{"title":"The enigmatic cytokine oncostatin m and roles in disease.","authors":"Carl D Richards","doi":"10.1155/2013/512103","DOIUrl":"10.1155/2013/512103","url":null,"abstract":"<p><p>Oncostatin M is a secreted cytokine involved in homeostasis and in diseases involving chronic inflammation. It is a member of the gp130 family of cytokines that have pleiotropic functions in differentiation, cell proliferation, and hematopoetic, immunologic, and inflammatory networks. However, Oncostatin M also has activities novel to mediators of this cytokine family and others and may have fundamental roles in mechanisms of inflammation in pathology. Studies have explored Oncostatin M functions in cancer, bone metabolism, liver regeneration, and conditions with chronic inflammation including rheumatoid arthritis, lung and skin inflammatory disease, atherosclerosis, and cardiovascular disease. This paper will review Oncostatin M biology in a historical fashion and focus on its unique activities, in vitro and in vivo, that differentiate it from other cytokines and inspire further study or consideration in therapeutic approaches. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"512103"},"PeriodicalIF":0.0,"publicationDate":"2013-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31992900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ISRN inflammationPub Date : 2013-10-31eCollection Date: 2013-01-01DOI: 10.1155/2013/783190
Courtney M Crawford, Okezie Igboeli
{"title":"A review of the inflammatory chorioretinopathies: the white dot syndromes.","authors":"Courtney M Crawford, Okezie Igboeli","doi":"10.1155/2013/783190","DOIUrl":"https://doi.org/10.1155/2013/783190","url":null,"abstract":"<p><p>The white dot syndromes are a group of inflammatory chorioretinopathies of unknown etiology which have in common a unique and characteristic appearance of multiple yellow-white lesions affecting multiple layers of the retina, retinal pigment epithelium (RPE), choriocapillaris, and the choroid. They also have overlapping clinical features. We discuss acute retinal pigment epitheliopathy, multiple evanescent white dot syndrome, acute posterior multifocal placoid pigment epitheliopathy, multifocal choroiditis and panuveitis, acute zonal occult outer retinopathy, birdshot chorioretinopathy, and serpiginous choroidopathy. Some of these diseases are associated with a viral prodrome suggesting a possible viral/infectious etiology, while others are associated with a number of systemic processes suggesting an autoimmune etiology. We also review the presentation, evaluation/diagnosis, and treatment of these entities as well as the prognosis. Where applicable we discuss recent advancements in diagnosing and treating the white dot syndromes. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"783190"},"PeriodicalIF":0.0,"publicationDate":"2013-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/783190","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31918020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ISRN inflammationPub Date : 2013-10-21eCollection Date: 2013-01-01DOI: 10.1155/2013/539305
Rupak Chowdhury, Ramadevi Nimmanapalli, Thomas Graham, Gopal Reddy
{"title":"Curcumin attenuation of lipopolysaccharide induced cardiac hypertrophy in rodents.","authors":"Rupak Chowdhury, Ramadevi Nimmanapalli, Thomas Graham, Gopal Reddy","doi":"10.1155/2013/539305","DOIUrl":"https://doi.org/10.1155/2013/539305","url":null,"abstract":"<p><p>To study the ameliorating effects of curcumin in lipopolysaccharide (LPS) induced cardiac hypertrophy, mice were assigned to 4 groups (3 males and 3 females in each group): (A) control, (B) curcumin: 100 μ g/kg of body weight by intraperitoneal route (IP), (C) LPS: 60 mg/kg (IP), and (D) LPS + curcumin: both at previously stated concentrations by IP route. All mice were sacrificed as 12 hr and 24 hrs groups accordingly after LPS injection. The hearts were collected, photographed for cardiomegaly, and weighed to compare heart weight/brain weight (HW/BW) in mg/mg. For immunohistochemistry, the tissue sections were exposed to histone H3, H4 and acetylated histone H3, H4 antibody. LPS induced a significant increase in histone acetylation as shown by intense staining. In curcumin + LPS treated mice nuclear staining was similar to the control group indicating that curcumin traversed the histone acetylation activity of the LPS. To further check the mechanism of action of curcumin, p300 protein acetylation levels were analyzed. This study suggests that the probable mechanism of action of curcumin is via the reduction of p300 HAT activity. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"539305"},"PeriodicalIF":0.0,"publicationDate":"2013-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/539305","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31867167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ISRN inflammationPub Date : 2013-10-10eCollection Date: 2013-01-01DOI: 10.1155/2013/483646
