{"title":"Monocyte Migration Driven by Galectin-3 Occurs through Distinct Mechanisms Involving Selective Interactions with the Extracellular Matrix.","authors":"Cláudia Danella Polli, Karina Alves Toledo, Luís Henrique Franco, Vânia Sammartino Mariano, Leandro Licursi de Oliveira, Emerson Soares Bernardes, Maria Cristina Roque-Barreira, Gabriela Pereira-da-Silva","doi":"10.1155/2013/259256","DOIUrl":"https://doi.org/10.1155/2013/259256","url":null,"abstract":"<p><p>Monocyte migration into tissues, an important event in inflammation, requires an intricate interplay between determinants on cell surfaces and extracellular matrix (ECM). Galectin-3 is able to modulate cell-ECM interactions and is an important mediator of inflammation. In this study, we sought to investigate whether interactions established between galectin-3 and ECM glycoproteins are involved in monocyte migration, given that the mechanisms by which monocytes move across the endothelium and through the extravascular tissue are poorly understood. Using the in vitro transwell system, we demonstrated that monocyte migration was potentiated in the presence of galectin-3 plus laminin or fibronectin, but not vitronectin, and was dependent on the carbohydrate recognition domain of the lectin. Only galectin-3-fibronectin combinations potentiated the migration of monocyte-derived macrophages. In binding assays, galectin-3 did not bind to fibronectin, whereas both the full-length and the truncated forms of the lectin, which retains carbohydrate binding ability, were able to bind to laminin. Our results show that monocytes migrate through distinct mechanisms and selective interactions with the extracellular matrix driven by galectin-3. We suggest that the lectin may bridge monocytes to laminin and may also activate these cells, resulting in the positive regulation of other adhesion molecules and cell adhesion to fibronectin. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"259256"},"PeriodicalIF":0.0,"publicationDate":"2013-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/259256","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31745640","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 : 2013-02-17eCollection Date: 2013-01-01DOI: 10.1155/2013/735158
Gaurav Kaithwas, Dipak K Majumdar
{"title":"Effect of L. usitatissimum (Flaxseed/Linseed) Fixed Oil against Distinct Phases of Inflammation.","authors":"Gaurav Kaithwas, Dipak K Majumdar","doi":"10.1155/2013/735158","DOIUrl":"https://doi.org/10.1155/2013/735158","url":null,"abstract":"<p><p>The present investigation summarizes the effect of Linum usitatissimum fixed oil against different phases of acute inflammatory reaction, namely, protein exudation, peritoneal capillary permeability, and leukocyte migration. The fixed oil exhibited dose-dependent inhibition of protein exudation vascular permeability, comparable to standard aspirin. The oil also inhibited the leukocyte migration in pleural exudates in a dose-dependent manner. Production of less vasodilatory (PGE3) and chemotactic (LTB5) eicosanoids through EPA (derived from linolenic acid) metabolism could account for the above observations. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"735158"},"PeriodicalIF":0.0,"publicationDate":"2013-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/735158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744475","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 : 2013-02-17eCollection Date: 2013-01-01DOI: 10.1155/2013/531026
Maqsood M Elahi, Bashir M Matata
{"title":"Nitric Oxide-Dependent Regulation of Cytokines Release in Type-II Diabetes Mellitus.","authors":"Maqsood M Elahi, Bashir M Matata","doi":"10.1155/2013/531026","DOIUrl":"https://doi.org/10.1155/2013/531026","url":null,"abstract":"<p><p>The mechanism of release of proinflammatory cytokines by blood granulocytes in diabetes is unknown. We investigated whether diabetes mellitus affects the production of cytokines by granulocytes (PMN) and mononuclear cells (PBMCs) and whether this is modulated by NO. Isolated PMN and PBMC from with or without type-II diabetes mellitus were incubated at 37°C for 6 h with S-nitroso-N-acetylpenicillamine (SNAP) at 0, 1, and 100 μ M with or without lipopolysaccharides (LPS) stimulation (1 μ g/mL). Supernatants were assayed for tumor necrosis factor- α (TNF- α ) and interleukin-8 (IL-8) by sandwich ELISA. Significant increases in TNF- α and IL-8 were observed only in PMN from diabetic subjects with or without LPS stimulation and that exogenous NO inhibited further production of cytokines in a concentration-dependent manner. However, activity of PBMC when stimulated with LPS was greatly enhanced by diabetes, but not affected by NO production. Hence, suggesting that granulocytes activation and participation in diabetes related complications is modulated by NO bioavailability. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"531026"},"PeriodicalIF":0.0,"publicationDate":"2013-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/531026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744473","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 : 2013-02-13eCollection Date: 2013-01-01DOI: 10.1155/2013/496208
