correlated with IL-6 (r = -0.3188, P = 0.0479). Sufficient serum level of Vit. D is correlated with higher level of anti-inflammatory cytokines (IL-10 and IL-35) and lower level of IL-6. This support the immunomodulatory effect of Vit. D in RA.
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AVANZINI, M. "Specific synergic effect of IL-4 and IL-10 on in vitro IgA producction in IgA deficiency." Molecular Immunology 35, no. 11-12 (1998): 744. http://dx.doi.org/10.1016/s0161-5890(98)90424-2.

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Papoutsopoulou, Stamatia, Liam Pollock, Jonathan M. Williams, et al. "Interleukin-10 Deficiency Impacts on TNF-Induced NFkB Regulated Responses In Vivo." Biology 11, no. 10 (2022): 1377. http://dx.doi.org/10.3390/biology11101377.

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Interleukin-10 (IL-10) is an anti-inflammatory cytokine that has a major protective role against intestinal inflammation. We recently revealed that intestinal epithelial cells in vitro regulate NFkB-driven transcriptional responses to TNF via an autocrine mechanism dependent on IL-10 secretion. Here in this study, we investigated the impact of IL-10 deficiency on the NFkB pathway and its downstream targets in the small intestinal mucosa in vivo. We observed dysregulation of TNF, IkBa, and A20 gene and protein expression in the small intestine of steady-state or TNF-injected Il10-/- mice, compared to wild-type C57BL6/J counterparts. Upon TNF injection, tissue from the small intestine showed upregulation of NFkB p65[RelA] activity, which was totally diminished in Il10-/- mice and correlated with reduced levels of TNF, IkBa, and A20 expression. In serum, whilst IgA levels were noted to be markedly downregulated in IL-10-deficient- mice, normal levels of mucosal IgA were seen in intestine mucosa. Importantly, dysregulated cytokine/chemokine levels were observed in both serum and intestinal tissue lysates from naïve, as well as TNF-injected Il10-/- mice. These data further support the importance of the IL-10-canonical NFkB signaling pathway axis in regulating intestinal mucosa homeostasis and response to inflammatory triggers in vivo.
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Neven, Bénédicte, Emilie Mamessier, Julie Bruneau, et al. "A Mendelian predisposition to B-cell lymphoma caused by IL-10R deficiency." Blood 122, no. 23 (2013): 3713–22. http://dx.doi.org/10.1182/blood-2013-06-508267.

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Key Points Human inherited IL-10 receptor deficiency is associated with a very high risk of non-EBV–related diffuse large B-cell lymphoma. IL-10 signaling may be involved in the immune control of germinal center B-cell lymphoma.
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Kader, Muhamuda, Mounia Alaoui-El-Azher, Bhushan Kode, et al. "MyD88 suppresses IL-10 and IL-17 production in response to obligate intracellular Ehrlichia infection." Journal of Immunology 196, no. 1_Supplement (2016): 206.1. http://dx.doi.org/10.4049/jimmunol.196.supp.206.1.

