Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types – adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
The endothelial cells lining the blood vessels are tightly linked, forming a barrier that prevents the escape of other cells and molecules from the bloodstream into surrounding tissue. However, during an immune response, the leukocytes from the bloodstream must pass through this barrier and reach the target tissue. Inflammatory molecules like histamines, and signaling proteins like vascular endothelial growth factor (VGEF), trigger downstream processes, such as phosphorylation and internalization of cadherins present on the endothelial cell surface. This leads to the disassembly of adherens junctions and increases the endothelial permeability by creating gaps that allow immune cells and other molecules to pass through. The maintenance and breakdown of adherens junctions are thus dynamically regulated in response to specific stimuli.
Adherens Junctions and Infection
Infectious agents like Helicobacter pylori can enter the host tissue by disrupting the adherens junctions and moving through the intercellular gaps. These bacteria produce proteases that cleave the extracellular domain of cadherins, thus, causing junction disassembly. Cell surface cadherins are also hijacked as receptors by bacteria such as Streptococcus pneumoniae to adhere to the upper respiratory epithelium.
However, the most impressive hijacking is perhaps demonstrated by Listeria monocytogenes. This bacterium expresses cell wall proteins that attach E-cadherins and trigger the recruitment of ɑ, β, and p120-catenins to the site. This recruitment initiates dynamic actin polymerization, forming membrane protrusions that engulf the bacteria in a process called induced phagocytosis. The bacterium thus gains entry into a nonphagocytic cell and proliferates within the host.
