scholarly journals Effect of Camphor on the Behavior of Leukocytes In vitro and In vivo in Acute Inflammatory Response

2015 ◽  
Vol 13 (12) ◽  
pp. 2031 ◽  
Author(s):  
SE Silva-Filho ◽  
FM De Souza Silva-Comar ◽  
LAM Wiirzler ◽  
RJ Do Pinho ◽  
R Grespan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response

Recombinant P-selectin glycoprotein ligand–1 directly inhibits leukocyte rolling by all 3 selectins in vivo: complete inhibition of rolling is not required for anti-inflammatory effect

Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3249-3256 ◽  
Author(s):  
Anne E. R. Hicks ◽  
Sarah L. Nolan ◽  
Victoria C. Ridger ◽  
Paul G. Hellewell ◽  
Keith E. Norman
Keyword(s):  
Inflammatory Response ◽  
Clinical Benefit ◽  
Inflammatory Diseases ◽  
Neutrophil Migration ◽  
Acute Inflammatory Response ◽  
Leukocyte Rolling ◽  
Selectin Ligand ◽  
Inflammatory Effect

AbstractSelectin-dependent leukocyte rolling is one of the earliest steps of an acute inflammatory response and, as such, contributes to many inflammatory diseases. Although inhibiting leukocyte rolling with selectin antagonists is a strategy that promises far-reaching clinical benefit, the perceived value of this strategy has been limited by studies using inactive, weak, or poorly characterized antagonists. Recombinant P-selectin glycoprotein ligand–1–immunoglobulin (rPSGL-Ig) is a recombinant form of the best-characterized selectin ligand (PSGL-1) fused to IgG, and is one of the best prospects in the search for effective selectin antagonists. We have used intravital microscopy to investigate the ability of rPSGL-Ig to influence leukocyte rolling in living blood vessels and find that it can reduce rolling dependent on each of the selectins in vivo. Interestingly, doses of rPSGL-Ig required to reverse pre-existing leukocyte rolling are 30-fold higher than those required to limit inflammation, suggesting additional properties of this molecule. In support of this, we find that rPSGL-Ig can bind the murine chemokine KC and inhibit neutrophil migration toward this chemoattractant in vitro.

7,12-Dimethylbenz(a)anthracene-Induced Myelotoxicity Differs in Mice Selected for High or Low Acute Inflammatory Response

2014 ◽  
Vol 33 (2) ◽  
pp. 130-142 ◽  
Author(s):  
Iana Suly Santos Katz ◽  
Layra Lucy Albuquerque ◽  
Alessandra Paes Suppa ◽  
Débora Mathias de Siqueira ◽  
Cristiano Rossato ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Environmental Pollutants ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Phenotypic Selection ◽  
Acute Inflammatory Response ◽  
Aryl Hydrocarbon ◽  
Ahr Gene

Polycyclic aromatic hydrocarbons, such as 7,12-dimethylbenz(a)anthracene (DMBA), are environmental pollutants that exert multiple toxic and carcinogenic effects. Studies showed that these effects are mediated by activation of the aryl hydrocarbon receptor (AhR) and modulated by allelic variants of Ahr gene. Here, we investigated the effects of DMBA treatment in the inflammatory response and bone marrow (BM) hematopoietic function of maximal acute inflammatory response (AIRmax) and minimal acute inflammatory response (AIRmin) heterogeneous mouse lines selected for high and low acute inflammatory responsiveness, respectively. The phenotypic selection resulted in the segregation of the Ahrd and Ahrb1 alleles that confer low and high receptor ligand-binding affinity, respectively, in AIRmax and AIRmin mice. We observed a reduction in BM mature granulocyte population in AIRmin mice 24 hours after DMBA treatment while both blast and immature myeloid cells were increased. Proliferation and differentiation of BM myeloid cells in response to in vitro granulocyte-macrophage colony-stimulating factor stimulus were impaired in AIRmin-treated mice. These DMBA effects on myeloid BM cells (BMCs) affected the in vivo leukocyte migration to an inflammatory site induced by polyacrylamide beads (Biogel P-100, Bio-Rad, France) injection in AIRmin mice. On the other hand, these alterations were not observed in DMBA-treated AIRmax mice. These data indicate that DMBA affects myeloid cell differentiation and inflammatory response and Ahrb1 allele in the genetic background of AIRmin mice contributes to this effect.

scholarly journals In vivo and in vitro evaluation of hydroxyapatite nanoparticle morphology on the acute inflammatory response

Biomaterials ◽  
2016 ◽  
Vol 90 ◽  
pp. 1-11 ◽  
Author(s):  
Shiuli Pujari-Palmer ◽  
Song Chen ◽  
Stefano Rubino ◽  
Hong Weng ◽  
Wei Xia ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
In Vitro Evaluation ◽  
Nanoparticle Morphology

Effect of patchouli (Pogostemon cablin) essential oil on in vitro and in vivo leukocytes behavior in acute inflammatory response

2016 ◽  
Vol 84 ◽  
pp. 1697-1704 ◽  
Author(s):  
Saulo Euclides Silva-Filho ◽  
Luiz Alexandre Marques Wiirzler ◽  
Heitor Augusto Otaviano Cavalcante ◽  
Nancy Sayuri Uchida ◽  
Francielli Maria de Souza Silva-Comar ◽  
...  
Keyword(s):  
Essential Oil ◽  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Pogostemon Cablin

scholarly journals Combined In Silico, In Vivo, and In Vitro Studies Shed Insights into the Acute Inflammatory Response in Middle-Aged Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e67419 ◽  
Author(s):  
Rami A. Namas ◽  
John Bartels ◽  
Rosemary Hoffman ◽  
Derek Barclay ◽  
Timothy R. Billiar ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
In Silico ◽  
In Vitro Studies ◽  
Acute Inflammatory Response ◽  
Middle Aged ◽  
Aged Mice

