In the resolution of an infection, bacterial debris is removed by neutrophils or by antibody as soluble immune complexes.
Early antibody production is of the IgM class. There are five binding sites on IgM which enhance the binding efficiency. IgM is a good opsonin and activator of the classical component pathway. Opsonised bacteria are engulfed by phagocytes.
Mast cell degranulation causes increased blood flow and leaky blood vessels. You get oedema in the area and local irritation.
Surface lipopolysaccharides on bacteria activate the alternative complement pathway or the mannose binding lectin pathway leading to bacterial cell lysis. Complement activation also leads to mast cell activation, opsonisation and chemotaxis.
C-reactive protein can bind to bacteria and activate complement.
A break in the epithelial surface allows bacteria to enter and proliferate
Opsonised bacteria are phagocytosed and killed by neutrophils.
Dendritic cells engulf and internalise bacteria. They then migrate to a lymph node via the lymphatics
T cells are recruited to the lymph node by dendritic cells. Dendritic cells present bacterial peptide to naive T helper cells on their MHC II molecules which activates the T cells. The dendritic cells can activate T helper 1 and T helper 2 cells.
Activated T helper 2 cells cause B cells to become plasma cells and produce antibodies. Initially the IgM class of antibodies are produced followed by class switching to IgG or IgA
C3a and C5a lead to mast cell activation
C3b leads to opsonisation
C5a leads to chemotaxis
Opsonisation = using opsonins to tag foreign pathogens for elimination by phagocytes
bacteria enter through endothelial break
activation of alternative and MBL complement pathways
mast cell degranulation
neutrophil extravasation
phagocytosis (neutrophils and dendrites)
dendrites activate Th1 and Th2
Th2 convert B cells to plasma cells and they release antibodies (IgM then IgG)
opsonisation and classical complement activation
debris removed by neutrophils or as soluble antibody complexes