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Abstract Ehrlichia is an obligate intracellular gram negative bacterium that target macrophages, and causes the potentially fatal human monocytic ehrlichiosis (HME). In murine models of fatal ehrlichiosis (FE), Ixodes ovatus Ehrlichia (IOE) inhibits autophagy, suppresses protective acquired immunity, and causes immunopathology and toxic shock syndrome. Innate Ehrlichia detection by TLR2 mediates host resistance, while NOD2 signaling confers host susceptibility to FE. Recently, we have shown that deficiency of type I interferon receptor (IFNaR) phenocopy NOD2 deficiency in IOE-infected mice, implying a contribution of both NOD2-IFNaR pathways to susceptibility to FE. However, how TLR2 mediates protective function against Ehrlichia is not clearly defined. Here, we investigated the role of MyD88, the main adaptor molecule for the TLRs in host response to virulent IOE using MyD88 knockout mice (MyD88−/−). Our data showed that, MyD88−/− mice have an impaired bacterial clearance, increased liver injury, and a heightened mortality when compared to infected wild type (WT) mice. Increased bacterial load in MYD88−/− mice correlates with decreased levels of TNF-α in both in vivo and in vitro {serum and IOE- infected bone marrow-derived macrophages (BMM)}, and increased frequency of splenic CD4+ T cells producing IL-10 and IL-17. Protective anti-Ehrlichia immunity and minimal pathology in WT mice infected with low virulent Ehrlichia species correlates with a high Th1 response, but a low frequency of IL-10 and IL-17 producing splenic T cells, suggesting that IL-10 and IL-17 may play pathogenic roles in host defense against Ehrlichia. Together these data suggest that MYD88 plays a protective role in ehrlichiosis via suppression of IL-10 and IL-17.
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Moriaitis, Andreas, Lita Freeman, Robert Shamburek, et al. "Elevated Interleukin-10 and “Disappearing HDL Syndrome” in Lymphoproliferative Disorders." Blood 124, no. 21 (2014): 4134. http://dx.doi.org/10.1182/blood.v124.21.4134.4134.

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Abstract BACKGROUND: Acquired severe HDL deficiency is relatively uncommon. It may occur with use of high doses of anabolic steroids or in severe liver diseases, which can lead to low LCAT activity and decreased apoA-I production. “Disappearing HDL Syndrome”*, a term first used by Goldberg and Mendez, refers to cases of severe HDL deficiency in patients that are not critically ill, sometimes long before the clinical or biochemical features of the underlying primary disease become evident. Disappearing HDL Syndrome can also result from an idiosyncratic reaction to medications, such as peroxisome proliferation-activated receptor (PPAR) agonists. Additionally, autoantibodies against LCAT in non-Hodgkin lymphoma have been described as a possible cause. Low high-density lipoprotein-cholesterol (HDL-C) is a risk factor for coronary artery disease. OBJECTIVE: To determine the cause of low HDL-C in patients with severe acquired HDL deficiency noted as an incidental finding associated with lymphoma and autoimmune lymphoproliferative syndrome (ALPS)** as well as following recombinant human IL10 therapy in psoriatric arthritis patients. Investigating mechanisms underlying acquired severe HDL deficiency in non-critically ill patients (“Disappearing HDL Syndrome”) could provide new insights into HDL metabolism and its role in lymphomagenesis. PATIENTS AND RESULTS: Patients with intravascular large B-cell lymphoma (IVLBCL, n=2), diffuse large B-cell lymphoma (DLBCL, n=1), and ALPS-FAS (n=1) presenting with markedly decreased HDL-C, low LDL-C and elevated triglycerides were identified. The abnormal lipoprotein profile returned to normal following therapy in all four cases (Figure). All of them were found to have markedly elevated serum interleukin-10 (IL-10) levels at presentation that also normalized following therapy. Besides accumulation of abnormal lymphocytes in lymph nodes and spleen, ALPS patients have elevated serum IL-10. In a cohort of ALPS patients with genetic mutations in FAS (n=93), IL-10 showed a strong inverse correlation with HDL-C (R2=0á3720, P<0á0001). A direct causal role for increased serum IL-10 in inducing the observed changes in lipoproteins was established in a randomized, placebo-controlled clinical trial of recombinant human IL-10 (rhIL-10) in psoriatic arthritis patients (n=18). Within a week of initiating subcutaneous rhIL-10 injections, HDL-C precipitously decreased to near-undetectable levels. LDL-C also decreased by over 50% (P<0.0001) and triglycerides increased by approximately 2-fold (P<0.005). All values returned to baseline after stopping IL-10 therapy. CONCLUSION: Increased IL-10 causes severe HDL-C deficiency, low LDL-C and elevated triglycerides. IL-10 is thus a potent modulator of lipoprotein levels, a potential new biomarker for B-cell disorders, and a novel cause of Disappearing HDL Syndrome. Elevated IL-10 plays a key role in linking inflammation and lipoprotein metabolism. As evidence for its causality, rhIL-10 treatment in a clinical trial of psoriasitic arthritis patients precipitously lowered HDL-C. Finding elevated IL-10 as a cause of “Disappearing HDL Syndrome” in patients with 3 different types of B-cell disorders suggests that IL-10 and low HDL-C could be useful biomarkers of disease activity in these conditions. Finally, future research focusing on strategies to alter lipoprotein levels by modulating circulating IL-10 levels or its signaling pathways may be useful for developing novel targeted therapies. *Ref: Severe acquired (secondary) high-density lipoprotein deficiency. Goldberg RB, Mendez AJ. J Clin Lipidol. 2007;1:41-56 **Ref: Natural history of autoimmune lymphoproliferative syndrome associated with FAS gene mutations. Price S, Shaw PA, Seitz A et al. Blood. 2014 Mar 27;123(13):1989-99. Figure. Concomitant drop in IL-10 associated with HDL-C recovery during treatment in patients with B-cell disorders. IL-10 and HDL-C time course before and after chemotherapy in: (A, B) 2 IVLBCL and (C) 1 DLBCL patients. The first time point (“Day 0”) represents the last lipid time point before initiating chemotherapy (arrow). D. Recovery of HDL-C and IL-10 in an ALPS patient after treatment with sirolimus over a period of 6 years. P* denotes high dose (15 mg/day) prednisone pulse therapy in this 2 year old ALPS patient. Figure. Concomitant drop in IL-10 associated with HDL-C recovery during treatment in patients with B-cell disorders. IL-10 and HDL-C time course before and after chemotherapy in: (A, B) 2 IVLBCL and (C) 1 DLBCL patients. The first time point (“Day 0”) represents the last lipid time point before initiating chemotherapy (arrow). D. Recovery of HDL-C and IL-10 in an ALPS patient after treatment with sirolimus over a period of 6 years. P* denotes high dose (15 mg/day) prednisone pulse therapy in this 2 year old ALPS patient. Disclosures No relevant conflicts of interest to declare.
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Abston, Eric D., Michael J. Coronado, Adriana Bucek, et al. "TLR3 deficiency induces chronic inflammatory cardiomyopathy in resistant mice following coxsackievirus B3 infection: role for IL-4." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 4 (2013): R267—R277. http://dx.doi.org/10.1152/ajpregu.00516.2011.

