Immunity to Bacterial Infections

摘要

Abstract: Co-evolution of pathogenic bacteria and hosts has led to the development of an array of virulence genes (the nvirulome) and a set of mechanisms of defense which constitute the immune system. Mechanisms of innate or non-specific nimmunity involve mucosal epithelial surface barriers, antibacterial peptides and enzymes, defensive molecules (collectins, ncomplement), and cells (macrophages, dendritic cells, polymorphonuclear neutrophil leukocytes, natural killer cells). The npresence of bacterial products in host tissues induces a complex series of non-specific responses which constitute the ninflammatory reaction. Inflammation is critical to the resolution of infection, the key process being the ingestion and nkilling of bacteria by phagocytes, but inflammation also causes tissue damage and contributes to the pathology. The innate nimmunity is the initial step in the host defense against pathogens, but some pathogenic bacteria with appropriate virulence nfactors can overcome the innate immunity mechanisms. In these cases, the goal of innate immunity is to contain the ninfectious process until specific immunity is developed. The specific immune responses are performed by lymphocytes: B ncells, T helper (TH) cells, and cytotoxic T lymphocytes (CTL). Specific antibodies are produced by B cells, usually with nthe cooperation of TH2 cells. In general terms, extracellular bacteria can be killed by antibodies and complement proteins, nor cleared by phagocytosis after opsonization by antibodies, and bacterial exotoxins are neutralized by their specific nantibodies. In contrast, resistance to intracellular bacteria requires the induction of TH1 and CTL responses. In this review, nwe will focus on current knowledge about the defensive mechanisms against bacterial infections. We will discuss the ninnate immunity mechanisms, connections between innate and specific immunity, the key role of T helper 1 (TH1) and nTH2 cells, and the antibody and cell-mediated responses.