Chapter 15- Innate immunity

Innate immunity

No change between what we do if we are infected with salmonella vs E. coli. No learning, no adaption. Most important part of our immune system.

First line defense

Bacteria hits exterior surface or interior tube(digestive system)- no tissue.

1. Skin

2. Mucosal lining/system

3. Lacrimal system

4. Normal microbiota

5. Other: saliva, stomach acid, urine, vomiting, and secretions.

Skin

• Few pathogens can penetrate these layers

• Shedding of dead skin cells removes microorganisms

• We have pores that produce salts and binds available H2O so it prevents water from being useable and prevents bacteria from being successful at hanging out there.

• Oil in skin makes it placid so it can stretch. Important so that we don’t have gaps in our skin after movement to prevent bacteria from getting into our system.

• Skin also produces lysozyme from our prose and it destroys bonds between NAG-NAM.

Mucosal lining/system

• Any bacteria that land on ciliated cells in mucosal lining will produce mucus on the surface of these cells.

• Any bacteria that attach to mucus in the nose/mouth will fall into stomach where acid and bile salts will digest them.

• Not all bacteria will die to acid and bile salts and if these bacteria survive, they can contribute to our gut microflora.

Lacrimal system (eyes)

• Produce tears and tears drain through drains in corner of eye and fall into the back of the throat which constantly washes bacteria away from the surface of our eye.

• Also have lysozymes in our tears that destroy bacteria.

• Blinking spreads tears and washes surface of eye.

Normal microbiota

Compete with potential pathogens. Compete for nutrients and create and environment unfavorable to other microorganisms.

Saliva

Has digestive enzymes and washes bacteria toward stomach acid.

Urine

Flow through urethra fast enough that bacteria can’t hang on to establish a population.

Vomiting

Expel bad bacteria back out into the environment.

Second line defense

Bacteria associated with tissue or bloodstream.

1. Leukocytes

2. Non-specific chemical defense with interferons

3. Complement system

Leukocytes

• Involved in defending the body against invader. Divided into agranulocytes and granulocytes.

• Neutrophil- bacteria gets into cells/tissues and a few cells have been damaged and open. Foreign bacteria and damaged cells will send signals to cell walls to start to produce proteins. Neutrophil has proteins on tis surface which like to interact with the newly produced proteins. The proteins connect and the neutrophil starts to roll, which triggers diapedesis or flattening of neutrophil. The neutrophile squeezes through cell wall of the blood vessel to enter the tissue and eventually accumulate a large number of neutrophils in that area. Neutrophils surround bacteria and bring it into a phagosome. In neutrophiles are lysosomes which contain lysozyme, reactive oxygen species, and proteases. Lysozyme starts degrading bacterial cell wall and protease chews up bacteria protein and reactive oxygen species will help with metabolism and steals electrons. When phagolysosome membrane touches neutrophil membrane, release waste of phagolysosome.

Nonspecific chemical defense with interferons

Enveloped COVID virus gets into cell and releases nucleic acid. Cell is forced to utilize viral genome to make viral proteins and cell will release chemical signals alpha and beta interferons). Receptors for alpha and beta interferons are on our cells. Two nearby cells received the signals and the third farthest did not. The signal tells the cell to produce AVP’s. Both cells that received the signal will upregulate AVP’s and ABBEC which modifies nucleic acid. IF the virus tries to infect these cells, they have a better defense against the virus.

Complement system

Classical pathway:

• Gram +, staph pathogen, protein C1qrs binds to pathogen.

• C1qrs becomes active and other proteins floating around are C2 and C4.

• When active C4 will get converted to C4a and C4b.

• C2 will get converted to C2a and C2b.

• C4b can bind to C2b to make C3 convertase.

• C3 convertase takes C3 to C3a and C3b.

• C3b will start to attach to bacterial cell surface.

• C4b, C2b, and C3b interact to make C5 convertase.

• C5 convertase cuts C5 into C5a and C5b.

• C5b will start to accumulate at various spots on pathogen surface and is the first component of the MAC complex.

• C5b will interact with C6.

• When C6 interacts, we get proteins to bind to C7 and allows C8 to bind which allows C9 to bind.

• With C9 also interacting with C5b we get MAC complex.

• MAC makes hole/pore in membrane of cell

• The bacterial will start to get many MAC’s and primary active transport is ruined because ions pumped out will just come back in through hole.

• Lost ability to make nutrients, lost ability to pump out wastes, lost ability to move flagella, not proton motive force.

• C3b will bind to CR1 on neutrophil which enhances phagocytosis of bacteria.