Host Defence Mechanisms and Microbial Strategies to Overcome This Flashcards
Microbes rinsed from epithelial surface via host secretions and secretion immunolglobulin (IgA)
Bind firmly to epithelial surface by binding to a receptor, and can produce ciliotoxic/ciliostatic molecules.
Released IgA protease to break down IgA.
Host cell membrane is a barrier to intracellular microbe
They traverse membrane and endure or trigger uptake by phagocyte and resist killing.
Use fusion proteins in viral envelope and inject proteins that trigger uptake or block intracellular signalling.
Ingestion and killing of microbe by phagocyte
Block phagocyte chemotaxis, kill the phagocyte, inhibit phagocytosis, inhibit lyososme fusion and resist killing and multiply in phagocyte.
Can release leucocidins, antiphagocytic haemolysins ect… diversion of toxic compounds from microbe escape phagosome into cytosol.
Restriction of Fe (III)
Scavange iron in competition with the host by secreting siderophores which bind Fe (III) in the host with an extremely high affinity and are imported into the cytosol where Fe is released.
Production of reactive oxygen and nitrogen species
Avoid oxidative burst or removes ROS and RNS. Diverts vesicles bearing NADPH oxidase so they don’t fuse with phagosome and produce enzymes like catalase, super oxide dismutase to inactivate ROS and RNS.
Production of complement and antimicrobial peptides
Microbes alter their cell surface via sialylation or LPS structure alteraltions or production of proteases.
They can inactivate complement or bind to it non-productively - C3b receptor on microbe competes with that on the phagocyte to hinder production of membrane attack complex.
Production of antimicrobial antibodies
They can destroy antibodies, prevent induction of protective antibody, express Fc receptor, prevent antibody or complement from binding near surface and avoid immune recognition.
They can secrete IgA protease, infect lymphoid cells, bind antibody so its not orientated correctly (180 degrees) and produce long LPS chain to keep antibodies away.
They can coat themsleves in host fibronectin to remain undetected.
Antimicrobial cell-mediated response
Invasion of T cells to block their function or kill them, switch on T or B cells non-specifically or non-productively.
Virus envelope component binds CD4 on helper T cell surface, polyclonal activation of B cells anf polyclonal activation of T cells by release of T cell mitogens.
Antimicrobial Immune response
Infect glands or epithelial surface that are relatively inaccessible to circulating antibody or immune cells, suppress immune responses, vary microbial antigens either in a single host during spread in host communities.
Trophism for cells in glands or on surfaces, invade immune tissues, switch on different surface antigens, use of mutation/genetic recombination.
Non-apparent immune responses (shedding)
Stimulate host processes that increase change of transmission by key routes, transmission via other routes e.g. blood via needles.
Trigger sneezing, diarrhoea, induction of processes that favour survival in biofluids/environment.
