The body’s immediate, localized response to injury is inflammation. When the skin suffers a thermal burn, the heat causes damage that triggers this mechanism. The familiar signs of a burn—redness, swelling, and pain—are the physical manifestations of the body’s rapid deployment system. This process is designed to prevent further harm, clean the wound site, and lay the groundwork for tissue repair.
How Thermal Injury Triggers the Immune System
Thermal energy directly damages cell structures, causing them to rupture and die (necrosis). This event is the initial signal that initiates the inflammatory cascade. The contents of these damaged cells are released into the surrounding tissue, acting as chemical alarm bells.
These released intracellular contents are known as Danger-Associated Molecular Patterns (DAMPs). Molecules like High Mobility Group Box 1 (HMGB1) and cellular DNA function as DAMPs, which are normally confined within healthy cells. Once free, DAMPs bind to specialized pattern recognition receptors (PRRs) on nearby immune cells, such as mast cells and macrophages.
The binding of DAMPs alerts the immune system that significant tissue damage has occurred, initiating sterile inflammation. This signaling prompts local immune cells to immediately release various inflammatory mediators, including cytokines and histamine. This prompt response explains why the characteristic signs of inflammation begin within moments of the burn, establishing the context for healing.
The Core Biological Functions of Acute Inflammation
The visible changes that occur immediately following a burn are rooted in specific biological actions. The acute inflammatory phase lasts approximately five to seven days, and its main goals are containment, debridement, and protection.
Containment and Restriction
The redness and heat at the burn site result from the dilation of local blood vessels (vasodilation). This increases blood flow, delivering a higher concentration of immune cells and plasma proteins to the injured area. Simultaneously, the vessels become more permeable, allowing fluid and plasma proteins to leak into the tissue spaces, causing swelling (edema).
The purpose of this fluid leakage is to dilute toxins or DAMPs released from damaged cells, reducing their impact. The leaked plasma also contains clotting factors, which quickly form a fibrin barrier around the injury. This barrier walls off the damaged zone, preventing the spread of cellular debris and potential contaminants.
Debridement and Cleaning
Chemical signals released by activated immune cells drive the physical cleaning of the wound. These signals, called chemokines, recruit specialized immune cells from the bloodstream to the injury site (chemotaxis). Neutrophils are the first responders, migrating rapidly to consume dead tissue and cellular debris.
Following the neutrophils, monocytes arrive and differentiate into macrophages, which are powerful phagocytic cells. Macrophages continue debridement by engulfing and breaking down remaining necrotic tissue, spent neutrophils, and any invading microorganisms. This cellular cleaning is essential because a wound cannot heal until all damaged material has been removed.
Protection and Signaling
The sensation of pain is a function of the inflammatory process, serving as a protective mechanism. Chemical mediators like bradykinin and prostaglandins are released into the tissue, stimulating local nerve endings. The resulting pain signal discourages use or movement of the injured area.
This immobilization helps prevent further mechanical damage to the newly forming tissue and allows the containment and cleaning phases to proceed. The pain signal is a biological command to rest the affected area.
Resolution and Transition to Tissue Repair
Once immune cells have contained the injury, removed debris, and neutralized inflammatory triggers, the acute phase must resolve for healing to begin. This transition is actively managed and sets the stage for tissue reconstruction.
The resolution phase involves clearing inflammatory cells, particularly accumulated neutrophils. Macrophages play a dual role; they clean up debris and change their signaling profile. They switch from releasing pro-inflammatory signals to secreting anti-inflammatory cytokines and growth factors.
These growth factors, such as Transforming Growth Factor-beta (TGF-β), signal surrounding cells to transition from a cleaning state to a repair state. This shift activates fibroblasts, which synthesize new tissue matrix. Fibroblasts lay down a framework of new collagen, which will ultimately form the final healed skin or scar tissue.