scholarly journals Ephrin B2 Regulates Inflammatory Cell Accumulation in a Rat Aortic Transplant Model

2021 ◽  
Vol 233 (5) ◽  
pp. S271
Author(s):  
John T. Langford ◽  
Luis H. Gonzalez ◽  
Ryosuke T. Taniguchi ◽  
Anand H. Brahmandam ◽  
Weichang T. Zhang ◽  
...  
2003 ◽  
Vol 82 (3) ◽  
pp. 232-237 ◽  
Author(s):  
N. Broggini ◽  
L.M. McManus ◽  
J.S. Hermann ◽  
R.U. Medina ◽  
T.W. Oates ◽  
...  

The inflammatory response adjacent to implants has not been well-investigated and may influence peri-implant tissue levels. The purpose of this study was to assess, histomorphometrically, (1) the timing of abutment connection and (2) the influence of a microgap. Three implant designs were placed in the mandibles of dogs. Two-piece implants were placed at the alveolar crest and abutments connected either at initial surgery (non-submerged) or three months later (submerged). The third implant was one-piece. Adjacent interstitial tissues were analyzed. Both two-piece implants resulted in a peak of inflammatory cells approximately 0.50 mm coronal to the microgap and consisted primarily of neutrophilic polymorphonuclear leukocytes. For one-piece implants, no such peak was observed. Also, significantly greater bone loss was observed for both two-piece implants compared with one-piece implants. In summary, the absence of an implant-abutment interface (microgap) at the bone crest was associated with reduced peri-implant inflammatory cell accumulation and minimal bone loss.


2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
S. F. Wang ◽  
X. Q. Gao ◽  
Y. N. Xu ◽  
D. N. Li ◽  
H. Y. Wang ◽  
...  

Interferon- (IFN-)λ1 is regarded as a potent bio-active molecule in innate immunity. However, little is known about its role in chronic spontaneous urticaria (CSU). We therefore investigated expression of IFN-λ1 in CSU, its cellular location, and its influence on inflammatory cell accumulation by using flow cytometry analysis, skin tissue dispersion, immunohistochemical stain, and a mouse peritoneal inflammation model. The results showed that level of IFN-λ1 was 2.0-fold higher in plasma of the patients with CSU than the level in healthy control (HC) subjects. Among leukocytes examined, only CD8+T cells expressed more IFN-λ1 in CSU blood. Double labeling immunohistochemical staining revealed that IFN-λ1+inflammatory cells such as mast cells, eosinophils, B cells, neutrophils, and macrophages were mainly located in dermis, whereas epidermis tissue highly expressed IFN-λ1. IFN-λ1 induced a dose-dependent increase in number of eosinophils, lymphocytes, mast cells, macrophages, and neutrophils in the peritoneum of mice at 6 h following injection, which was inhibited by pretreatment of the animals with anti-intercellular adhesion molecule- (ICAM-) 1 and/or anti-L-selectin antibodies. In conclusion, IFN-λ1 is likely to play a role in the pathogenesis of CSU. Blocking IFN-λ1 production may help to reduce the accumulation of inflammatory cells in the involved CSU skin.


PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77274 ◽  
Author(s):  
Junio Dort ◽  
Nadine Leblanc ◽  
Julie Maltais-Giguère ◽  
Bjørn Liaset ◽  
Claude H. Côté ◽  
...  

2021 ◽  
Vol Volume 14 ◽  
pp. 1375-1385
Author(s):  
Hong-Xia Mei ◽  
Yang Ye ◽  
Hao-Ran Xu ◽  
Shu-Yang Xiang ◽  
Qian Yang ◽  
...  

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 347-348 ◽  
Author(s):  
Gail G. Shapiro

It is impossible to read about asthma in the 1990s without being informed that it is an inflammatory disease and that all but the mildest cases require anti-inflammatory therapy for optimal management.1 Bronchoalveolar lavage studies document the influx of inflammatory cells and the upregulation of inflammatory cytokines in bronchial washings of patients with chronic asthma.2 Biopsy specimens confirm an inflammatory cell accumulation and the destructive change to the epithelium that one would expect from this insult.3 The pathophysiology of asthma would seem to justify the use of corticosteroids for its management. A single dose of prednisone can be shown to decrease inflammatory leukotrienes while there is a concomitant increase in forced expiratory volume in 1 second.4


2006 ◽  
Vol 85 (5) ◽  
pp. 473-478 ◽  
Author(s):  
N. Broggini ◽  
L.M. McManus ◽  
J.S. Hermann ◽  
R. Medina ◽  
R.K. Schenk ◽  
...  

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 ± 691 vs. 2398 ± 1077 neutrophils/mm2). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.


2007 ◽  
Vol 52 (1) ◽  
pp. 74-82 ◽  
Author(s):  
Amit R Vora ◽  
Sarah M Bodell ◽  
Alison R Loescher ◽  
Keith G Smith ◽  
Peter P Robinson ◽  
...  

Oncogene ◽  
2014 ◽  
Vol 34 (35) ◽  
pp. 4664-4672 ◽  
Author(s):  
K U Sales ◽  
S Friis ◽  
L Abusleme ◽  
N M Moutsopoulos ◽  
T H Bugge

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