What is chemotaxis?

After exiting the circulation, leukocytes move in the tissues toward the site of injury by a process called chemotaxis, which is defined as locomotion along a chemical gradient. 

Both exogenous and endogenous substances can act as chemoattractants. 

Exogenous agents are bacterial products, including peptides that possess an N-formylmethionine terminal amino acid and some lipids. 

Endogenous chemoattractants include several chemical mediators 

(1) Cytokines, particularly those of the chemokine family

(2) Components of the complement system, particularly C5a

(3) Arachidonic acid (AA) metabolites, mainly leukotriene B4.

Mechanism of Increased Vascular Permeability in Acute Inflammation

Several mechanisms involved in increased vascular permeability in acute inflammation:

1. Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism of vascular leakage.
2. Endothelial injury, resulting in endothelial cell necrosis and detachment.
3. Increased transport of fluids and proteins, called transcytosis, through the endothelial cell. This process may involve intracellular channels that may be stimulated by certain factors, such as vascular endothelial growth factor (VEGF), that promote vascular leakage.

What vascular changes occur in acute inflammation?

Vascular changes in acute inflammation are as follows:

1. Vasodilation is induced by the action of several mediators, mainly histamine, on vascular smooth muscle.
2. Vasodilation is quickly followed by increased permeability of the microvasculature.
3. Engorgement of small vessels with slowly moving red cells, a condition termed stasis,
   which is seen as vascular congestion and localized redness of the involved tissue.
4. As stasis develops, blood leukocytes, principally neutrophils, accumulate along the vascular endothelium.

What are the components of acute inflammation?

There are three components of acute inflammation:

1. Dilation of small vessels leading to an increase in blood flow, 
2. Increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation.
3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent