Differential expression tight junction proteins infection
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Answer:
Tight junctions (TJs) are the most apical intercellular junctions of epithelial cells formed by occludin, claudins, junctional adhesion molecules (JAMs), and zonula occludens (ZO). Tight junction proteins can sense the presence of bacteria and regulate the transcription of target genes that encode effectors and regulators of the immune response. The aim of this study was to determine the impact of TJ proteins in response to Porphyromonas gingivalis (P. gingivalis), P. gingivalis lipopolysaccharide (P. gingivalis LPS), and extracellular adenosine triphosphate (ATP) in the oral epithelial cell culture model. Quantified real time-polymerase chain reaction (RT-PCR), immunoblots, and immunostaining were performed to assess the gene and protein expression in TJs. It was found that P. gingivalis infection led to transient upregulation of the genes encoding occludin, claudin-1, and claudin-4 but not JAM-A, claudin-15, or ZO-1, while P. gingivalis LPS increased claudin-1, claudin-15, and ZO-1 and decreased occludin, JAM-A, and claudin-4. Tight junction proteins showed significant upregulation in the above two groups when cells were pretreated with ATP for 3 h. The findings indicated that P. gingivalis induced the host defence responses at an early stage. P. gingivalis LPS exerted a more powerful stimulatory effect on the disruption of the epithelial barrier than P. gingivalis. ATP stimulation enhanced the reaction of TJ proteins to P. gingivalis invasion and LPS destruction of the epithelium.
Introduction
Tight junctions (TJs), the most apical intercellular junctions of epithelial cells, are formed by occludin, claudins, junctional adhesion molecules (JAMs), and zonula occludens (ZO)-1, 2, and 3.1 Tight junctions are transmembrane proteins that control the paracellular passage and create a regulatable semipermeable diffusion barrier between individual cells.2 As the first integral membrane protein of TJs, occludin is the most ubiquitously expressed and the most reliable immunohistochemical marker for TJs.3 ZO-1 is critical to junction assembly.4 In the absence of ZO-1, cells fail to form TJs.5 JAM-A, another crucial transmembrane component of TJs, controls the passage of nutrients and solutes across epithelial surfaces6 and modulates many cellular functions, including cell migration, cell polarity, paracellular permeability, and proliferation.7 The claudin family is regarded as the backbone of TJs8 and contributes to the epithelial barrier in the junctional epithelium.9 The network of adhesion molecules in protein–protein interactions in gingival epithelial cells provides a clear picture for understanding the regulation of TJ proteins in periodontitis.10