Khan Mubashir, Bashir A Ganai, Khalid Ghazanfar, Seema Akbar, Akhtar H Malik, Akbar Masood
{"title":"Evaluation of Artemisia amygdalina D. for Anti-Inflammatory and Immunomodulatory Potential.","authors":"Khan Mubashir, Bashir A Ganai, Khalid Ghazanfar, Seema Akbar, Akhtar H Malik, Akbar Masood","doi":"10.1155/2013/483646","DOIUrl":"https://doi.org/10.1155/2013/483646","url":null,"abstract":"<p><p>Artemisia amygdalina D. is a critically endangered endemic medicinal plant of Kashmir Himalayas. In the current study anti-inflammatory and immunomodulatory activity of the plant was carried out. Carrageenan paw edema model was used to study the potential of the drug in inflammation in Wistar rats. SRBC-specific haemagglutination titre and DTH assays were carried out in Balb/C mice for observing the effect of test drugs on immune system. The plant extracts used as test drugs showed to have anti-inflammatory potential. The methanolic fraction was observed to have the maximum effect on the inhibition of paw edema formation with the inhibitory potential of 42.26%, while in the immunomodulation studies the test drugs were found to have the immunosuppressant activity with methanolic fraction again showing the maximum potential for the suppression of both humoral (55.89% and 47.91%) and cell-mediated immunity (62.27% and 57.21%). The plant in total seems to have the anti-inflammatory potential. The suppression of immune system suggests some mechanistic way by which the inhibition of inflammation takes place. Since, in chronic inflammation like arthritis, there is the involvement of immune system, the plant in that way may serve as an alternative for the treatment of such autoimmune diseases. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"483646"},"PeriodicalIF":0.0,"publicationDate":"2013-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/483646","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31859401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pentraxins: structure, function, and role in inflammation.","authors":"Terry W Du Clos","doi":"10.1155/2013/379040","DOIUrl":"10.1155/2013/379040","url":null,"abstract":"<p><p>The pentraxins are an ancient family of proteins with a unique architecture found as far back in evolution as the Horseshoe crab. In humans the two members of this family are C-reactive protein and serum amyloid P. Pentraxins are defined by their sequence homology, their pentameric structure and their calcium-dependent binding to their ligands. Pentraxins function as soluble pattern recognition molecules and one of the earliest and most important roles for these proteins is host defense primarily against pathogenic bacteria. They function as opsonins for pathogens through activation of the complement pathway and through binding to Fc gamma receptors. Pentraxins also recognize membrane phospholipids and nuclear components exposed on or released by damaged cells. CRP has a specific interaction with small nuclear ribonucleoproteins whereas SAP is a major recognition molecule for DNA, two nuclear autoantigens. Studies in autoimmune and inflammatory disease models suggest that pentraxins interact with macrophage Fc receptors to regulate the inflammatory response. Because CRP is a strong acute phase reactant it is widely used as a marker of inflammation and infection. