Non specific host defence- bacteria overcome it & how specific interact.

The non specific immune system consists of barriers like skin and mucous membranes. The immune system is non specific meaning it will react the same way weather it’s the first or second time its being attacked. The non specific immune system can have phagocytic cells, NK, complement (lyse/opsonise bacteria) or iron binding protein ( starve bacteria for iron).the innate immune system will slow down the phatogen. If the bacteria gets past this system the adaptive immune system will take over. The adaptive immune system is a slower response, but is pore precise. The main difference is that adaptive has antibodies T & B cells. The adaptive immune system have developed a memory : eg LPS has different O side chains and adaptive can develop ab against each type of O chain.

The skin epithelium and the epithelium lining the gastrointestinal tract, uritogenital tract and respiratory tract are part of the protective barrier of the innate immune system, some also secretes mucous that prevents the bacteria living on the surface. The epithelial lining provides a tight junction and mount a non specific chemical attach like the acidic environment of the stomach. If there is a hole in the epithelium so that the pathogens get through the barrier there are macrophages patrolling the lining. They have many receptors on their surfaces that recognise common pathoges (lipopolysaccharides/ liptoeichoic acids – found in the bacterial walls). When the mø’s recognises the pathogen they engulf them called phagocytosis. Once inside the lysosome(containting many different substaces like Nitric oxide, hydrogen peroxide, Lacroferrin can deprive bacteria of nutrients (iorn & B12) etc) will help destroy the pathogen. Once the mø’s are activated they secrete chemicals called cytokines that recruite other pahgocytes to the site if infection. These might cause inflammation that bring other effector cells to help fight the infectionand not allowing the pathogens to get into the bloods stream. Another aspect of the innate immune system is the activation of the complement cascade (enzyme cascade). There are 3 main outcomes of the complement. 1) more inflammatory cells are signalled to come to the site of infection. 2) the pathogens are opsonised (pathogen surface is coated with protein- making them easier to recognise) for the  phagocytes to engulf and destroy the pathogen. 3) pathogens are directly killed.

Some bacteria have a capsule (made of polysaccharides) that will protect the bacteria from phagocytosis. Without help phagocytes find it hard to deal with capsulated bacteria.

 

 

Acquired immune system: the main focus is to amplify and focus the activity of the components of the innate immune response. Making complement and phagocytes more efficient. Memory is very important to have a quicker response the next time it encounter the bacteria with a more amplified response. Dendritic cells engulf bacteria and break down the pathogens to present them on the surface of the cell. This leads to activation and proliferation and differential of lymphocytes.  T cells provide stimulus that allows B cells to prolifereate and then differentiate into lymphoblasts. This again helps macrophage activation.

Many intracellular bacterial pathogens can survive and grow inside the macrophages. Macrophages needs to be activated by TH1 cells to deal with the pathogens. When mø’s are activated they are cleared by all bacteria that might live inside them (mycobacteria).

How bacteria cause disease?

Bacteria have to be able to colonize host at mucosal surfaces and adherer to host. The pathogen needs to get nutrients and counter act host defence. This is done by contact/entry, conisation and replication, before transmitting to new host. To adhere avidly to host cells and tissues some bacteria have developed special pili that allow attachment (so they are not flushed away- eg. Urinary tract). Adhesion is hard for the bacteria and it often needs a virus  first to kill the cilia (cant bind to cilia) for then to attack as a secondary bacterial infection. The pili attach to mucous( where they replicate at high rate that beats out rate they are flushed) or bind to chards or surface proteins or extracellular matrix proteins. The bacteria needs to bind to the host tissues and resist defences. This is done by two ways extracellular vs intracellular mechanisms.

Extracellular consist of 1) adhestion, 2) anti phagocytic factors like a capsule that often consist of polysaccharides. This capsule will resist complement cascade and is often non immunogenic because if might have host components. The capsule might have surface proteins or toxins that prevents it from being phagocytosed. Exotoxis are toxic proteins that affect phagocytes, chemotaxis and degranulation. 3) nutrient acquisition systems like iron & infecton. Iron is needed for the  bacteria to grow. If there are low Fe in the environment the bacteria can starve and therefore they have special adaptive systems to overcome this. Sidephores are made that have higher affinity for Fe and capture Fe from lactoferrin. Or TF or LF binding protein that bind lactoferrin or transferring to the surface of itself for then to pull Fe off and into the bacteria.

Intracellular pathogens invade cells, modify intracellular environment, counter intracellular defences and aquire nutrients. Some will evade the system by getting inside and living inside the macrophages. This is beneficial because macrophages are long lived (compared to neutrophils), mobile and have a rich nutrient supply. Once inside the macrophage they escape the phagosome. Some inhibit phagolysosome fusion and coxiella is even able to live inside the phagolysosome. C5a is a peptidase, a protein that interrupts the complement cascade. Some bacteria also produce different proteins that kill neutrophils. M protein on the surface of the capsule of the bacteria is very variable and will  avade the host even when they have mounted a humoral response (memory) because it might infect with a different M type strain thereby evading the memory antibodies.

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About Annettevet

I'm a Norwegian practicing as a veterinarian in Durham, England. I`ve recently qualified as a veterinarian at Glasgow University. This is a blog about my experiences as a vet student and now as a veterinarian. “The greatness of a nation and its moral progress can be judged by the way its animals are treated”
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