Microbiology Innate Immunity
chp. 16 (chp. 9), Innate Immunity Dr. Collins
Terms in this set (60)
Defenses against any pathogen (general)
Lack of resistance to a disease
Ability to ward off disease
Immunity, resistance to a specific pathogen
First line of defense
Intact Skin, Mucous Membranes and their secretions, Normal Microbiota
Second Line of defense
NK cells, phagocytic white blood cells, inflammation, fever, antimicrobial substances
third line of defense
specialized lymphocytes: T cells and B cells, antibodies
What are the physical factors of skin?
The epidermis consists of tightly packed cells with keratin
a protective protein found in skin
What are the physical factors of Mucous Membranes
Ciliary Escalator, Lacrimal apparatus, Saliva, urine, vaginal secretions
How does the ciliary escalator work?
Microbes trapped in mucus are transported away from the lungs
how does the lacrimal apparatus work?
manufactures and drains tears that wash the eye
how does saliva work as a first line of defense
washes off microbes
how do vaginal secretions/urine work as a first line of defense?
flows microbes out of th ebody
Chemical Factors of the second line of defense
Fungistatic fatty acid in sebum; Low pH of skin (3-5); lysozyme in perspiration, tears, saliva, and tissue fluids; Low pH of gastric juice (1.2-3.0); Transferrins in blood find iron; NO inhibits ATP production
Microbial antagonism/competetive exclusion
Normal microbiota compete with pathogens inside the host
Formed elements in blood
red blood cells (erythrocytes), platelets, Neutrophils, Basophils, Eosinophils, Dendritic Cells, monocytes, natural killer cells, T cells, B cells
List the Granulocytes
Neutrophils (60-70%), Basophils (0.5-1%), Eosinophils (2-4%)
List the Agranulocytes
Monocytes (3-8%), Dendritic Cells, Lymphocytes (20-25%)
Function of Neutrophils
Function of Basophils
Production of histamine
Function of Eosinophils
Production of toxic proteins against certain parasites; some phagocytosis
Function of Monocytes
Phagocytosis (when they mature into macrophages)
Function of Dendritic Cells
phagocytosis and initiation of adaptive immune response; derived from monocytes
List the Lymphocytes
NK cells, T Cells, B Cells
Function of NK cells
Destroy target cells by cytolysis and apoptosis
Function of T Cells
Function of B Cells
Descendants of B cells (plasma cells) produce antibodies
Macrophages that are ALWAYS in the lungs, liver and bronchi
Roam tissuses searching for microbes to destroy
From the Greek meaning "eat"
From the Greek meaing "cell"
Ingestion of microbes or particals by a cell performed by phagocytes
Phases of Phagocytosis
1. Chemotaxis and adherence of microbe to phagocyte; 2. Ingestion of microbe by phagocyte; 3. Formation of a phagosome; 4. Fusion of the phagosome with a lysosome to form a phagolysosome; 5. Digestion of ingested microbe by enzymes; 6. Formation of residual body containing indigestible material; 7. discharge of waste materials
What are the ways that microbes evade phagocytosis?
Inhibit adherence: M protein capsules; kill phagocytes: leukocidins; Lyse phagocytes: membrane attack complex; prevent phagosome-lusosome fusion; survive in phagolysosome
What are the signs of Inflammation
Redness, pain, heat, swelling (edema), acute-phase proteins activated, vasodilation, margination of emigration of WBCs, tissue repair
Chemicals released by damaged cells
Histamine, Kinins, Prostaglandins, Leukotrienes
Function of Histamine
Vasodilation, increased permeability of blood vessels
Function of Kinins
Vasodilation, increased permeability of blood vessels
Intensity histamine and kinin efect
Increased permeability of blood vessels, phagocytic attachment
The process of inflammation
1. Chemicals such as histamines, kinins, prostaglandins, and leukotrienes are released by the damaged cells; 2. blood clot forms; 3. Abscess starts to form; 4. magination-phagocytes stick to the endothelium; 5. Diapedesis-Phagocytes squeeze between endothelial cells; 6. Phagocytosis of invading bacteria. 7. tissue repair
What temperature is the body normally set at by the hypothalamus?