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Recent findings indicate that TLR3 polymorphisms increase susceptibility to enteroviral myocarditis and inflammatory dilated cardiomyopathy (iDCM) in patients. TLR3 signaling has been found to inhibit coxsackievirus B3 (CVB3) replication and acute myocarditis in mouse models, but its role in the progression from myocarditis to iDCM has not been previously investigated. In this study we found that TLR3 deficiency increased acute ( P = 5.9 × 10−9) and chronic ( P = 6.0 × 10−7) myocarditis compared with WT B6.129, a mouse strain that is resistant to chronic myocarditis and iDCM. Using left ventricular in vivo hemodynamic assessment, we found that TLR3-deficient mice developed progressively worse chronic cardiomyopathy. TLR3 deficiency significantly increased viral replication in the heart during acute myocarditis from day 3 through day 12 after infection, but infectious virus was not detected in the heart during chronic disease. TLR3 deficiency increased cytokines associated with a T helper (Th)2 response, including IL-4 ( P = 0.03), IL-10 ( P = 0.008), IL-13 ( P = 0.002), and TGF-β1 ( P = 0.005), and induced a shift to an immunoregulatory phenotype in the heart. However, IL-4-deficient mice had improved heart function during acute CVB3 myocarditis by echocardiography and in vivo hemodynamic assessment compared with wild-type mice, indicating that IL-4 impairs cardiac function during myocarditis. IL-4 deficiency increased regulatory T-cell and macrophage populations, including FoxP3+ T cells ( P = 0.005) and Tim-3+ macrophages ( P = 0.004). Thus, TLR3 prevents the progression from myocarditis to iDCM following CVB3 infection by reducing acute viral replication and IL-4 levels in the heart.
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Sun, Xiaofei, Monica Cappelletti, Yingju Li, Christopher L. Karp, Senad Divanovic, and Sudhansu K. Dey. "Cnr2 Deficiency Confers Resistance to Inflammation-Induced Preterm Birth in Mice." Endocrinology 155, no. 10 (2014): 4006–14. http://dx.doi.org/10.1210/en.2014-1387.

