The major role of neutrophils is to phagocytose and destroy infectious agents but they also limit the growth of some microbes, thereby buying time for adaptive (specific) immunological responses. With many microbes, however, neutrophil defences are ineffective in the absence of opsonins and various agents that amplify the cytotoxic response.
Opsonization is a process, in which opsonins adsorb to the surface of bacteria or other particles and facilitate their adherence to the phagocyte cytoplasmic membrane through opsonin receptors. Specific binding between the particle and phagocyte which occurs during immune phagocytosis is mediated by immunoadherent receptors. There are two types of immunoadherent receptors: Fc-receptors mainly for IgG antibodies (FcçR) and complement receptors (CR1, CR3). It means that function of opsonins in the first case is realized by antibodies and in the second case by iC3b. Specific binding between the particle and phagocyte may be also performed by lectins and lectin receptors ( lectinophagocytosis).
To the phagocytosis itself chemotaxis of phagocytes precede into the site where phagocytosable material occurs. This is regulated by chemotactic factors generated by infectious agents themselves, as well as those release as a result of their initial contact with phagocytes and other components of the immune system.
Phagocytosis is a complex process composed of several morphological and biochemical steps. After recognition and particle binding to the phagocyte surface, ingestion (engulfment), phagosome origination, phagolysosome formation (fusion of phagosome with lysosomes), killing and degradation of ingested cells or other material proceed. Simultaneously with the recognition and particle binding a dramatic increase in oxygen consumption (the respiratory burst) is observed. It is responsible for the production of superoxide and other oxygen radicals, and also for the secretion of a variety of enzymes and biologically active substances controlling inflammatory and cytotoxic reactions.
During phagocytosis, cytosolic granules (lysosomes) fuse with the invaginating plasma membrane (around the engulfing microorganism) to form a phagolysosome into which they release their contents, thereby creating a higly toxic microenvironment. This step is of the first importance because during it two categories of cytotoxic substances, present in the preformed state in azurophil and specific granules and synthesized de novo during the respiratory burst, arrive at the same cell compartment. This degranulation normally prevents release of the toxic components into the extracellular milieu. However, some target may be too large to be fully phagocytosed or they avoid engulfment, resulting in frustrated phagocytosis in which no phagosome is formed. These may be killed extracellularly. However, tissue damage occurs when neutrophil microbicidal products are released extracellularly to such an extent that host defences (antioxidant and antiprotease screens) in the immediate vicinity are overwhelmed.
The importance of neutrophils in fighting bacterial and fungal infections is well recognized. Recently, it has been shown that neutrophils are in abundance also in virally induced lesions. Neutrophils bind to opsonized viruses and virally infected cells via antibody (Fc) and complement (iC3b) receptors. Viruses such as influenza can be inactivated by neutrophils trough damage to viral proteins (e.g. hemagglutinin and neuraminidase) mediated by the myeloperoxidase released during degranulation. In contrast to these acute diseases, chronic influenza infections can diminish or exhaust the microbicidal potency of neutrophils.