[Bacterial aggression]

In all living species, the first line of defence against microbial aggressions is constituted by innate immunity. During Evolution, it appears in invertebrates and plants, long before adaptive immunity, which appears in vertebrate. Adaptive immunity induces acquired resistance against microorganisms through random somatic rearrangements of genes encoding immunoglobulins and T cell receptors, thus generating a high level of diversity of receptors (>10(9)) in response to microbial aggressions. Acquired resistance is not vertically transmitted and reflects the "infectious history" of every individual. In contrast, innate immunity relies on recognition of antigens by a small number of weakly specific receptors (>10(2)) designated Pattern-Recognition Receptors (PRR) and is vertically transmitted by germinal cells. The PRR are expressed on macrophages dendritic cells and B lymphocytes and recognize antigenic structures highly conserved in the living world, termed Pathogen-Associated Molecular Patterns (PAMP), as lipopolysaccharides peptidoglycanes and lipoteichoic acids. PRR are secreted (complement, lectins), or expressed at the cell surface of cells to induce endocytosis or signaling (Toll-like receptors or TLRs). The recognition of antigens induces an immediate inflammatory response and triggers adaptive immunity. Among secreted PRR, the system of complement plays a major role in the immediate inflammatory response, controlling infections by its major role in opsonization, chemotactism and activation of leucocytes. TLRs induce the inflammatory response against microorganisms through NF-kB, a cytoplasmic factor controlling transcription of many genes, including cytokines (TNF, INF, IL-1, IL-2, IL-8, IL-12.) and defensines. So, within few minutes following microbial aggression, the inflammatory response is rapidly triggered to destroy infectious agents and to generate a long-term memory against pathogens.