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Abstract Infection-induced inflammation, frequently associated with increased production of proinflammatory cytokines, is considered a significant contributor to preterm birth. A G protein-coupled cannabinoid receptor 2 (CB2), encoded by Cnr2, is expressed in various immune cells and was shown to modulate immune responses. We show here that Cnr2, but not Cnr1, deficient mice are resistant to lipopolysaccharide (LPS)-driven preterm birth and suppression of serum progesterone levels. After LPS challenge, Cnr2−/− mice exhibited increased serum levels of IL-10 with decreased IL-6 levels. These changes were associated with reduced LPS-induced Ptgs2 expression at the maternal-conceptus interface on day 16 of pregnancy. LPS stimulation of Cnr2−/− dendritic cells in vitro resulted in increased IL-10 with reduced IL-6 production and correlated with increased cAMP accumulation. Collectively, our results suggest that increased IL-10 production occurring via augmented cAMP accumulation represents a potential mechanism for the resistance of Cnr2−/− mice to LPS-induced preterm birth. These results may have clinical relevance, because currently, there are limited options to prevent preterm birth.
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Moon, Sung, Jeong-Im Woo, Sejo Oh, Yoojin Lee, Okjin Ahn, and David Lim. "IL-10-mediated modulation of cochlear inflammation (P6228)." Journal of Immunology 190, no. 1_Supplement (2013): 115.10. http://dx.doi.org/10.4049/jimmunol.190.supp.115.10.

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Abstract Inflammatory response is commonly involved in the pathogenesis of various cochlear diseases such as acoustic trauma and cisplatin ototoxicity. Previously, we have demonstrated that the spiral ligament fibrocytes play a pivotal role in cochlear inflammation through secretion of chemokines such as CCL2 and CXCL2 in response to pro-inflammatory signals. In this study, we aim to determine molecular mechanism involved in negative modulation of cochlear inflammation. We found that IL-10 inhibits SLF’s CCL2 up-regulation and migration of THP-1 cells in response to SLF-derived molecules. The SLFs appeared to up-regulate HMOX1 expression via NRF-2 activation. The inhibitory effect of IL-10 was mimicked by CoPP and CORM-3 but was blocked by silencing of IL-10RA and HMOX1. IL-10 was found to inhibit binding of p65 NFκB to the enhancer region of the CCL2 gene. IL-10 deficiency appeared to enhance cochlear inflammation secondary to nontypeable H. influenzae-induced otitis media. Furthermore, we demonstrated that the cochlear macrophages serve as a local source of IL-10, which appeared to be primarily distributed in the stria vascularis. Our results suggest that cochlear macrophage-derived IL-10 modulates cochlear inflammation by inhibition of SLF’s CCL2 up-regulation through HMOX1-mediated CO production. This study is anticipated providing us with a novel strategy for the management of inflammation-associated cochlear diseases.
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Jeong, Eui-Suk. "Role of IL-10 Deficiency in Pneumonia Induced by Corynebacterium kutscheri in Mice." Journal of Microbiology and Biotechnology 19, no. 4 (2009): 424–30. http://dx.doi.org/10.4014/jmb.0807.436.

