Distinct Distribution of Immunocytes in a Retropharyngeal Lymphadenopathy Associated with Kawasaki Disease: A Case Study Compared with Tonsillitis

Cardiology ◽  
2017 ◽  
Vol 137 (4) ◽  
pp. 237-243 ◽  
Author(s):  
Seigo Okada ◽  
Yuki Kobayashi-Fujiwara ◽  
Atsunori Oga ◽  
Takashi Furuta ◽  
Kenzo Ikemoto ◽  
...  

Objectives: Retropharyngeal lesions are often associated with Kawasaki disease (KD). A 4-year-old male first presented a peritonsillar and retropharyngeal abscess-like lesion. Surgical tonsillectomy was performed to avoid a risk of mediastinal abscess, but he fulfilled the diagnostic criteria of KD after the operation. This prompted us to perform a histological study on the KD tonsils. Methods: The histopathology of the KD tonsil specimens were compared with hypertrophic tonsils obtained from 4 patients with chronic tonsillitis unrelated to KD assessed by the immunostainings. Results: KD tonsils showed small lymphatic follicles and neutrophil infiltration in the peritonsillar muscle layer, with no evidence of vasculitis or abscess formation. The KD tonsils exclusively showed (1) predominant activated CD4+ T cells in the perifollicular interstitium, (2) sparse scattering of CD68+ monocytes/macrophages in the lymphatic follicles, and (3) polyclonal carcinoembryonic antigen-positive cells in the lymphatic follicles and venules with the high endothelial cells. Conclusions: The uniquely distributed immunocytes suggest the inflammatory process of KD involving the pathogen-associated molecules.

2012 ◽  
Vol 7 (4) ◽  
pp. 179-182 ◽  
Author(s):  
Maria Elena Cavicchiolo ◽  
Paola Berlese ◽  
Silvia Bressan ◽  
Elena Trincia ◽  
Ingrid Inches ◽  
...  

2001 ◽  
Vol 125 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Mark W. Lingen

Abstract The basic signs and symptoms of inflammation and wound healing have been appreciated for thousands of years. However, the specific cells involved and their roles in this complex environment are still being elucidated today. In 1926, the origin of the phagocytic mononuclear ameboid wandering cell (macrophage) had not been determined. One popular theory was that the cells were differentiated from the endothelial cells of the nearby blood vessels, whereas others believed that the cells came from the peripheral blood or resting wandering cells. The purpose of this article is to review the seminal article published by Lang regarding this topic nearly 75 years ago. In addition, this article will review what is now known with regard to the role of the macrophage and endothelial cells in the development of angiogenesis, which is arguably the most critical component of successful inflammatory process or wound healing.


QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Eman Gomaa El Saeed ◽  
Manal H Moussa ◽  
Gehad A Hammouda ◽  
Sahar M. M Omar

Abstract Background Repairing urinary bladder (UB) defect by enterocystoplasty remains the gold standard surgical bladder reconstruction procedure to increase the capacity and compliance of dysfunctional bladders. However, many complications were recorded. Aim of the work This work aimed to compare the consequences of reconstruction of urinary bladder defect using untreated small intestinal submucosal (SIS) matrix versus seeded and unseeded decellularized SIS matrix. Material and Methods Fifty female albino rats were used in this study. The animals were divided into three groups: Group I (Control) included ten adult rats from which ileal tissue was obtained. Group II included ten adult rats in which their UB defect was repaired by untreated cellular SIS. Group III included twenty adult rats that were subdivided into two subgroups, 10 rats each; Subgroup IIIA where rats had their UB defect repaired by acellular SIS and subgroup IIIb where rats had their UB defect repaired by acellular SIS seeded with adipose mesenchymal stem cells (AMSCs).Ten young rats were used for preparation of AMSCs. Morphometric and statistical analysis were also performed. Results In rats where UB defect was repaired by untreated cellular SIS, the graft area showed loss of epithelial polarity, presence of intraepithelial cysts and occasional extension of urothelium to the outer surface forming fistula. There were areas of metaplasia with the appearance PAS positive cells. In the lamina propria, there was areas of lymphocytic infiltration together with significant increase in the collagen fiber deposition (p < 0.05). There was a significant decrease thickness of muscle layer as compared to control (p < 0.05). In rats where UB defect was repaired by acellular SIS, urothelium in the graft area showed occasional squamous metaplasia and often the urothelium extended to the deeper layers forming Brunn's nest. There was minimal muscle regeneration in the graft area. However, in rats where UB defect was repaired by acellular SIS seeded with AMSCs, the urothelium in the graft area was nearly similar to control group with uniform urothelium thickness, minimal collagen fibers deposition and thick muscle layer that showed no significant difference from the control (p > 0.05). Conclusion Acellular SIS seeded with AMSCs showed better results compared to non-seeded and cellular SIS in reconstructing urinary bladder defects.