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":" ","pages":"379040"},"PeriodicalIF":0.0,"publicationDate":"2013-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3791837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40274190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adipocytokines in thyroid dysfunction.","authors":"Berna İmge Aydogan, Mustafa Sahin","doi":"10.1155/2013/646271","DOIUrl":"https://doi.org/10.1155/2013/646271","url":null,"abstract":"<p><p>Adipocytokines are important mediators of interorgan crosstalk in metabolic regulation. Thyroid diseases have effects on metabolism and inflammation. The mechanism of these effects is not clear. Recently, there are several reports suggesting this interrelation between adipocytokines and thyroid dysfunction. In this review, we summarize this relation according to the literature. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"646271"},"PeriodicalIF":0.0,"publicationDate":"2013-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mariarita Dessì, Annalisa Noce, Pierfrancesco Bertucci, Simone Manca di Villahermosa, Rossella Zenobi, Veronica Castagnola, Eliana Addessi, Nicola Di Daniele
{"title":"Atherosclerosis, dyslipidemia, and inflammation: the significant role of polyunsaturated Fatty acids.","authors":"Mariarita Dessì, Annalisa Noce, Pierfrancesco Bertucci, Simone Manca di Villahermosa, Rossella Zenobi, Veronica Castagnola, Eliana Addessi, Nicola Di Daniele","doi":"10.1155/2013/191823","DOIUrl":"10.1155/2013/191823","url":null,"abstract":"<p><p>Phospholipids play an essential role in cell membrane structure and function. The length and number of double bonds of fatty acids in membrane phospholipids are main determinants of fluidity, transport systems, activity of membrane-bound enzymes, and susceptibility to lipid peroxidation. The fatty acid profile of serum lipids, especially the phospholipids, reflects the fatty acid composition of cell membranes. Moreover, long-chain n-3 polyunsatured fatty acids decrease very-low-density lipoprotein assembly and secretion reducing triacylglycerol production. N-6 and n-3 polyunsatured fatty acids are the precursors of signalling molecules, termed \"eicosanoids,\" which play an important role in the regulation of inflammation. Eicosanoids derived from n-6 polyunsatured fatty acids have proinflammatory actions, while eicosanoids derived from n-3 polyunsatured fatty acids have anti-inflammatory ones. Previous studies showed that inflammation contributes to both the onset and progression of atherosclerosis: actually, atherosclerosis is predominantly a chronic low-grade inflammatory disease of the vessel wall. Several studies suggested the relationship between long-chain n-3 polyunsaturated fatty acids and inflammation, showing that fatty acids may decrease endothelial activation and affect eicosanoid metabolism. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"191823"},"PeriodicalIF":0.0,"publicationDate":"2013-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/191823","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31745641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Paprika Pigments Attenuate Obesity-Induced Inflammation in 3T3-L1 Adipocytes.","authors":"Hayato Maeda, Shuuichi Saito, Nozomi Nakamura, Takashi Maoka","doi":"10.1155/2013/763758","DOIUrl":"https://doi.org/10.1155/2013/763758","url":null,"abstract":"<p><p>Obesity is related to various diseases, such as diabetes, hyperlipidemia, and hypertension. Adipocytokine, which is released from adipocyte cells, affects insulin resistance and blood lipid level disorders. Further, adipocytokine is related to chronic inflammation in obesity condition adipocyte cells. Paprika pigments (PPs) contain large amounts of capsanthin and capsorubin. These carotenoids affect the liver and improve lipid disorders of the blood. However, how these carotenoids affect adipocyte cells remains unknown. Present study examined the effects of PP on adipocytokine secretion, which is related to improvement of metabolic syndrome. In addition, suppressive effects of PP on chronic inflammation in adipocyte cells were analyzed using 3T3-L1 adipocyte cells and macrophage cell coculture experiments. PP promoted 3T3-L1 adipocyte cells differentiation upregulated adiponectin mRNA expression and secretion. Further, coculture of adipocyte and macrophage cells treated with PP showed suppressed interleukin-6 (IL-6), tumor necrosis factor- α (TNF- α ), monocyte chemotactic protein-1 (MCP-1), and resistin mRNA expression, similarly to treatment with troglitazone, which is a PPAR γ ligand medicine. Conclusion. These results suggest that PP ameliorates chronic inflammation in adipocytes caused by obesity. PP adjusts adipocytokine secretion and might, therefore, affect antimetabolic syndrome diseases. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"763758"},"PeriodicalIF":0.0,"publicationDate":"2013-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/763758","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ISRN inflammationPub Date : 2013-03-17eCollection Date: 2013-01-01DOI: 10.1155/2013/817901
