Lecture 4 - Inflammation part 2 Flashcards
List the contents of leukocytes granules.
Bactericidal permeability increasing protein (BPI), lysozyme, lactoferrin
Defensins (punch holes in membranes).
List the defects of leukocyte function of adhesion.
LFA-1 and Mac-1 subunit defects lead to impaired adhesion (LAD-1),
Absence of sialyl-Lewis X, and defect in E- and P-selectin sugar epitopes (LAD-2)
List the defects of leukocyte function of chemotaxis/phagocytosis.
Microtubule assembly defect leads to impaired locomotion and lysosomal degranulation (Chediak-Higashi Syndrome).
List the defects of leukocyte function of microbicidal activity.
Deficiency of NADPH oxidase that generates superoxide… no oxygen-dependent killing mechanism (chronic granulomatous disease)
What are the chemical mediators of inflammation?
Plasma derived: Complement, kinins, coagulation factors, many in “pro-form” requiring activation.
Cell-derived: Preformed, sequestered and released (mast cell histamine), synthesized as needed (prostaglandin)
What are the systematic effects of inflammation?
Fever (One of the easily recognized cytokine- mediated, acute phase reactions including: anorexia, skeletal muscle protein degradation, hypotension)
Fever speeds up immune responses and makes it difficult for pathogens to survive at elevated temperature.
Leukocytosis: Elevated white blood cell count
List the possible outcome of inflammation.
Complete resolution, little tissue damage capable of regeneration, scarring (fibrosis), in tissues unable to regenerate, excessive fibrin deposition organized into fibrous tissue, abscess formation occurs with some bacterial or fungal infections
What is the specific mediators of PFA (platelet activating factor) Causes what?
Derived also from cell membrane phospholipid; causes vasodilation, increased vascular permeability, increases leukocyte adhesion
What are the specific mediators of arachidonic acid metabolites? Causes what?
Prostaglandins and thromboxane: via cyclooxygenase pathway
cause vasodilation and prolong edema but also protective.
Describe the Kinin system.
Leads to formation of bradykinin from cleavage of precursor (HMWK), vascular permeability Arteriolar dilation, non-vascular smooth muscle contraction (e.g., bronchial smooth muscle), causes pain
What does serotonin do as a mediator? Released by what?
Has vasodilatory effects similar to those of histamine, platelet dense-body granules; release is triggered by platelet aggregation, plasma proteases, clotting system, complement, kinins
What does histamine do as a mediator? Released by what?
Causes vasodilation and venular endothelial cell contraction, junctional widening; mast cells, basophils, platelets in response to injury
State 4 things about chemical mediators.
May or may not utilize a specific cell surface receptor for activity; may signal target cells to release other effector molecules that either amplify or inhibit initial response; are tightly regulated; quickly decay, inactivated enzymatically (kininase), or are scavenged (antioxidants)
Where is histamine released by? In response to what?
The granules of mast cells, basophils, platelets; to injury and immune reactions
How are the complement factors in the complement system named? How many factors are there?
W/ numbers: C1-C9; 20 factors