scholarly journals Dysregulation of DPP4-CXCL12 Balance by TGF-β1/SMAD Pathway Promotes CXCR4+ Inflammatory Cell Infiltration in Keloid Scars

2021 ◽  
Vol Volume 14 ◽  
pp. 4169-4180
Author(s):  
ZongAn Chen ◽  
Zhen Gao ◽  
LingLing Xia ◽  
XiaoQing Wang ◽  
LiMing Lu ◽  
...  
2021 ◽  
Author(s):  
Bo Wang ◽  
Ye Tian ◽  
Yong Ban ◽  
Zhen Wang ◽  
Bing Yang ◽  
...  

Abstract Background: To clarify the expression of histological inflammation and major inflammatory factors in prostate of castrated rats induced by different concentrations estrogen/ androgen. Methods: Male Sprague-Dawley (SD) rats aged 3-4 months were randomly divided into the blank group (sham operation group, bilateral testicular specimens were retained), and the castration group (surgical removal of bilateral testes) and different concentrations of estrogen/androgen treatment after castration. Dihydrotestosterone (DHT) and estradiol (E) were administered daily by subcutaneous injection for one month, and the rats in each group were sacrificed by neck-broken method after one month. Obtained prostate specimens by surgery, and performed routine paraffin embedding and sectioning of prostate tissue. Observed the changes of prostate tissue structure and prostate inflammation under light microscope after Hematoxylin-eosin (HE) staining. Immunohistochemical method was used to detect the expression of TGF-β1, IL-6 and IL-8 in the rats prostate tissues. Results: After castration, when the exogenous E concentration was constant, the exogenous DHT(0-0.15mg/kg) concentration of SD rats in each group increased gradually, and the anatomical position score of inflammatory cell infiltration in each group of rats gradually increased. Further, even if the DHT concentration increased again after the exogenous DHT concentration reached at 0.5mg/kg, the score did not increase but decreased insteadly. From the area of tissues involved in inflammatory cell infiltration and the density of typical inflammatory cells, the inflammation score of each group of rats increased gradually with the increase of DHT concentration. When the exogenous DHT concentration was constant, from the anatomical location and the area of tissues involved in inflammatory cell infiltration in each group of SD rats, the inflammation score of each group of rats increased gradually with the increase of exogenous E concentration. The results of the immunohistochemical reaction showed that the positive rates of TGF-β1, IL-6 and IL-8 in SD rats after castration were higher than those in the blank group, and the positive rate of TGF-β1 was statistically significant compared with the blank group (P<0.05). When the concentration of exogenous E was constant, the positive rates of TGF-β1 and IL-8 in each group of DHT0.015-0.5mg/kg increased with the increase of the concentration of exogenous DHT. However, even if the exogenous DHT concentration increased again after the exogenous DHT concentration exceeded 0.5mg/kg, the positive rates of TGF-β1 and IL-8 in the E0.05+DHT1.5 group did not increase with the further increase of exogenous DHT, but decreased to a certain extent. In addition, when the exogenous DHT concentration was constant, the exogenous E concentration was gradually increased, and the positive rates of TGF-β1, IL-6 and IL-8 in SD rats in each group increased to some extent with the increase of exogenous E concentration. Conclusions: Sex hormone levels are involved in the regulation of prostate inflammation in SD rats. Different levels of estrogen and androgen have different levels of inflammatory response to prostate inflammation and the expression of TGF-β1, IL-6, IL-8 in castrated SD rats, and the positive expression of TGF-β1, IL-6, IL-8 can reflect the inflammation of prostate tissue in SD rats to a certain extent. In addition, there may be an inflection point between the ratio of estrogen/ androgen and prostate inflammation. After crossing this inflection point, the inflammation of the prostate did not further deepen even if the concentration of exogenous androgens increased again. Of course, it needs to be confirmed by more systematic and comprehensive experiments in vivo and vitro.