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Tewari, N., SP Murphy, and S. Sharma. "1141635485 Genetic stress (IL-10 deficiency) and toxicant (PCB)-induced disruption of pregnancy." American Journal of Reproductive Immunology 55, no. 6 (2006): 408. http://dx.doi.org/10.1111/j.1600-0897.2006.00383_39.x.

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Kobbe, Philipp, Burkhard Stoffels, Joachim Schmidt, et al. "IL-10 deficiency augments acute lung but not liver injury in hemorrhagic shock." Cytokine 45, no. 1 (2009): 26–31. http://dx.doi.org/10.1016/j.cyto.2008.10.004.

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de Lemos Rieper, Carina, Pia Galle, Bente Klarlund Pedersen, and Morten Bagge Hansen. "A state of acquired IL-10 deficiency in 0.4% of Danish blood donors." Cytokine 51, no. 3 (2010): 286–93. http://dx.doi.org/10.1016/j.cyto.2010.06.009.

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Koh, Byunghee, and Mark H. Kaplan. "Etv5 promotes IL-10 production in Th2 cells." Journal of Immunology 196, no. 1_Supplement (2016): 58.15. http://dx.doi.org/10.4049/jimmunol.196.supp.58.15.

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Abstract The anti-inflammatory cytokine, IL-10, suppresses inflammatory responses at mucosal surfaces. Among T helper cell subsets, Th2 cells produce the highest concentrations. However, the transcription factors that regulate Il10 gene expression have not been completely defined. Etv5 is a member of the ETS transcription factor family that promotes production of IL-17 in Th17 cells and IL-9 in Th9 cells. To define the effects of Etv5 deficiency on cytokine expression in Th2 cells, T cells from CD4 specific Etv5 knockout (Etv5fl/flCD4-Cre+, termed Etv5 KO below) and littermate control (Etv5fl/fl CD4-Cre-, termed WT below) mice were differentiated under Th2 conditions. Etv5 was required for maximal IL-10 production and modestly repressed the Th2 cytokines IL-4, IL-5 and IL-13. In mice sensitized with Aspergilus fumigatus extract, IL-10 production in both BAL and lung was significantly reduced in Etv5 KO mice, consistent with in vitro data. Using ChIP and reporter assays, we showed that Etv5 directly binds to the Il10 locus, specifically at the CNS3 region. Etv5 promotes IL-10 production by recruiting IL-10 inducing transcription factors including Jun family members, IRF4 and E4BP4, and the binding of these factors to the Il10 locus, but not the expression of these factors, was decreased in the absence of Etv5. Ectopic GATA3 and E4BP4 expression recovers IL-10 production to wild type amounts, suggesting that Etv5 enhances the efficiency of function of these factors. Importantly, ectopic Etv5 expression in Etv5 KO Th2 cells restored binding of the factors to the Il10 locus. Thus, Etv5 promotes IL-10 production by enhancing the recruitment of IL-10 inducing transcription factors.
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Wang, Lei, Li Zhang, Xiaoxia Feng, et al. "The Functional Difference of Dendritic Cells in HBeAg Negative Chronic Hepatitis B Patients with Three Different Spleen Deficiency Syndromes and the Therapeutic Evaluation of Chinese Medicine Intervention Based on Syndrome Differentiation." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/802402.

