Chapter 7 Flashcards
Hematopoietic pluripotent cells
Becomes either Common Myeloid or Common Lymphoid progenitor cells.
Common Myeloid progenitor
Becomes either erythrocyte, Megakaryocyte (platelets), neutrophils, eosinophil, basophil, monocyte (macrophage).
Common lymphoid progenitor
Becomes B-cells, T-cells, or NK-Cells (lymphocytes)
Hematopoiesis
refers to the formation and development of the cells of the blood.
Recognition mechanism of innate immunity
Rapid response, fixed (specific), limited number of specificities, constant during response.
Recognition mechanism of acquired immunity
Slow response (days or weeks), variable, numerous highly selective specific, improve during response (memory).
Innate immunity
First line defense, phagocytosis, inflammation, complement.
Adaptive immunity
Humoral immunity, cell mediated, Antigen processing and presentation.
Lysozyme
Destroys cell wall of gram (+) bacteria. Found in sweat glands and lacrimal glands.
Sebaceous Glands
Helps keep skin pliable and less likely to break or tear. Lowers skin pH to a level inhibitory to many bacteria
Sweat Glands
Salt inhibits growth of pathogens. Antimicrobial peptides act against microorganisms. Lysozyme destroys cell wall of Gram (+) bacteria
Activities of normal microbiota
Consumption of nutrients. Create an environment unfavorable to other microorganisms. Help stimulate the body’s second line of defense. Promote overall health by providing vitamins to host
Antimicrobial peptides
Present in skin, mucous membranes, neutrophils.
Act against a variety of microbes. Work in several ways: by inducing holes in bacterial membranes and intracellular killing.
Nonspecific Chemical Defenses Against Pathogens
Complement proteins (serum), Antimicrobial peptides (all body secretions), and interferons (3 types).
Body’s Second Line of Defense (Innate immunity)
Phagocytic cells (blood and tissues), Nonspecific Chemical Defense Against Pathogens, Inflammation (fever).
Plasma
Mostly water containing electrolytes, dissolved gases, nutrients, and proteins.
Serum
The fluid remaining when clotting factors are removed. Includes iron-binding compounds, complement proteins and antibodies.
Buffy coat
WBCs and platelets
Erythrocytes
Carry oxygen and carbon dioxide in the blood. 99.9% of formed elements.
Leukocytes
Involved in defending the body against invaders. divided into granulocytes and a granulocytes. WBCs and platelets make up 0.1% of formed elements.
Basophil (Leukocyte)
Inflammation (second line of defense)
Neutrophil, Eosinophil, Monocyte (Leukocytes)
Phagocytosis (second line of defense)
Lymphocyte (Leukocyte)
Adaptive immunity
Neutrophil and Eosinophils
Phagocytize pathogens, capable of diapedesis (chemotaxis).
Granulocytes
Basophils (Stain blue with methylene blue)
Esoinophils (Stain red/orange with acidic dye eosin)
Neutrophils (Stain lilac with mix of acidic and basic dyes)
Agranulocytes
Lymphocytes (Most involved in adaptive immunity) and Monocytes (Leave blood and mature into macrophages)
Lab analysis: Increased eosiniphils
Indicate allergies or parasitic worm infection.
Bacterial diseases
Often show increase in leukocytes which are mostly neutrophils.
Viral infections
Show increase in lymphocytes
The events of phagocytosis
1) Chemotaxis of phagocytes to microbes
2) Adherence
3) Ingestion of microbes by phagocytes (in phagosome)
4) Fusion of lysosome
5) Killing of microbes be enzymes
6) Elimination (exocytosis)
Killing by eosiniphils (Nonphagocytic Killing)
Attack parasitic helminths by attaching to their surface. Secret toxins that weaken helminth. Eosinophilia (elevated eosinophils) is often indicated of a helminth infestation.
Killing by natural killer lymphocytes (Nonphagoctic Killing)
Secrete toxins onto surface of virally infected cells and tumors. Differentiate normal body cells because they have membrane proteins similar to the NK cells.
Toll-like Receptors (Nonspecific Chemical Defense Against Pathogens)
Integral membrane proteins produced by phagocytic cells. Bind pathogen associated molecular patterns (PAMPs). Initiate defensive responses: Apoptosis of infected cells, secretion of inflammatory mediators (interferons), production of stimulants of adaptive immune responses.
Interferons (Nonspecific Chemical Defense Against Pathogens)
Protein molecules released by host cells to nonspecifically inhibit the spread of viral infections.
Cause many symptoms associated with viral infections: Type 1- non immune interferon (Alpha and beta). Type 2- immune interferon (Gamma)
Complement (Nonspecific Chemical Defenses Against Pathogens)
Set of serum proteins designated numerically according to their order of discovery. Activated by proteolytic cleavage, forming a cascade of peptides. Complement components: Opsonins and chemotactic factors, indirect triggers of inflammation and fever, lysis of foreign cels.
Complement pathways
Classical Pathway- activated by antibody molecules coating microbes
Alternate Pathway- Activated by surface components of microbes directly (PG & LPS)
Lectin pathway- Activated by microbial polysaccharides (sugars)
Opsonins
An antibody or product of complement activation in blood serum that causes bacteria or other foreign cells to become more susceptible to the action of phagocytes.
C3b
A split product of C3 which can bind to cell membranes and then an opsonin for neutrophils and macrophages.
C3a and C5a (anaphylatoxins)
Smooth muscle contraction, Histamine release from mast cells, and enhanced vascular permeability.
C5a
Is an chemotactic agent for neutrophils (PMN) and macrophages.
C5678(9)
Membrane attack complex. Induces holes in cytoplasmic membrane of pathogens.
Inflammation
Nonspecific response to tissue damage from various causes. Characterized by redness, heat, swelling, pain, and loss of function. Can be local or systemic. Acute or Chronic.
Acute inflammation
develops quickly and is short lived. Typically beneficial. Stages: Vascular events (Dilation and increased permeability of the blood vessels), Cellular events (Migration of phagocytes), tissue repair.
Vascular events of inflammation
Dilation and increased permeability of vessels are mediated by: prostaglandins and leukotriens (produced by damaged cells), Histamine (released by mast cells and basophils), Anaphylotoxins (C3a and C5a components of complement cascade.
Cellular events of inflammation
Leading to the phagocytes to the site of injury is mediated by; Release of chemotactic factors PMN and Macrophages. Chemotactic factors: C5a of complement cascade, Interleukin (IL-8) released by macrophages, C3b opsonises pathogens to increase uptake by phagocytic cells (Antibody IgG is also an opsonin).
C3a and C5a fragments of Complement Cascade
Cause mast cells to release inflammatory mediators (cause vasodilatation of capillaries)
Fever
Body temperature over 37 celsius. Results when pyrogens trigger the hypothalamus to increase the body’s core temperature.
Pyrogens
Fever producing bacterial toxins. Cytoplasmic contents of bacteria released by lysis. Antibody-antigen complexes: These signal for the production of interleukin-I (IL-1) by macrophages.
