Characterization of Cytokines and Proliferation Marker Ki67 in Cleft Affected Lip Tissue.

Medicina (Kaunas)

Institute of Anatomy and Anthropology, Riga Stradins University, Kronvalda Boulevard 9, LV-1010 Riga, Latvia.

Published: August 2019

Cleft lip palate takes the second place among all anomalies. The complex appearance of cytokines and proliferation markers has still not been clarified despite their possible crucial role in cleft tissue. Therefore, the aim of work was the detection of appearance of pro- and anti-inflammatory cytokines and proliferation marker Ki67, and their inter-correlations in cleft affected lip (CAL). The lip material was obtained from 16 children aged before primary dentition during plastic surgery. Control was obtained from 7 non-CAL oral tissue. Tissues were stained for IL-1, IL-4, IL-6, IL-8, IL-10 and Ki67 immunohistochemically. Non-parametric statistic, Mann-Whitney and Spearman's coefficient were used. All cytokines positive cells were observed more into the epithelium. Statistically significant difference was seen between epithelial IL-1, IL-10, IL-8 and Ki67 positive cells and IL-10-, IL-4-containing connective tissue cells in comparison to the control. Strong positive correlation was detected in CAL epithelium between IL-10 and IL-8, IL-10 and IL-4, IL-10 and IL-1, IL-1 and IL-8, IL-1 and IL-4, IL-4 and IL-8, IL-8 and Ki67, IL-10 and Ki67, but moderate-in connective tissue between IL-1 and IL-10, IL-1 and IL-4. The CAL epithelium is the main source for the interleukins. Rich similar expression of IL-1 and IL-10 suggests the balance between pro-and anti-inflammatory tissue response on basis of dysregulated tissue homeostasis (increase of IL-8). The correlations between the different ILs -1, -4, -8, -10 in CAL epithelium seem to indicate the self-protection compensatory mechanism for intensification of local inflammatory-immune response without involvement of IL-6. The correlations between Ki67 and cytokines indicate the involvement of IL-8 and IL-10 in stimulation of cellular proliferation. IL-4 and IL-10 expression from CAL connective tissue simultaneously to IL-1, IL-4 and IL-10 inter-correlations there suggests the intensification of local immune response regulated probably by main pro-inflammatory cytokine-IL-1.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6780708PMC
http://dx.doi.org/10.3390/medicina55090518DOI Listing

Publication Analysis

Top Keywords

il-1 il-4
16
cytokines proliferation
12
cleft lip
12
il-8 il-10
12
il-1 il-10
12
connective tissue
12
cal epithelium
12
il-4 il-10
12
il-10
11
il-1
9

Similar Publications

Obesity is a complex health risk influenced by genetic, environmental, and lifestyle factors. This review systematically assessed the association between interleukin gene polymorphisms (rs16944, rs17561, rs1143623, rs1143633, rs1143634, rs1800587, rs2234677, and rs4848306), (rs180275, rs1805010, rs13306435, rs1800795, rs1800796, rs1800797, rs2228145, rs2228145, rs2229238, and rs4845623), (rs1518110, rs1518111, rs1800871, rs1800872, rs1800896, rs1878672, rs2834167, rs3024491, rs3024496, rs3024498, and rs3024505), (rs3136617, rs3136618, and rs2296135), and (rs187238, rs1946518, rs2272127, rs2293225, and rs7559479) and the risk of overweight and obesity in adults, focusing on rs1800795 through a meta-analysis. The focus on in this review arises from its pleiotropic nature and unclear effect on obesity risk.

View Article and Find Full Text PDF

As a key inflammatory factor, the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome plays a crucial role in neuroinflammation and the progression of neurodegenerative diseases. Dysregulation of NLRP3 signaling can trigger various inflammatory responses in the brain, contributing to the development of neurodegenerative diseases such as ischemic stroke, vascular dementia (VaD), Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Therefore, the NLRP3 signaling pathway is a promising therapeutic target for the treatment of neurodegenerative diseases, including VaD.

View Article and Find Full Text PDF
Article Synopsis
  • The study investigates how interleukin-17 (IL-17) affects CD4+ T-cell immune regulation and the JAK/STAT signaling pathway, potentially leading to new therapies for dilated cardiomyopathy.
  • Naive CD4+ T cells from mice were manipulated to either overexpress or knockdown IL-17, with multiple proteins measured via methods like Western blotting and PCR to assess inflammatory responses and signaling pathways.
  • Results showed that overexpressing IL-17 increased levels of inflammatory factors and apoptosis in CD4+ T cells, while knocking it down decreased these levels, highlighting IL-17's significant regulatory role in inflammation and immune response.
View Article and Find Full Text PDF

Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila.

Ecotoxicol Environ Saf

January 2025

NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China. Electronic address:

Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.

View Article and Find Full Text PDF

Introduction Zinc deficiency (ZnD) impairs the development of acquired immunity and contributes to growth failure in children under five years of age. However, the prevalence of ZnD and its association with immunity in this age group in Uganda have not been well explored. This study aimed to determine the prevalence of ZnD and explore the associations between low serum zinc levels and total white blood cell count, differential cell counts, and levels of IL-1 and IL-2 in children aged 12 to 59 months.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!