Nonspecific Defenses Of The Host Flashcards
Innate immunity vs adaptive immunity
Innate immunity vs. adaptive immunity
Susceptibility
lack of resistance to a disease
Immunity
ability to ward off disease
Innate immunity
defenses against any pathogen
Normal body functions
Adaptive immunity:
immunity or resistance to a specific pathogen
Physical/Mechanical Factors of innate immunity
Physical/Mechanical Factors of innate immunity
Skin
Epidermis consists of tightly packed cells with
Keratin, a protective protein
Physical Factors
Mucous membranes
Mucus: traps microbes
Ciliary escalator: transports microbes trapped in mucus away from the lungs
Physical Factors
Lacrimal apparatus:
Washes eye
Saliva:
washes microbes off
Urine:
Flows out
Vaginal secretions:
Flows out
Chemical Factors of innate immunity
Fungistatic fatty acid in sebum
Low pH (3–5) of skin
Lysozyme in perspiration, tears, saliva, and urine Low pH (1.2–3.0) of gastric juice
Low pH (3–5) of vaginal secretions
Microbial antagonism/competitive exclusion:
normal microbiota compete with pathogens or alter the environment
Commensal microbiota:
one organism (microbe)
benefits, and the other (host) is unharmed
May be opportunistic pathogens
Host Toll-like receptors (TLRs) attach to
pathogen-associated molecular patterns (PAMPs)
TLRs induce cytokines that..
regulate the intensity and duration of immune responses
Second line of defense
Blood
Percentage of each type of white cell in a sample of 100 white blood cells
Neutrophils 60-70%
Basophils 0.5-1%
Eosinophils 2-4%
Monocytes 3-8%
Lymphocytes 20-25%
Second line of defense
Lymphatic system
Phagocytosis
Phago: from Greek, meaning eat
Cyte: from Greek, meaning cell
Ingestion of microbes or particles by a cell, performed by phagocytes
Phagocytes
Neutrophils
Fixed macrophages Wandering macrophages Dendritic cells
The phases of phagocytosis
Microbial evasion of phagocytosis
Inflammation
Activation of acute-phase proteins (complement, cytokine, and kinins)
Vasodilation (histamine, kinins, prostaglandins, and leukotrienes)
Redness
Swelling (edema)
Pain
Heat
Chemicals released by damaged cells
Fever
Abnormally high body temperature
Hypothalamus is normally set at 37°C
Gram-negative endotoxins cause phagocytes to release interleukin-1 (IL-1)
Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature
Body increases rate of metabolism, and shivering occurs, which raise temperature
Vasodilation and sweating: body temperature falls (crisis)
Advantages of fever
Increases transferrins ● Increases IL-1 activity ● Produces interferon ● Many microbes can’t ●
survive in the higher temperature
Disadvantages of fever
Tachycardia (fast heart rate)
Acidosis
Dehydration
44–46°C fatal
The complement system (immune response)
Serum proteins activated in a cascade (domino effect)
Activated by
Antigen–antibody reaction
Proteins C3, B, D, P and a pathogen
The Complement System
C3b causes opsonization
C3a + C5a cause inflammation: inflammatory mediator
C5b + C6 + C7 + C8 + C9 cause cell lysis (Mac attack)
C:complement protein
B:opsonization
Effects of Complement Activation
Opsonization, or immune adherence: enhanced phagocytosis
Membrane attack complex: cytolysis (MAC attack) Attract phagocytes
Act as inflammatory mediators
Classical pathway of a complement activation
Alternative pathway of complement activation
Lectin pathway of complement activation
Some Bacteria Evade Complement
Capsules prevent C activation
Surface lipid–carbohydrate complexes prevent formation of membrane attack complex (MAC)
Enzymatic digestion of C5a
Interferons (IFNs)
IFN- α and IFN- β: cause cells to produce antiviral proteins that inhibit viral replication
IFN-y:
causes neutrophils and macrophages to phagocytize bacteria
Innate Immunity
Transferrins
Bind serum iron
Innate Immunity
Antimicrobial peptides
Lyse bacterial cells