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Objective. To investigate the dendritic cells (DCs) maturity differences of HBeAg negative chronic hepatitis B (CHB) patients with different spleen deficiency (SD) syndromes and explore the role of syndrome differentiation in the therapeutic evaluation of Chinese medicine.Methods. 120 participants were recruited including three treatment groups in different SD syndrome categories as spleen deficiency with liver depression (SDLD), spleen deficiency with damp heat (SDDH), and spleen deficiency with kidney deficiency (SDKD) and one healthy control group; each group had 30 participants. Corresponding drugs were applied. The outcome measures included DC phenotype, liver function, IL-10, IL-12, and HBV-DNA levels.Results.The surface markers of mature DCs and cytokines levels were different in each group; the positive rate of CD80, CD1a, HLA-DR, and CD1a was the lowest in SDKD group. After 3-month intervention, the expression of CD80, CD86, CD1a, HLA-DR, and IL-12 significantly increased, while ALT, AST, and IL-10 significantly decreased (P<0.05) in treatment groups. HBV-DNA level also significantly reduced in both SDKD and SDLD groups (P<0.05).Conclusions.HBeAg negative patients had DCs dysmaturity, and there were differences between different SD syndromes. Chinese medicine intervention according to syndrome differentiation could advance the maturity and function of DCs and improve the therapeutic effect.
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Nguyen, Deanna, Jeremy Goettel, Marc-Andre Wurbel, et al. "Colitis in mice with WASP deficiency in innate immune cells is associated with impairment in IL-10 production (71.10)." Journal of Immunology 188, no. 1_Supplement (2012): 71.10. http://dx.doi.org/10.4049/jimmunol.188.supp.71.10.

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Abstract Colitis occurs in mice and some patients deficient in the Wiskott-Aldrich Syndrome protein (WASP), a hematopoietic-specific molecule that regulates the actin cytoskeleton. This colitis is lymphocyte-dependent, but severe disease is observed in chimeric mice with WT T cells and WASP KO innate immune cells, generated by transfer of WT CD4+ T cells into WASP/RAG DKO mice. Given the immunomodulatory function of IL-10, coupled with our findings that mixed bone marrow chimeras are free of colitis, we investigated whether alterations in IL-10 play a role in our colitis model. We found reduced IL-10 transcript levels in mesenteric lymph nodes of chimeric mice. To tease out the cellular source of decreased IL-10 production, WASP/RAG DKO DCs were stimulated in vitro and observed to produce less IL-10. We then transferred IL-10GFP CD4+ cells and found a reduction in the IL-10-expressing proportion of T cells in WASP/RAG DKO compared to RAG KO mice. Lastly, exogenous administration of IL-10-Ig completely abrogated disease in chimeric mice. In summary, besides impaired Treg homeostasis and function, severe colitis in our chimeric mice is associated with reduced IL-10 production in MLNs and in vitro stimulated DCs. Taken together with prevention of disease with IL-10 treatment, colitis in this model may result from decreased IL-10 production by WASP KO innate immune cells.
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Yang, Xi, Shuhe Wang, Yijun Fan, and Xiaobing Han. "IL-10 deficiency prevents IL-5 overproduction and eosinophilic inflammation in a murine model of asthma-like reaction." European Journal of Immunology 30, no. 2 (2000): 382–91. http://dx.doi.org/10.1002/1521-4141(200002)30:2<382::aid-immu382>3.0.co;2-l.

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Turner, Joanne, Joshua Cyktor, Bridget Carruthers, Rachel Kominsky, Paul Stromberg, and Gillian Beamer. "Deficiency in interleukin 10 reverses the susceptibility phenotype of CBA/J mice during infection with Mycobacterium tuberculosis. (43.23)." Journal of Immunology 188, no. 1_Supplement (2012): 43.23. http://dx.doi.org/10.4049/jimmunol.188.supp.43.23.