2008 ◽  
Vol 70 (3) ◽  
pp. 269-273
Author(s):  
Taisuke KAMIYAMA ◽  
Yoshihiro KAWAGUCHI ◽  
Masami SASAKI ◽  
Masamichi SATOU ◽  
Kumiko MIURA ◽  
...  

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1126
Author(s):  
Giovanna Iezzi ◽  
Francesca Di Lillo ◽  
Michele Furlani ◽  
Marco Degidi ◽  
Adriano Piattelli ◽  
...  

Symmetric and well-organized connective tissues around the longitudinal implant axis were hypothesized to decrease early bone resorption by reducing inflammatory cell infiltration. Previous studies that referred to the connective tissue around implant and abutments were based on two-dimensional investigations; however, only advanced three-dimensional characterizations could evidence the organization of connective tissue microarchitecture in the attempt of finding new strategies to reduce inflammatory cell infiltration. We retrieved three implants with a cone morse implant–abutment connection from patients; they were investigated by high-resolution X-ray phase-contrast microtomography, cross-linking the obtained information with histologic results. We observed transverse and longitudinal orientated collagen bundles intertwining with each other. In the longitudinal planes, it was observed that the closer the fiber bundles were to the implant, the more symmetric and regular their course was. The transverse bundles of collagen fibers were observed as semicircular, intersecting in the lamina propria of the mucosa and ending in the oral epithelium. No collagen fibers were found radial to the implant surface. This intertwining three-dimensional pattern seems to favor the stabilization of the soft tissues around the implants, preventing inflammatory cell apical migration and, consequently, preventing bone resorption and implant failure. This fact, according to the authors’ best knowledge, has never been reported in the literature and might be due to the physical forces acting on fibroblasts and on the collagen produced by the fibroblasts themselves, in areas close to the implant and to the symmetric geometry of the implant itself.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Weigang Jia ◽  
Wei Wang ◽  
Rui Li ◽  
Quanyu Zhou ◽  
Ying Qu ◽  
...  

Abstract Background In recent years, it has been reported that Qinbai Qingfei Concentrated Pellet (QQCP) has the effect of relieving cough and reducing sputum. However, the therapeutic potentials of QQCP on post-infectious cough (PIC) rat models has not been elucidated. So the current study was aimed to scientifically validate the efficacy of QQCP in post infectious cough. Methods All rats were exposed to sawdust and cigarette smokes for 10 days, and intratracheal lipopolysaccharide (LPS) and capsaicin aerosols. Rats were treated with QQCP at dose of 80, 160, 320 mg/kg. Cough frequency was monitored twice a day for 10 days after drug administration. Inflammatory cell infiltration was determined by ELISA. Meanwhile, the histopathology of lung tissue and bronchus in rats were evaluated by hematoxylin-eosin staining (H&E). Neurogenetic inflammation were measured by ELISA and qRT-PCR. Results QQCP dose-dependently decreased the cough frequency and the release of pro-inflammatory cytokines TNF-α, IL-1β, IL-6 and IL-8, but exerted the opposite effects on the secretion of anti-inflammatory cytokines IL-10 and IL-13 in BALF and serum of PIC rats. The oxidative burden was effectively ameliorated in QQCP-treated PIC rats as there were declines in Malondialdehyde (MDA) content and increases in Superoxide dismutase (SOD) activity in the serum and lung tissue. In addition, QQCP blocked inflammatory cell infiltration into the lung as evidenced by the reduced number of total leukocytes and the portion of neutrophils in the broncho - alveolar lavage fluid (BALF) as well as the alleviated lung damage. Furthermore, QQCP considerable reversed the neurogenetic inflammation caused by PIC through elevating neutral endopeptidase (NEP) activity and reducing Substance P (SP) and Calcitonin gene related peptide (CGRP) expression in BALF, serum and lung tissue. Conclusions Our study indicated that QQCP demonstrated a protective role of PIC and may be a potential therapeutic target of PIC.


2013 ◽  
Vol 114 (1) ◽  
pp. 66-72 ◽  
Author(s):  
Peter Marklund ◽  
C. Mikael Mattsson ◽  
Britta Wåhlin-Larsson ◽  
Elodie Ponsot ◽  
Björn Lindvall ◽  
...  