Zdenek Pelikan
{"title":"Delayed asthmatic response to allergen challenge and cytokines released by nonspecifically stimulated blood cells.","authors":"Zdenek Pelikan","doi":"10.1155/2013/496208","DOIUrl":"https://doi.org/10.1155/2013/496208","url":null,"abstract":"<p><p>Background. Bronchial asthma patients can develop various asthmatic response types following bronchial allergen challenge, such as immediate (IAR), late (LAR), dual late (DLAR), or delayed (DYAR), due to different immunologic mechanisms. The DYAR, recorded in 24 patients, beginning between 26 and 32 hrs and lasting up to 56 hrs after the bronchial allergen challenge, differs from the IAR, LAR, and DLAR in clinical, diagnostic, and immunologic aspects. Objective. To investigate amounts of particular cytokines released by the blood cells after an additional nonspecific stimulation with Phorbol 12-myristate 13-acetate (PMA) during the DYAR. Methods. In 24 patients, the repeated DYAR was supplemented with determination of cytokines both in the nonstimulated plasma and in the supernatants of the blood cells stimulated with PMA before and up to 72 hours after the bronchial challenge, by means of enzyme-linked immunoassay. Results. No significant changes of the prechallenge cytokine concentrations in the non-stimulated serum were recorded in the DYAR patients as compared with the healthy subjects. The DYAR was accompanied by significantly increased postchallenge concentrations (P < 0.05) of IL-2, IL-8, IL-12p70, IL-13, IL-18, IFN- γ , G-CSF, TNF- α , and TGF- β , while decreased concentration of IL-7 (P < 0.05) in the nonstimulated plasma. The significantly increased postchallenge concentrations of IL-2, IL-8, IL-12p70, IL-13, IL-18, IFN- γ , TNF- α , and TGF- β were released by peripheral blood cells after stimulation with PMA, as compared with both their prechallenge concentrations and with the PBS control values. Conclusions. These results would support evidence for an important role of the Th1 cells, neutrophils, monocytes, and probably also NK cells in the immunologic mechanism(s) leading to the development of the clinical DYAR. Nevertheless, an additional role of macrophages, endothelial and epithelial cells in these mechanisms cannot be even excluded. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"496208"},"PeriodicalIF":0.0,"publicationDate":"2013-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744472","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 : 2013-02-12eCollection Date: 2013-01-01DOI: 10.1155/2013/431739
Fernando A Rivera-Chávez, Ryan M Huebinger, Agnes Burris, Ming-Mei Liu, Joseph P Minei, John L Hunt, Brett D Arnoldo, Robert C Barber
{"title":"A TREM-1 Polymorphism A/T within the Exon 2 Is Associated with Pneumonia in Burn-Injured Patients.","authors":"Fernando A Rivera-Chávez, Ryan M Huebinger, Agnes Burris, Ming-Mei Liu, Joseph P Minei, John L Hunt, Brett D Arnoldo, Robert C Barber","doi":"10.1155/2013/431739","DOIUrl":"https://doi.org/10.1155/2013/431739","url":null,"abstract":"<p><p>Background. The triggering receptor expressed in myeloid cells (TREM-1) is a key mediator in the activation of the local inflammatory response during lung infections. We aimed to evaluate the effect of a functionally relevant TREM-1 single nucleotide polymorphism within the exon 2 (A→T) on the development of pneumonia in burn patients. Objective. To determine whether a single nucleotide polymorphism (SNP) within the exon 2 (A→T) in the TREM-1 gene is associated with ventilator-associated pneumonia (VAP) in burn-injured patients. Methods. 540 patients with ≥10% total body surface area (TBSA) burn injuries or inhalation injury were prospectively enrolled. The influence of a polymorphism (A→T) in exon 2 of the TREM-1 gene was evaluated for association with increased risk of pneumonia by logistic regression analysis. Measurements and Main Results. 209 patients met criteria for VAP. Multivariate regression analysis showed that, after adjustment for potential confounders, we found that carriage of the TREM-1 T allele is associated with more than a 3-fold increased risk of VAP (OR 6.3, 95% CI 4-9). Conclusions. A TREM-1 single nucleotide polymorphism within the exon 2 (A→T) is associated with the development of pneumonia in burn patients. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"431739"},"PeriodicalIF":0.0,"publicationDate":"2013-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/431739","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31745643","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 : 2013-01-29eCollection Date: 2013-01-01DOI: 10.1155/2013/907821