Blood ◽  
2018 ◽  
Vol 132 (17) ◽  
pp. 1818-1828 ◽  
Author(s):  
Laurel E. Hind ◽  
Patrick N. Ingram ◽  
David J. Beebe ◽  
Anna Huttenlocher

Abstract Neutrophil infiltration into tissues is essential for host defense and pathogen clearance. Although many of the signaling pathways involved in the transendothelial migration of neutrophils are known, the role of the endothelium in regulating neutrophil behavior in response to infection within interstitial tissues remains unclear. Here we developed a microscale 3-dimensional (3D) model that incorporates an endothelial lumen, a 3D extracellular matrix, and an intact bacterial source to model the host microenvironment. Using this system, we show that an endothelial lumen significantly increased neutrophil migration toward a source of Pseudomonas aeruginosa. Surprisingly, we found neutrophils, which were thought to be short-lived cells in vitro, migrate for up to 24 hours in 3D in the presence of an endothelial lumen and bacteria. In addition, we found that endothelial cells secrete inflammatory mediators induced by the presence of P aeruginosa, including granulocyte-macrophage colony-stimulating factor (GM-CSF), a known promoter of neutrophil survival, and interleukin (IL)-6, a proinflammatory cytokine. We found that pretreatment of neutrophils with a blocking antibody against the IL-6 receptor significantly reduced neutrophil migration to P aeruginosa but did not alter neutrophil lifetime, indicating that secreted IL-6 is an important signal between endothelial cells and neutrophils that mediates migration. Taken together, these findings demonstrate an important role for endothelial paracrine signaling in neutrophil migration and survival.


2020 ◽  
Author(s):  
Xue Fan ◽  
Meng Li ◽  
Min Xiao ◽  
Cong Liu ◽  
Mingguo Xu

Abstract Background: Kawasaki disease (KD) leads to coronary artery damage and the etiology of KD is unknown. The present study was designed to explore the differentially expressed genes (DEGs) in KD serum-induced human coronary artery endothelial cells (HCAECs) by RNA-sequence (RNA-seq). Methods: HCAECs were stimulated with serum (15% (v/v)), which were collected from 20 healthy children and 20 KD patients, for 24 hours. DEGs were then detected and analyzed by RNA-seq and bioinformatics analysis. Results: The expression of SMAD1, SMAD6, CD34, CXCL1, PITX2, and APLN was validated by qPCR. 102 genes, 59 up-regulated and 43 down-regulated genes, were significantly differentially expressed in KD groups. GO enrichment analysis showed that DEGs were enriched in cellular response to cytokines, cytokine-mediated signaling pathway, and regulation of immune cells migration and chemotaxis. KEGG signaling pathway analysis showed that DEGs were mainly involved in cytokine−cytokine receptor interaction, chemokine signaling pathway, and TGF−β signaling pathway. Besides, the mRNA expression levels of SMAD1, SMAD6, CD34, CXCL1, and APLN in the KD group were significantly up-regulated compared with the normal group, whilePITX2 was significantly down-regulated. Conclusion: 102 DEGs in KD serum-induced HCAECs were identified, and six new targets were proposed as potential indicators of KD.


Author(s):  
Robin P. Choudhury ◽  
Edward A. Fisher

Formation of an atheromatous plaque—this is an inflammatory process that involves the contribution of endothelial cells, monocytes, and smooth muscle cells in conjunction with the deposition of atherogenic lipoproteins in the intimal layer of the vascular wall. The initial stage involves activation of the endothelium at regions of nonlaminar flow in vessels resulting in increased permeability to Apo B-containing lipoproteins (LDL). Inflammatory cells, in particular monocytes, are recruited into the intimal layer of the vessel wall via the action of chemokines and adhesion molecules mobilized by activated endothelium....


Metabolism ◽  
2020 ◽  
Vol 104 ◽  
pp. 154096
Author(s):  
Ying Wang ◽  
Jian Hu ◽  
Jingjing Liu ◽  
Zhimin Geng ◽  
Yijing Tao ◽  
...  

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