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Abstract Interleukin 10 is a known correlate of susceptibility to tuberculosis (TB) in man and similarly, elevated levels of IL-10 (either natural or induced) in mice can accelerate TB disease progression. The CBA/J mouse strain is a model that naturally produces abundant IL-10 and is also highly susceptible to infection with Mycobacterium tuberculosis (M.tb). We have generated CBA/J mice deficient in IL-10 (IL-10 KO) to determine the mechanisms of influence of IL-10 on TB disease progression in this highly susceptible mouse strain. In contrast to IL-10 KO on resistant mouse strain backgrounds where the lack of IL-10 has little impact on TB outcome, the CBA/J IL-10 KO was fully capable of limiting M.tb growth within the lung and spleen for an extended period of time, with over 2 Log fewer M.tb colony forming units (CFU), compared to CBA/J wild type. This reduction in bacterial growth correlated with a highly significant extension in survival, relative to CBA/J wild type mice. The ability to control M.tb infection was associated with an early detection of IFN-gamma within the lung and the detection of IFN-gamma producing antigen specific T cells throughout infection. Of particular significance was the finding that CBA/J IL-10 mice developed mature granulomas (encircled by collagen) with necrotic centers containing M.tb bacillus of variable acid-fast staining.
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Makris, A., B. Xu, B. Yu, C. Thornton, and A. Hennessy. "Placental Deficiency of Interleukin-10 (IL-10) in Preeclampsia and its Relationship to an IL10 Promoter Polymorphism." Placenta 27, no. 4-5 (2006): 445–51. http://dx.doi.org/10.1016/j.placenta.2005.05.003.

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Brufau, Gemma, Marion J. J. Gijbels, Ine M. J. Wolfs, et al. "Deleting myeloid IL-10 receptor signalling attenuates atherosclerosis in LDLR-/- mice by altering intestinal cholesterol fluxes." Thrombosis and Haemostasis 116, no. 09 (2016): 565–77. http://dx.doi.org/10.1160/th16-01-0043.

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Abstract:
SummaryInflammatory responses and cholesterol homeostasis are interconnected in atherogenesis. Interleukin (IL)-10 is an important anti-inflammatory cytokine, known to suppress atherosclerosis development. However, the specific cell types responsible for the atheroprotective effects of IL-10 remain to be defined and knowledge on the actions of IL-10 in cholesterol homeostasis is scarce. Here we investigated the functional involvement of myeloid IL-10-mediated atheroprotection. To do so, bone marrow from IL-10 receptor 1 (IL-10R1) wild-type and myeloid IL-10R1-deficient mice was transplanted to lethally irradiated female LDLR-/- mice. Hereafter, mice were given a high cholesterol diet for 10 weeks after which atherosclerosis development and cholesterol metabolism were investigated. In vitro, myeloid IL-10R1 deficiency resulted in a pro-inflammatory macrophage phenotype. However, in vivo significantly reduced lesion size and severity was observed. This phenotype was associated with lower myeloid cell accumulation and more apoptosis in the lesions. Additionally, a profound reduction in plasma and liver cholesterol was observed upon myeloid IL-10R1 deficiency, which was reflected in plaque lipid content. This decreased hypercholesterolaemia was associated with lowered very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) levels, likely as a response to decreased intestinal cholesterol absorption. In addition, IL-10R1 deficient mice demonstrated substantially higher faecal sterol loss caused by increased non-biliary cholesterol efflux. The induction of this process was linked to impaired ACAT2-mediated esterification of liver and plasma cholesterol. Overall, myeloid cells do not contribute to IL-10-mediated atheroprotection. In addition, this study demonstrates a novel connection between IL-10-mediated inflammation and cholesterol homeostasis in atherosclerosis. These findings make us reconsider IL-10 as a beneficial influence on atherosclerosis.Supplementary Material to this article is available online at www.thrombosis-online.com.
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49

Yakovlev, A. T., T. F. Danilina, and V. F. Mikhalchenko. "Diagnostic information content of indicators of cytokine profile of gingival fluid in pregnant women with iron deficiency anemia." Parodontologiya 25, no. 4 (2020): 295–300. http://dx.doi.org/10.33925/1683-3759-2020-25-4-295-300.