Inhibitory effects of epimedium herb water extract on the inflammatory response in vitro and in vivo

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
YC Oh ◽  
YH Jeong ◽  
WK Cho ◽  
SJ Lee ◽  
JY Ma
Keyword(s):  
Inflammatory Response ◽  
Water Extract ◽  
Inhibitory Effects

Stanniocalcin-1, an inhibitor of macrophage chemotaxis and chemokinesis

2004 ◽  
Vol 286 (2) ◽  
pp. F356-F362 ◽  
Author(s):  
John Kanellis ◽  
Roger Bick ◽  
Gabriela Garcia ◽  
Luan Truong ◽  
Chun Chui Tsao ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Intracellular Calcium ◽  
In Vivo Studies ◽  
Cellular Processes ◽  
Multiple Organs ◽  
Chemotactic Protein ◽  
Stromal Cell Derived Factor ◽  
Mammalian Counterpart

In macrophages, changes in intracellular calcium have been associated with activation of cellular processes that regulate cell adhesion and motility and are important for the response of macrophages to antigenic stimuli. The mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in multiple organs including the thymus and spleen, and hence, we hypothesized that it may have a role in modulating the immune/inflammatory response. Using murine macrophage-like (RAW264.7) and human monoblast-like (U937) cells to study chemotaxis in vitro, we found that STC1 attenuated chemokinesis and diminished the chemotactic response to monocyte chemotactic protein-1 (MCP-1) and stromal cell-derived factor-1α. Consistent with these findings, STC1 blunted the rise in intracellular calcium following MCP-1 stimulation in RAW264.7 cells. In vivo studies suggested differential expression of STC1 in obstructed kidney and localization to macrophages. MCP-1 and STC1 transcripts were both upregulated following ureteric obstruction, suggesting a functional association between the two genes. Our data suggest a role for mammalian STC1 in modulating the immune/inflammatory response.

scholarly journals MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xudong Wang ◽  
Yali Wang ◽  
Mingjian Kong ◽  
Jianping Yang
Keyword(s):  
Acute Kidney Injury ◽  
Inflammatory Response ◽  
Periodic Acid ◽  
Kidney Injury ◽  
Luciferase Reporter ◽  
Tunel Staining ◽  
Tnf Α

Abstract Background: Septic acute kidney injury is considered as a severe and frequent complication that occurs during sepsis. The present study was performed to understand the role of miR-22-3p and its underlying mechanism in sepsis-induced acute kidney injury. Methods: Rats were injected with adenovirus carrying miR-22-3p or miR-NC in the caudal vein before cecal ligation. Meanwhile, HK-2 cells were transfected with the above adenovirus following LPS stimulation. We measured the markers of renal injury (blood urea nitrogen (BUN), serum creatinine (SCR)). Histological changes in kidney tissues were examined by hematoxylin and eosin (H&E), Masson staining, periodic acid Schiff staining and TUNEL staining. The levels of IL-1β, IL-6, TNF-α and NO were determined by ELISA assay. Using TargetScan prediction and luciferase reporter assay, we predicted and validated the association between PTEN and miR-22-3p. Results: Our data showed that miR-22-3p was significantly down-regulated in a rat model of sepsis-induced acute kidney injury, in vivo and LPS-induced sepsis model in HK-2 cells, in vitro. Overexpression of miR-22-3p remarkably suppressed the inflammatory response and apoptosis via down-regulating HMGB1, p-p65, TLR4 and pro-inflammatory factors (IL-1β, IL-6, TNF-α and NO), both in vivo and in vitro. Moreover, PTEN was identified as a target of miR-22-3p. Furthermore, PTEN knockdown augmented, while overexpression reversed the suppressive role of miR-22-3p in LPS-induced inflammatory response. Conclusions: Our results showed that miR-22-3p induced protective role in sepsis-induced acute kidney injury may rely on the repression of PTEN.

scholarly journals A dynamic equilibrium between TTP and CPEB4 controls mRNA stability and inflammation resolution

2021 ◽  
Author(s):  
Clara Suñer ◽  
Annarita Sibilio ◽  
Judit Martín ◽  
Chiara Lara Castellazzi ◽  
Oscar Reina ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mrna Stability ◽  
Regulatory Network ◽  
Dynamic Equilibrium ◽  
Relative Number ◽  
Mapk Signalling Pathway ◽  
Mapk Signalling ◽  
Inflammation Resolution

SUMMARYTemporal control of inflammation is critical to avoid pathological developments, and is largely defined through the differential stabilities of mRNAs. While TTP-directed mRNA deadenylation is known to destabilize ARE-containing mRNAs, this mechanism alone cannot explain the variety of mRNA expression kinetics observed during inflammation resolution. Here we show that inflammation resolution requires CPEB4 expression, in vitro and in vivo. Our results identify that CPEB4-directed polyadenylation and TTP-mediated deadenylation compete during the resolutive phase of the LPS response to uncouple the degradation of pro-inflammatory mRNAs from the sustained expression of anti-inflammatory mRNAs. The outcome of this equilibrium is quantitatively defined by the relative number of CPEs and AREs in each mRNA, and further shaped by the coordinated regulation by the MAPK signalling pathway of the levels and activities of their trans-acting factors, CPEB4 and TTP. Altogether, we describe a temporal- and transcript-specific regulatory network controlling the extent of the inflammatory response.

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