The complement system is an important factor in innate immunity. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. During complement activation, C3 is proteolytically cleaved resulting in release of the anaphylatoxic peptide C3a.C3a is a small polypeptide consisting of 74 amino acids. C3a itself is very short-lived and in serum cleaved rapidly into the more stable C3a-desArg (also called acylation stimulating protein, ASP) . Therefore, measurement of C3a-desArg allows reliable conclusions about the level of complement activation in the samples. For convenience, both forms will be referred to in the following text as C3a.C3a is a mediator of local inflammatory processes. It induces smooth muscle contraction, increases vascular permeability, and causes histamine release from mast cells and basophilic leukocytes. C3a is involved in inflammatory reactions seen in gram-negative bacterial sepsis, trauma, ischemic heart disease, post-dialysis syndrome and a variety of autoimmune diseases. Normal values in plasma of control persons range between 48 - 150 ng/ml (median: 86.4 ng/ml, SD: 29.3 ng/ml).Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. The human C3a ELISA kit is based on a catching monoclonal antibody that recognizes a neo-epitope on C3a-desArg. This prevents cross-reactivity with C3.