A S Golovkin, V G Matveeva, I V Kudryavtsev, M N Chernova, Y V Bayrakova, D L Shukevich, E V Grigoriev
{"title":"Perioperative Dynamics of TLR2, TLR4, and TREM-1 Expression in Monocyte Subpopulations in the Setting of On-Pump Coronary Artery Bypass Surgery.","authors":"A S Golovkin, V G Matveeva, I V Kudryavtsev, M N Chernova, Y V Bayrakova, D L Shukevich, E V Grigoriev","doi":"10.1155/2013/817901","DOIUrl":"https://doi.org/10.1155/2013/817901","url":null,"abstract":"<p><p>Hypercytokinemia plays a key role in the pathogenesis of systemic inflammatory response syndrome (SIRS). Monocytes are the main source of cytokines in the early inflammatory phase. Simultaneous stimulation of toll-like receptors (TLRs) and triggering receptor expressed on myeloid cells (TREM-1) activating receptor on monocytes results in the amplification of the inflammatory signal and multiple increase in proinflammatory cytokine production. The dynamics of those receptors expression on monocyte surface of patients with uncomplicated SIRS course followed coronary artery bypass surgery (CABG) was studied. The increase in TLR2 and TREM-1 expression on the first day after CABG induces proinflammatory and amplification potentials of monocytes in that period. The decrease in TLR2 surface expression on the seventh day compared to the preoperative values can be regarded as a mechanism limiting inflammatory response. The highest level of TLR2, TLR4, and TREM-1 surface expression was observed in CD14(hi)CD16(+) monocyte subpopulation, confirming its proinflammatory profile. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"817901"},"PeriodicalIF":0.0,"publicationDate":"2013-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/817901","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ISRN inflammationPub Date : 2013-02-28eCollection Date: 2013-01-01DOI: 10.1155/2013/419823
Gustavo Duarte Pimentel, Fábio Santos Lira, José César Rosa, Cláudia Maria Oller do Nascimento, Lila Missae Oyama, Regina Lúcia Harumi Watanabe, Eliane Beraldi Ribeiro
{"title":"High-fat fish oil diet prevents hypothalamic inflammatory profile in rats.","authors":"Gustavo Duarte Pimentel, Fábio Santos Lira, José César Rosa, Cláudia Maria Oller do Nascimento, Lila Missae Oyama, Regina Lúcia Harumi Watanabe, Eliane Beraldi Ribeiro","doi":"10.1155/2013/419823","DOIUrl":"https://doi.org/10.1155/2013/419823","url":null,"abstract":"<p><p>Whether PUFA diets affect inflammatory mediators in central and peripheral sites is not clear. We investigated the effect of high-fat PUFA diets on the expression of proteins involved in inflammatory pathways in hypothalamus, muscle, and liver. Male rats were fed for 2 months with either chow or high-fat diets enriched with either soy (n-6 PUFAs) or fish oil (n-3 PUFAs). The fish group had normal body weight, low serum NEFA, reduced hypothalamic levels of TNF- α , IL-6, and TRAF6, and increased levels of IL-10 receptor. In contrast, the soy group had increased body weight and hypothalamic levels of TRAF6 and NF κ Bp65. In muscle, the fish diet reduced TNF- α and IL-6 levels. Both PUFA diets increased muscle IL-10 levels and reduced liver TNF- α and IL-6 levels. The data showed that the high-fat soy diet induced activation of the hypothalamic NF κ B inflammatory pathway, a feature predisposing to feeding and energy expenditure disturbances associated with the development of obesity. On the other hand, the high-fat fish diet improved the central and the peripheral inflammatory profile via reduction of intracellular inflammatory mediators, suggesting a protection against obesity. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"419823"},"PeriodicalIF":0.0,"publicationDate":"2013-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/419823","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31745642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}