Acute inflammation is the initial physiological response to tissue damage, such as that caused by mechanical, thermal, electrical, irradiation, chemical, or infective insults. It can be acute (lasting for a few days) or chronic (in response to an ongoing and unresolved insult). Inflammation can develop into permanent tissue damage or fibrosis.

The outcome of acute inflammation can be:
1. **Complete resolution:** With total repair and destruction of the insult.
2. **Fibrosis and scar formation:** Occurs in cases of significant inflammation.
3. **Chronic inflammation:** From a persisting insult or failure of resolution.
4. **Formation of an abscess:** A localized collection of pus.
5. **Organization:** The replacement of inflamed tissue by granulation tissue and scar tissue.

Chemical mediators of inflammation are substances that are responsible for many of the inflammatory events. According to their origin, they are either plasma-derived or cell-derived. Most mediators perform their job by binding to specific receptors on target cells. One mediator can stimulate the release of other mediators. The secondary mediators may have identical or similar actions to the initial mediators but may have opposing activities.

The functions of chemical mediators of inflammation include:
– **Stimulating release and mediation of target cells themselves:** The secondary mediators have similar or opposite effects.
– **Chemical action:** One or many target cells with different effects.
– **Scavenging oxygen species**.
– **Causing tissue damage:** Histamine and serotonin are examples of mediators that cause tissue damage.