Current problems in burn immunology

Innate Immune System Response to Burn Damage—Focus on Cytokine Alteration

“…Immune cells, similar to macrophages and neutrophils, produce oxygen free radicals (ROS) to destroy pathogens, which damage skin structures, and which results in a strong inflammatory response in the immune system, defined as systemic inflammatory response syndrome (SIRS) [ 3 ]. Innate immunity provides non-specific and rapid responses to infection [ 17 ], and its mechanisms are the first to respond and recognize microbial pathogen-related molecular patterns (PAMPs) and danger-related molecular patterns (DAMPs). This is achieved using the instrumentation of pattern recognition receptors (PRRs), which include several classes: Toll-like receptors (TLR), NOD-like receptors (NLR), RIG-I-like receptors (RLR) and C-type lectin receptors (CLR) [ 2 , 18 ].…”

“…This is achieved using the instrumentation of pattern recognition receptors (PRRs), which include several classes: Toll-like receptors (TLR), NOD-like receptors (NLR), RIG-I-like receptors (RLR) and C-type lectin receptors (CLR) [ 2 , 18 ]. Outside of the body, epithelial cells secrete defensins, lysozymes and cathelicidins, whose roles are to destroy the cell walls of pathogens and provide antibacterial activity [ 17 ]. Inside the body, the innate immune system consists of macrophages, neutrophils, dendritic cells (DC) and more.…”

“…Binding of PAMP to TLRs leads to rapid phagocytosis of suspect pathogens. In addition, innate immunity involves the recruitment of non-cellular defense mechanisms such as complement, coagulation and proinflammatory cytokine proteins that enhance the acquired immune system [ 17 ].…”

“…Hampson et al [ 10 ] reported that, within 24 hours after the injury, the number of neutrophils increases significantly, and the state normalizes 3 days after the injury; then, it increases significantly on day 7 and remains elevated for 28 days after the burn [ 10 ]. Neutrophils produce oxidants, antimicrobial peptides and proteolytic enzymes and provide non-specific antimicrobial defense [ 17 ]. After the burn, the ability of neutrophils’ oxidative burst decreases, which in turn weakens phagocytosis [ 10 , 29 ]; there is a decrease in the speed of motility during chemotaxis [ 30 , 31 ] and decreased bactericidal capacity [ 14 ], which ultimately reduce innate immune function.…”

“…Monocytes are primarily responsible for phagocytosis, production of cytokines and antigen presentation [ 28 ]. Activated by the injury, monocytes initiate the production of chemokines and cytokines that attract other cells of the immune system, such as, e.g., neutrophils, to the site of injury and enhance their response [ 17 , 28 , 41 ]. Production of cytokines and chemokines are stimulated after monocytes recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) [ 42 ].…”