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Relevance. Modern literature and clinical dental practice do not provide enough information about the value of local immunity parameters for early diagnosis of inflammatory periodontal diseases in pregnant women with iron deficiency anemia. Conventional anti-inflammatory medications used to treat inflammatory periodontal disease are frequently contraindicated during pregnancy. It is important to make a reasonable choice of safe medications, prevention methods, and treatment at early stages of inflammatory periodontal diseases in pregnant women with iron deficiency anemia. The aim of the present study is to determine informative cytokine levels in gingival fluid for early diagnosis of inflammatory periodontal disease and evaluation of effectiveness of “Lysobact” medication in pregnant women with iron deficiency anemia (IDA).Materials and methods. Cytokine levels (IL-8, IL-10; IgA, IgG) in gingival crevicular fluid were investigated in 46 pregnant women aged 18-35: among them 16 (n = 16) had mild IDA (D50), 15 (n = 15) didn't have IDA, 15 (n = 15) were non-pregnant controls. «Lysobact» (Reg. #ПN0179/01-2002) was used in pregnant women with IDA; conventional antiinflammatory therapy was used to treat pregnant women without IDA, before and after drug therapy (8-10 days) according to clinical examinations.Results. There was determined diagnostic value of cytokine levels (IgA, IgG; IL-8, IL-10) that are of great importance for early diagnosis, evaluation of the course of the disease and effectiveness of “Lysobact” immunomodulating drug, and that significantly increase in pregnant women with IDA (IL-10 from 0.010 [1.790] to 3.050 [8.550] ng/ml) versus pregnant women without IDA (from 0.001 [1.259] to 2.900 [18.640] ng/ml) in comparison with controls (4.5 [1.13] ng/ml).Conclusion. Clinical laboratory results in pregnant women with inflammatory periodontal disease allowed to determine diagnostic value of gingival crevicular fluid parameters (sIgA, IgG; IL-8, IL-10) that are related to clinical periodontal index levels, and are informative non-invasive method and are of practical importance for early diagnosis of inflammatory periodontal disease and effectiveness of “Lysobact” drug in pregnant women with iron deficiency anemia.
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50

Gunasekera, Dilini C., Amritha Ramakrishnan, Jinxia Ma, et al. "IL-22-deficiency mediates resolution of colitis in Il10 −/− mice." Journal of Immunology 198, no. 1_Supplement (2017): 201.4. http://dx.doi.org/10.4049/jimmunol.198.supp.201.4.

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Abstract The cytokines IL-10 and IL-22 play important, but presumably distinct roles in promoting intestinal homeostasis. Although the anti-inflammatory actions of IL-10 in the gut are well established, the role(s) of IL-22 remain unclear. Il10−/− mice develop chronic colitis characterized by rectal prolapse, colonic thickening and inflammatory infiltrates, including abundant Th17 cells. We have also observed a modest, but consistent elevation in IL-22 (mRNA and IL-22+CD4 T cells) in colons of Il10−/− mice. This is accompanied by an increased expression of IL-22-target bactericidal genes such as Reg3g, s100a8, and s100a9 and reduced intestinal microbial diversity in Il10−/− mice. To define a potential role for IL-22 in spontaneous colitis, we generated Il10−/− Il22−/− mice by backcrossing. Unexpectedly, concurrent IL-22 deficiency prevented colitis in Il10−/− mice, normalizing histopathology inflammatory scores and restoring microbial diversity to WT levels in Il10−/− Il22−/− mice, despite endemic Helicobacter spp. infection, an established risk factor for colitis in Il10−/− mice. Interestingly, prevention of disease was not accompanied by a reduction in Th17 cells. Importantly, introduction of recombinant IL-22 into the GI tracts of both Il10−/− Il22−/− and WT mice resulted in colonic shortening and thickening after only 2 weeks of treatment, suggesting that IL-22 is at least partially responsible for the immunopathology observed in Il10−/− mice. Thus, although beneficial during certain bacterial infections and in response to acute tissue damage, our data suggest that left unchecked, IL-22 expression can contribute to chronic colitis and appears to be negatively regulated by IL-10.
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