37 degrees Celsius
Mechanisim of a Fever
1. Body temp is normally set at 37 degrees; 2. Gram-negative endotoxin cause phagcytes to release interleukin-1 (IL-1); 3. Body increases rate of metabolism and shivering which raises temperature; 4. When IL-1 is eliminated, body temperature falls (crisis).
Advantages of Fever
Increses Transferrins, Increases IL-1 activity
Tachycardia, acidosis, dehydration
The Complement System
1. Inactivated C3 splits into activated C3a and C3b; 2. C3b binds to microbe, resulting in opsonization; 3. C3b splits C5 into C5a and C5b; 4. C5b, C6, C7 and C8 bind together sequentially and insert into the microbiobial plasma membrane, C5b through C8 act as a receptor to attact a C9 fragment, and additional C9 fragments are added to form a channel. Together, C5b through C8 and the multiple C9 fragments form the membrane attac complex resulting in cytolysis; 5. C3a and C5a cause mast cells to release histamine, resulting in inflammation; C5a attracts phagocytes.
Key concept of the Complement System
One complement protein triggers the next. The cascade can be activated by a pathogen directly or by an antibody-antigen reaction. Together these proteins destroy microbes by cell lysis, inflammation, or enhanced phagocytosis.
Effects of complement activation
Opsonization or immune adherence results in enhanced phagocytosis; Membrane attack complex (MAC) results in Cytolysis; Inflammation attracts phagocytes.
Inflammation stimulated by complement
C3a and C5a bound to mast cells, basophils, and platelets trigger the release of histamine, which increases blood vessel permeability. C5a functions as a chemotactic factor that attracts phagocytes to the site of complement activation
Classical pathway of complement
1. antibodies attach to antigens forming antigen-antibody complexes which bind and activate C1. 2. Activated C1 activates C2 and C4 by splitting them. C2 is split into C2a, C2b and C4 is split into C4a and C4b. 3. C2a and C4b combine and together they activate C3 by splitting into C3a and C3b. The C3 fragments then initiate cytolysis, inflammation, and opsonization.
Does not involve antibodies. It is activated by contact between certain complement proteins and a pathogen. C3 combines with factors B, D, and P on the surface of a microbe. This causes C3 to split into fragments C3a and C3b which intitiate cytolysis, inflammation, and opsonization.
Lectin binds to an invading cell. Bound lectin splits C2 and C4. C2a and C4b combine and activate C3 which splits into C3a and C3b. The C3 fragments initiate cytolysis, inflammation, and opsoniation.
Some bacteria can evade complement through
Capsules prevent C actviation. Surface lipid-carbohydrates prevent MAC formation. Enzymatic digestion of C5a.
Helps initiate immune response. They are host cell specific but not virus specific
Alpha IFN and Beta IFN
Cause cells to produce antiviral proteins that inhibit viral replication
Causes neutrophils and macrophages to phagocytize bacteria
Antiviral Action of of alpha and beta interferons
1. Viral RNA from an infecting virus enters the cell. 2. The infecting virus replicates into new viruses. 3. The infecting virus also induces the host cell to produce interferon mRNA (IFN-mRNA), which is translated into alpha and beta interferons. 4. Interferons released by the virus-infected host cell bind to plasma membrane or nuclear membrane receptors on uninfected neighboring host cells, inducing them to synthesize antiviral proteins (AVPs). These include oligoadenylate synthesis and protein kinase. 5. New viruses released by the virus-infected host cell infect neighboring host cells. 6. AVPs degrade viral mRNA and inhibit protein synthesis and thus interfere with viral replication.
Bind serum iron
Lyse bacterial cells