In this article we will discuss about the mechanisms of innate immunity in bacterial infection.
Bacteria-Host Interactions at Body Surfaces:
The totality of mechanisms constitutes our immunity to infection. Infection is caused rarely due to multifunctional systems of innate immunity. It is divided into those systems which (a) act at body surfaces (epithelium or submucosa), and (b) those which are present in the submucosal tissue (Fig. 27.23).
Fig. 27.23 : Innate immune systems of the epithelia and submucosal tissues.
It can be further subdivided into those activities which act on external body surface (i.e. lining of mouth, lungs, intestine, etc.) and those which function within the body. The various mucosal surfaces (epithelial lining) have evolved the mechanism which inhibit the growth and infection of pathogens. At different epithelial sites, there exists site-specific mechanisms to inhibit the infection.
These mechanisms include:
(a) Synthesis and release of antibacterial components e.g. lysozyme which degrade peptidoglycan of bacterial cell walls (or antibacterial peptides which kill bacteria),
(b) Constantly removing bacteria adhered to epithelium through sloughing off cells, and
(c) The inhibitory effect of normal microflora on growth of pathogenic bacteria.
The antibacterial mechanism employed by external epithelia are given in Table 27.11.
Recognition of Bacteria/Bacterial Infection by Innate Immunity:
The innate immune system recognises key molecular structures of pathogen i.e. the molecules that are essential for bacterial survival and unlikely evolve their structure, as such mutation would be lethal. Such molecules are called PAMPS (pathogen-associated molecular pattern).
Such molecules are called the structural components such as lipopolysaccharide and peptidoglycan, possibly DNA with high CpG content (where cytosine is unmethylated). Molecular chaperones play a role in bacterial recognition.
The invertebrates and vertebrates have evolved a range of receptors referred to as pattern recognition receptors (PRRs) which are cell bound and able to recognise bacterial molecules PAMPs which are essential for cell function.
Binding of PAMPs to the PRRs on the cells of vertebrate results in production of antibacterial peptide, cytokines (e.g. interleukin IL-4 nad IL-12) for the induction of Th1 and Th2 responses and the stimulatory molecules B7-1, B7-2 (Fig. 27.24).
Fig. 27.24 : Recognition of bacteria by innate immune responses.
The first PRR identified was CD14 present on monocytes and plasma which binds to bacterial carbohydrates including lipopolysaccharide, peptidoglycan and lipoarabinomannan and activate cells bearing this receptor. Binding of PAMPs to their receptors is an early evolved recognition system which stimulates the production of a range of molecules required for defence against bacterial parasite.