HOST DEFENSE MECHANISMS - LEC 1

• Host defense mechanism


  Resistance or protection against environmental agents to ward-off pathogens or diseases
• Mechanism of host defense

  1. Prevent entry of possible pathogen

  2. Eliminate pathogens from the body when it gets in

  3. Fight it if it keeps on entering the host
• Immune system

  • Variable from one individual to another
  • Different immune system from each other
  • Most susceptible - host is easily infected by infection
• Variable factors affecting immune system

  • Socioeconomic
  • Physical stress
  • Environmental factors
  • Species resistance
  • Racial resistance
  • Individual resistance
• Species resistance

  Anatomical and physiological differences among species that affect immunity
• Racial resistance

  Genetic factors that make certain races of people more resistant or susceptible to diseases
• Individual resistance

  Due to the combination of innate (non-specific) and adaptive (specific) factors inherited from parent
• Innate immunity

  Present at birth, non-specific, activated as long as foreign material enters the host cell, immediate and maximal response
• Innate immunity

  • Doesn't have immunological memory, doesn't recognize or remember any foreign substance that has entered before, only knows that it is foreign and must be removed from the system
• Toll-Like Receptors (TLRs)

  Responsible for immediate response, protein receptors that can detect chemical component of a pathogen, warning device to host cell indicating that an antigen is about to gain entry
• External barriers

  Skin and mucous membrane - prevent entry of pathogen
• Skin

  • Sheds every 2-3 months, keratin is water-phobic and maintains low moisture to inhibit microbial growth, sebum has antimicrobial activity, lysozyme, fatty acid & lactic acid maintain acidic pH to inhibit microbial growth
• Mucous membrane

  • Cilia can remove microbes, vibrissae and mucus trap harmful microbes, lysozyme and lactoferrin inhibit microbial growth, gastric juice maintains acidic pH, saliva and urine can wash away potential microbes, tears wash off microbes
• Internal defenses


  Blood cells, complement systems, other substances that act when pathogens escape the external barrier and gain entry to the host cell
• Blood cells involved in internal defenses

  • WBC (neutrophil, eosinophil, basophil, lymphocyte, monocyte)
  • RBC
  • Platelets
• Phagocytosis

  • Process correlated with neutrophil and monocyte, major players in innate immunity
• Steps of phagocytosis


  1. Chemotaxis

  2. Adherence

  3. Ingestion

  4. Digestion
• Microbes can escape phagocytosis if they are encapsulated or produce mycolic acid and M protein, which avoid the adherence step
• Microbes can also escape phagocytosis by killing the phagocytic cell with toxins or by replicating within the phagocytes and destroying the phagolysosome
• Inflammation

  A defense mechanism where phagocytosis occurs, body's first line of defense that promotes healing and repair by destroying and limiting the injury
• Inflammation process

  1. Normal healthy tissue

  2. Sustains an injury, microbes release products

  3. Products released cause vasodilation and increase vascular permeability, allowing phagocytic cells to enter the injury site and increase blood flow
• Bradykinin

  A substance released during inflammation, injury, or infection that can cause vasodilation, increase vascular permeability, and stimulate nerve endings leading to pain and loss of function
• When there is an injury, neutrophils are supposed to escape the blood vessel and migrate to the site of injury through diapedesis
• Permeability of blood vessels

  Substances can more easily pass into the blood vessels
• Substance released during inflammation, injury, or infection

  Increases blood flow, binds to mast cells, and attaches to capillary walls
• Mast cell response

  1. Mast cell releases histamine

  2. Vasodilation occurs

  3. More fluid and cells leave, causing swelling
• Capillary wall response

  1. Substance attaches to capillary wall

  2. Prostaglandins are released

  3. Can stimulate nerve endings, causing pain and loss of function
• When there is an injury, neutrophils are supposed to escape the blood vessel and migrate to the site of injury (diapedesis)
• Neutrophils can squeeze through the tight junctions of the endothelial cell to reach the site of injury
• Pus formation

  Contains tissue debris, dead cells, and phagocytic cells
• Advantages of pus formation

  • It is the first line of defense against local injury
  • It can limit the injury and prevent the infection from spreading
  • It helps in the healing process
  • It indicates that the infection is subsiding
• Fever

  Can develop due to an inflammatory event and is advantageous to some extent as it speeds up cellular response, accelerates metabolism, and releases substances and phagocytic cells to fight off infection
• A high grade fever (>40) is dangerous, especially for pediatric patients, as it can lead to complications like convulsions
• Complement system

  A system of 30 interacting proteins (C1-C9) that undergo cascade activation, leading to inflammation, opsonization, and lysis
• Types of complement system

  • Alternative or properdin
  • Mannose binding lectin
  • Classical
• Alternative and mannose binding lectin complement systems

  • Associated with innate immunity
• Classical complement system

  • Associated with adaptive immunity
• Activation of complement system

  1. C3 is activated

  2. C3a causes inflammation

  3. C3b leads to opsonization
• Activation of C5

  C5 splits into C5a (inflammation) and C5b (forms membrane attack complex, leading to lysis of foreign cells)
• Interferon

  Immune cells associated with adaptive and innate immunity that have antiviral properties and can inhibit virus protein synthesis in uninfected cells