The impact of a 24-h ultraendurance exercise bout on systemic and local muscle inflammatory reactions was investigated in nine experienced athletes. Blood and muscle biopsies were collected before (Pre), immediately after the exercise bout (Post), and after 28 h of recovery (Post28). Circulating blood levels of leukocytes, creatine kinase (CK), C-reactive protein (CRP), and selected inflammatory cytokines were assessed together with the evaluation of the occurrence of inflammatory cells (CD3+, CD8+, CD68+) and the expression of major histocompatibility complex class I (MHC class I) in skeletal muscle. An extensive inflammatory cell infiltration occurred in all athletes, and the number of CD3+, CD8+, and CD68+ cells were two- to threefold higher at Post28 compared with Pre ( P < 0.05). The inflammatory cell infiltration was associated with a significant increase in the expression of MHC class I in muscle fibers. There was a significant increase in blood leukocyte count, IL-6, IL-8, CRP, and CK at Post. At Post28, total leukocytes, IL-6, and CK had declined, whereas IL-8 and CRP continued to increase. Increases in IL-1β and TNF-α were not significant. There were no significant associations between the magnitude of the systemic and local muscle inflammatory reactions. Signs of muscle degenerative and regenerative events were observed in all athletes with various degrees of severity and were not affected by the 24-h ultraendurance exercise bout. In conclusion, a low-intensity but very prolonged single-endurance exercise bout can generate a strong inflammatory cell infiltration in skeletal muscle of well-trained experienced ultraendurance athletes, and the amplitude of the local reaction is not proportional to the systemic inflammatory response.


Author(s):  
Kazuhiko Hashimoto ◽  
Yutaka Oda ◽  
Koichi Nakagawa ◽  
Terumasa Ikeda ◽  
Kazuhiro Ohtani ◽  
...  

Recent data suggest that the lectin-like oxidized low-density lipoprotein (ox-LDL) receptor-1 (LOX-1)/ox-LDL system may be involved in the pathogenesis of arthritis. We aimed to demonstrate the roles of the LOX-1/ox-LDL system in arthritis development by using LOX-1 knockout (KO) mice. Arthritis was induced in the right knees of C57Bl/6 wild-type (WT) and LOX-1 KO mice via zymosan injection. Saline was injected in the left knees. Arthritis development was evaluated using inflammatory cell infiltration, synovial hyperplasia, and cartilage degeneration scores at 1, 3, and 7 days after administration. LOX-1, ox-LDL, and matrix metalloproteinase-3 (MMP-3) expression in the synovial cells and chondrocytes was evaluated by immunohistochemistry. The LOX-1, ox-LDL, and MMP-3 expression levels in synovial cells were scored on a grading scale. The positive cell rate of LOX-1, ox-LDL, and MMP-3 in chondrocytes was measured. The correlation between the positive cell rate of LOX-1 or ox-LDL and the cartilage degeneration score was also examined. Inflammatory cell infiltration, synovial hyperplasia, and cartilage degeneration were significantly reduced in the LOX-1 KOmice with zymosan-induced arthritis (ZIA) compared to WT mice with ZIA. In the saline-injected knees, no apparent arthritic changes were observed. LOX-1 and ox-LDL expression in synovial cells and chondrocytes were detected in the knees of WT mice with ZIA. No LOX-1 and ox-LDL expression was detected in the knees of LOX-1 KOmice with ZIA or the saline-injected knees of both mice. MMP-3 expression in the synovial cells and chondrocytes was also detected in knees of both mice with ZIA, and was significantly less in the LOX-1 KO mice than in WT mice. The positive cell rate of LOX-1 or ox-LDL and the cartilage degeneration score showed a positive correlation. Our data show the involvement of the LOX-1/ox-LDL system in murine ZIA development. LOX-1-positive synovial cells and chondrocytes are potential therapeutic targets for arthritis prevention.


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