Yafeng Song, Per S Stål, Jiguo Yu, Sture Forsgren
{"title":"Marked Effects of Tachykinin in Myositis Both in the Experimental Side and Contralaterally: Studies on NK-1 Receptor Expressions in an Animal Model.","authors":"Yafeng Song, Per S Stål, Jiguo Yu, Sture Forsgren","doi":"10.1155/2013/907821","DOIUrl":"https://doi.org/10.1155/2013/907821","url":null,"abstract":"<p><p>Muscle injury and inflammation (myositis) in a rabbit model of an unilateral muscle overuse were examined. It is unknown if the tachykinin system has a functional role in this situation. In this study, therefore, the neurokinin-1 receptor (NK-1R) expression patterns were evaluated. White blood cells, nerve fascicles, fine nerve fibers, and blood vessel walls in myositis areas showed NK-1R immunoreaction. NK-1R mRNA reactions were observable for white blood cells and blood vessel walls of these areas. NK-1R immunoreaction and NK-1R mRNA reactions were also seen for muscle fibers showing degenerative and regenerative features. There were almost no NK-1R immunoreactions in normal muscle tissue. Interestingly, marked NK-1R expressions were seen for myositis areas of both the experimental side and the contralateral nonexperimental side. EIA analyses showed that the concentration of substance P in the muscle tissue was clearly increased bilaterally at the experimental end stage, as compared to the situation for normal muscle tissue. These observations show that the tachykinin system is very much involved in the processes that occur in muscle injury/myositis. The effects can be related to proinflammatory effects and/or tissue repair. The fact that there are also marked NK-1R expressions contralaterally indicate that the tachykinin system has crossover effects. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2013 ","pages":"907821"},"PeriodicalIF":0.0,"publicationDate":"2013-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/907821","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744478","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 : 2012-12-30eCollection Date: 2012-01-01DOI: 10.5402/2012/578149
J R Bannister, A L Khan, D W Eccleston, R K Deol-Poonia, S F Hughes
{"title":"Interleukin-17 Expression in the Barrett's Metaplasia-Dysplasia-Adenocarcinoma Sequence.","authors":"J R Bannister, A L Khan, D W Eccleston, R K Deol-Poonia, S F Hughes","doi":"10.5402/2012/578149","DOIUrl":"https://doi.org/10.5402/2012/578149","url":null,"abstract":"<p><p>Introduction. This pilot study evaluated the expression of the proinflammatory cytokine IL-17 along the Barrett's metaplasia-dysplasia-adenocarcinoma sequence by establishing the expression levels of IL-17 in columnar epithelium, intestinal metaplastic cells, and dysplastic/glandular neoplastic cells. Immunohistochemical techniques were used to examine the accumulation of the proinflammatory cytokine IL-17 in forty (n = 40) formalin-fixed, paraffin-embedded oesophageal archived specimens across a range of endoscopic diagnostic categories, and a highly significant difference was found, where P ≤ 0.001, in IL-17 expression (Kruskall Wallis and Mann-Whitney U) between all the cell types examined. There was also a strong positive correlation (Spearman's rank correlation) between disease progression and IL-17 expression (r s = 0.883, P < 0.001, n = 29), IL-17 expression was absent or absent/weak in columnar epithelium, weak to moderate in columnar metaplastic cells, and moderate to strong in dysplastic/neoplastic cells, which demonstrated that the elevation of IL-17 expression occurs in the progression of the disease. Understanding the differential expression of IL-17 between benign and malignant tissue potentially has a significant diagnostic, prognostic, and therapeutic value. Ultimately, this selective biomarker may be employed in routine clinical practice for the screening of oesophageal adenocarcinoma. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2012 ","pages":"578149"},"PeriodicalIF":0.0,"publicationDate":"2012-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744657","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 : 2012-12-17eCollection Date: 2012-01-01DOI: 10.5402/2012/382862
