Intercellular adhesion molecule

Name: Instructor’s Name: Course: Date: Cell Adhesion Molecules Introduction Cells are independent units of life. However, when a cell becomes part of an organism, it becomes part of a tissue and organ system. Cells in a tissue are joined to each other and to the extracellular matrix (ECM) by cell junctions. There are three kinds of cell junctions: Occluding junctions, anchoring junctions and communication junctions. Occluding junctions occur in the epithelium where the adjacent cells are so tightly

Acute Inflammation The survival of all organisms requires that they eliminate foreign invaders, such as infectious pathogens, and damaged tissues. These functions are mediated by a complex host response called inflammation. Definition of inflammation Inflammation is fundamentally a protective response, the ultimate goal of which is to rid the organism of both the initial cause of cell injury (e.g., microbes, toxins) and the consequences of such injury (e.g., necrotic cells and tissues)

tight junctions can be found between skin cells which makes human skin watertight. Differing from the tight junction, a gap junction is composed of proteins surrounding a pore which enables the passage of amino acids, small molecules and ions between cells with a larger intercellular space than the tight junction. They play a pivotal role in communication between cells such as the heart muscle cells. Desmosomes bind cells together to form stronger sheets of cells. The

systemic inflammation and autoantibody production precedes synovial inflammation by as much as 15 years (Gibofsky 2012). 2 The autoimmune reaction results in endothelial activation, involving the expression of vascular cell adhesion molecule, intercellular adhesion molecule (ICAM), and E-selectin. This enables leukocyte migration and accumulation in the synovium, and subsequent cytokine release, regional hypoxia, fibroblast activation, and synovial remodeling worsening the inflammation and destruction

transduction pathways (Duntas 2009). The other important anti-inflammatory mechanism of selenium is regulated via its effect on monocyte adhesion to endothelial cells and their infiltration toward tissues. Monocytes stick to the endothelium and are converted into macrophages, as the main effectors of innate immunity in inflammation (Cao et al. 2002). The monocytes adhesion to the endothelium is mediated by L-selectin, which simplify the neutrophil migration, during inflammatory response- mediated by different

These cells are able to produce and secrete such mediator molecules, like cytokines, chemokines, growth-factors, enzymes, and disintegrins, which activate endothelial cells, proliferation of smooth muscle cells, lesion progression, and the weakening of a vulnerable plaque by matrix degradation of its fibrous cap. Many of these molecules involved can be measured systemically and has been shown that elevated concentrations in the circulation are associated

inflammation. Step I is the initial low-affinity rolling interaction that is mediated by all three selectins. Step II involved activation of leukocytes that alter concentration gradients of various chemotactic factors. Step III is the high-affinity adhesion, change in shape of leukocyte, and finally extravasation. Figure 2 left out another important factor of selectin’s role in inflammation: PSGL-1. PSGL-1 on the plasma memebranes of neutrophils or monocytes binds to P-selectin translocated to the surfaces

cells were pushed out from the axial flow, resulting in the increased leukocytes concentration adjacent to the endothelial cell lining.[1] The process of accumulation of leukocytes at the peripheral of vessels is known as margination.[1]  Adhesion The adhesion of leukocytes to the endothelial surface is mediated by integrins which appears on the surface of leukocytes, interacting with their subsequent ligands on the endothelial cells.[1] The integrins are usually of low affinity and do not adhere

Siyana Praskov Professor Fair Microbiology MCB4404 2017 Scientific Article Analysis of Role of Phenol-Soluble Modulins in Formation of Staphylococcus aureus Biofilms in Synovial Fluid Abstract and Introduction Recently, Stapylococcus aureus joint infection pathogenesis has become a major burden for patients and healthcare providers. A unique biofilm formation process allows bacteria to resist standard treatments used for infections. Specifically, a serious medical issue confronted by orthopedic

gingivalisuses many mechanisms for adhesion and internalisation into host cells such a frimbriae, gingipains, and proteolytic enzymes. These and other processes cause induction of host’s immune-inflammatory activity, which affects the structures supporting the teeth. This may also lead to the destruction of the surrounding bone and connective tissue, and ultimately tooth loss. Adhesion Initial interactions with epithelial cells require adhesion. The adhesion in the human oral cavity is essential