Acute Inflammation

 

ACUTE INFLAMMATION

Previously we discussed the types of inflammation briefly and in here we will know more about acute inflammation 

general features of inflammation

steps of inflammation

causes of inflammation

Before discussing acute inflammation exclusively, we should know the general pathway of inflammation which is described below

Due to the presence of an injurious agent or dead cells or tissue damage the phagocytes present in the tissues or organ try to eliminate the causative agent. Along with killing abilities the also has release soluble substances which cause inflammation and also act as mediators which help the leukocytes to reach the affected place.

There are three basic steps in the 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, and

3.               Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury,           and their activation to eliminate the offending agent

We will discuss them briefly here

1.      REACTION OF BLOOD VESSELS IN ACUTE INFLAMMATION- Dilation of small vessels, leading to an increase in blood flow,

The vascular reactions of acute inflammation consist of changes in the flow of blood and the permeability of vessels, both designed to maximize the movement of plasma proteins and leukocytes out of the circulation and into the site of infection or injury.

These include the blood vessels and the lymphatics

Often the plasma proteins and the leukocytes that accumulate in the place of inflammation gets accumulated in different forms

a) exudate- this fluid is high in protein content and all the dead cells and leukocytes that were used during the inflammation. This form of the liquid has a whitish-yellow color and we in common terms call it pus.

b) transudate- it is a basic clear fluid, can be considered as the ultrafiltrate of the blood plasma. It has very little protein content and is mostly produced due to osmotic imbalance. The osmotic imbalance can occur during vasodilation.

c) edema- it can be an exudate os transudate and is a fluid buildup in the serous layer or the interstitium.

 

LEUKOCYTE RECRUITMENT TO SITES OF INFLAMMATION- Increased permeability of the microvasculature, enabling plasma proteins and leukocytes to leave the circulation

 

a)       Leukocytes are recruited from the blood into the extravascular tissue where infectious pathogens or damaged tissues maybe located, migrate to the site of infection or tissue injury, and are activated to perform their functions.

b)       Leukocyte recruitment is a multistep process consisting of loose attachment to and rolling on endothelium (mediated by selectins); firm attachment to the endothelium (mediated by integrins); and migration through interendothelial gaps.

c)       Various cytokines promote the expression of selectins and integrin ligands on endothelium (TNF, IL-1), increase the avidity of integrins for their ligands (chemokines), and promote directional migration of leukocytes (also chemokines). Tissue macrophages and other cells responding to the pathogens or damaged tissues produce many of these cytokines.

d)        Neutrophils predominate in the early inflammatory infiltrate and are later replaced by monocytes and macrophages.

 

LEUKOCYTE ACTIVATION AND REMOVAL OF OFFENDING AGENTS

a)       Leukocytes can eliminate microbes and dead cells by phagocytosis, followed by their destruction in phagolysosomes.

b)      Destruction is caused by free radicals (ROS, NO) generated in activated leukocytes and by granule enzymes.

c)       Neutrophils can extrude their nuclear contents to form extracellular nets that trap and destroy microbes.

d)       Granule enzymes may be released into the extracellular environment.

e)       The mechanisms that function to eliminate microbes and dead cells (the physiologic role of inflammation) also are capable of damaging normal tissues (the pathologic consequences of inflammation).

f)         Anti-inflammatory mediators terminate the acute inflammatory reaction when it is no longer needed.

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