A S Golovkin, V G Matveeva, E V Grigoriev, D L Shukevich, Y V Bayrakova, L S Barbarash
{"title":"sTREM-1 as a Prognostic Marker of Postoperative Complications in Cardiac Surgery.","authors":"A S Golovkin, V G Matveeva, E V Grigoriev, D L Shukevich, Y V Bayrakova, L S Barbarash","doi":"10.5402/2012/382862","DOIUrl":"https://doi.org/10.5402/2012/382862","url":null,"abstract":"<p><p>Cell-activating receptor TREM-1 (triggering receptor expressed on myeloid cells 1) regulates congenital immune response and contributes to systemic inflammatory response syndrome (SIRS) development. It is able to multiply cytokine production while stimulated together with the main receptors of the congenital immune system. The purpose of the paper is to study the potential use of soluble TREM-1 (sTREM-1) as a marker of intensive SIRS and a criterion for postoperative complications prediction following on-pump coronary artery bypass surgery (CABG). Results show that early postoperative sTREM-1 concentrations demonstrate their potential prognostic value regarding SIRS-associated complications. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2012 ","pages":"382862"},"PeriodicalIF":0.0,"publicationDate":"2012-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744653","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":"Angiotensin type 1a receptor signaling is not necessary for the production of reactive oxygen species in polymorphonuclear leukocytes.","authors":"Fumiko Yamato, Junji Takaya, Shoji Tsuji, Masafumi Hasui, Kazunari Kaneko","doi":"10.5402/2012/347852","DOIUrl":"10.5402/2012/347852","url":null,"abstract":"<p><p>Background. Although angiotensin II (Ang II) has inflammatory effects, little is known about its role in polymorphonuclear leucocytes (PMLs). To elucidate the role of Ang II in PMLs ROS production, we examined hydrogen peroxide (H2O2), one of the ROS, and NO production in AT1a receptor knockout (AT1KO) mice. Methods and Results. PMLs were analyzed from Ang II type 1a receptor knockout mice (AT1KO) and C57BL/6 wild type mice. Using flow cytometry, we studied hydrogen peroxide (H2O2) production from PMLs after Staphylococcus aureus phagocytosis or phorbol myristate acetate (PMA) stimulation. Nitric oxide (NO) production in the AT1KO was low at basal and after phagocytosis. In the AT1KO, basal H2O2 production was low. After PMA or phagocytosis stimulation, however, H2O2 production was comparable to wild type mice. Next we studied the H2O2 production in C57BL/6 mice exposed to Ang II or saline. H2O2 production stimulated by PMA or phagocytosis did not differ between the two groups. Conclusions. AT1a pathway is not necessary for PMLs H2O2 production but for NO production. There was a compensatory pathway for H2O2 production other than the AT1a receptor. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2012 ","pages":"347852"},"PeriodicalIF":0.0,"publicationDate":"2012-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31744651","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 : 2012-11-25eCollection Date: 2012-01-01DOI: 10.5402/2012/983420
Tamotsu Tsukahara, Hisao Haniu
{"title":"Lysophosphatidic Acid Stimulates MCP-1 Secretion from C2C12 Myoblast.","authors":"Tamotsu Tsukahara, Hisao Haniu","doi":"10.5402/2012/983420","DOIUrl":"https://doi.org/10.5402/2012/983420","url":null,"abstract":"<p><p>Chemokines are regulatory proteins that play an important role in muscle cell migration and proliferation. In this study, C2C12 cells treated with lysophosphatidic acid (LPA) showed an increase in endogenous monocyte chemotactic protein-1 (MCP-1) expression and secretion. LPA is a naturally occurring bioactive lysophospholipid with hormone- and growth-factor-like activities. LPA is produced by activated platelets, cytokine-stimulated leukocytes, and possibly by other cell types. However, the LPA analog cyclic phosphatidic acid (cPA) had no effect on the expression and secretion of MCP-1. LPA, although similar in structure to cPA, had potent inducing effects on MCP-1 expression in C2C12 cells. In this study, we showed that LPA enhanced MCP-1 mRNA expression and protein secretion in a dose-dependent manner. Taken together, these results suggest that LPA enhances MCP-1 secretion in C2C12 cells and thus may play an important role in cell proliferation. </p>","PeriodicalId":89952,"journal":{"name":"ISRN inflammation","volume":"2012 ","pages":"983420"},"PeriodicalIF":0.0,"publicationDate":"2012-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31745638","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}