# Inflammation: What's There and What's New?
## 2 Inflammatory Mechanisms
### Initiation of the Inflammatory Response
#### 2.1.1 Vasodilatation, Fluid Exudation, and Leukocyte Migration
Poor adhesive association occurs after imagination by neutrophils and endothelial vascular cells, allowing neutrophils to remain close to the vascular endothelium. Neutrophil action is stimulated by the tension of moving erythrocytes, with the speed being in accordance with the speed of red cells [10]. Selectins and their ligands promote the adhesive interaction that causes leukocyte rolling. Selectins are a family of surface molecules of glycoprotein expressed on leukocytes (L-selectin), endothelial cells (E-selectin), and platelets (Pselectin) that bind adjacent cells to sialylated carbohydrate determinants. A strong affinity in the adhesive association denominated as conformity occurs when rolling continues. For the subsequent neutrophil diapedesis and chemotaxis, adherence is needed and can occur through the activity of integrins and respective ligands. The most commonly researched and understood are the \(\beta\)-2 integrins, which are composed of different subunits that are bound to a specific \(\beta\)- subunit (CD11a, CD11b, and CD11c) (CD18). B-2 integrins appear in the neutrophils and interact with ligands on the endothelial surface, especially intercellular adhesion molecule-1 (ICAM-1). In neutrophils and endothelial cells, beta-2 integrins and ICAMs are constitutively present, with their expression being significantly up-regulated when inflammation occurs, and help in the transition from rolling to strict adherence [11]. After the adhesion process, to reach the extravascular inflammatory environment, the neutrophil must enter the endothelium and basement membrane. Neutroph migrate via endothelial cells, a mechanism partially supported by endothelial retraction. Diapedesis is also promoted by the adherence of compounds such as platelet-endothelial cell adhesion molecule-1 (PECAM-1), which is usually present both on the endothelial cells and on neutrophils. PECAM-1 bonds can reduce neutrophils' adherence to ICAM-1, which results in the inhibition of adherence and diapedesis. Rolling, adhesion, and diapedesis mechanisms are regulated via the interaction of neutrophil-adherent molecules with endothelial cells. The end purpose of such processes is to promote neutrophils' movements at sites of infection or damage from the intravascular compartment and into the interstitium [12]. To promote their migration to the damaged tissue, neutrophils and other leukocytes often need chemoattractts, soluble compounds that help to attract leukocytes to damaged tissues, which are usually by-products of a bacterial origin, complementary agents, and chemokines. Several chemoattractts are unique to subsets of leukocytes and can be categorized depending on the sensitivity of the leukocyte. Classical chemoattractts may be bacteria-produced N-formylated peptides, complementary agents, as well as leukotrienes [13]. Injury or invasion of tissue can lead to significant growth in the place of chemokine production, causing a selective caption of leukocytes to the injured tissue. The analysis of chemokine secretion due to the inflammatory stimulus defines the type of the inflammatory penetration of the damaged site. Chemokine receptors regulate the migration of leukocytes that are cell-type and chemokine-type specific. With seven transmembrane regions, these receptors are G-protein-coupled proteins that present an identic chemical structure, but have different functions. These molecules display ligand and leukocyte specificity, thereby evaluating the inflammatory infiltrate's type [14].