12- Acute Inflammation

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Exam 2

What is the goal of inflammation?

a protective response to dilute, isolate, and/or get rid of injurious stimulus, and the consequences of the injury

what can be a major consequence of inflammation?

it can be inappropriately triggered or poorly controlled leading to tissue injury

What is acute inflammation?

- rapid onset
- short duration (hrs to a few days)
- characterized by edema and emigration of White blood cells

What is chronic infammation?

- back-up plan
- long duration
- characterized by lymphocytes, macrophages, proliferation of vessels, fibrosis, and tissue destruction

What are the 4 events of acute inflammation?

- stimuli for acute inflammation
- vascular changes
- cellular reaction: white blood cells extravasation and phagocytosis
- termination of acute inflammatory response

What are the 5 cardinal signs of inflammation?

- calor, rubor, tumor, dolor, and lasesa

what is calor?

heat caused by vasodilation

What is rubor?

redness caused by increased blood flow

What is tumor?

swelling due to increased blood flow and vascular permeability

what is Dolor?

pain due to stimulation of nerolan pathways by bradykinin, prostaglandins, histamine and serotonin

what is lasea?

loss of function

What are the 3 major components of acute inflammation?

- increased blood flow
- leakage of plasma proteins= edema
- white blood cell emigration

What are the stimuli for acute inflammation?

- infections
- foreign bodies or environmental elements
- tissue necrosis
- immune reactions

What types of infections stimulate inflammation?

bacterial, viral, fungal, parasitic, and microbial toxins

What are some examples of foreign bodies and environmental elements?

UV light, radiation, trauma, thermal injury, chemicals

How does tissue necrosis cause inflammation?

necrotic cells release uric acid, ATP, DNA which induce inflammation

How does hypoxia induce inflammation?

via hypoxia-induced factor- 1a

What is hypoxia-induced factor-1a?

released by cells deprived of O2 activating the transcription of many mediators involved in inflammation
- VEGF

What is the function of VEGF?

known to increase vascular permeability

How is inflammation induced by immune reactions?

- hypersensitivity reactions
- cytokines for t cells

What is stimulated with inflammation?

innate immune system

What is the innate immune system?

non-specific defense for environmental stimuli

What are the 4 components of the innate immune system?

- physical barriers and microenvironments
- molecular products from mucosal epithelia
- preformed and synthesized chemical mediators from tissue effector cells
- effector molecules in the blood like plasma proteases and in certain nerve fibers

What are the physical barriers and microenvironments that make up the innate immune system?

skin, mucosa, pH, mucociliary escalator, salivia, mucous secretions, peristalsis

What are some molecular products for mucosal epithelia that make up the innate immune system?

lactoferrin, antimicrobial peptides, surfactant protiens

What are the chemical mediators of mast cells?

histamine and TNF-alpha

What are the chemical mediators of white blood cells?

cytokines, degradative enzymes

What are the chemical mediators of macrophages?

cytokines

What are the effector molecules in blood and nerve fibers that make up the innate immune system?

blood: complement, kinin, clotting fibers
nerves: sensory fibers, C-reactive fibers that release substance-P

What do the severity and clinical signs of acute inflammatory response depend on?

- the route of exposure
- the physical and biological characteristics of the stimulus

What is a TLR?

toll-like receptor

What are PAMPs?

pathogen associated molecular patterns

What does the TLR do?

recognizes the PAMPs

Once the TLR recognizes the PAMPs, what happens?

triggers release of chemokines and cytokines to activate cells

what are some examples of PAMPS?

LPS, lipotheicoic acids, and peptidoglycan

What are the chemical mediators of acute inflammation?

vasoactive amines, plasma proteases, lipid mediators, PAF, cytokines, chemokines and NO

In acute inflammation, how is vascular flow and caliber changed?

vasodilation, increased permeability of the microvasculature, loss of fluid, and leukocyte accumulation along the vascular endothelium

What is vasodilation?

- early manifestation
- constriction of arterioles for a few seconds, then opening of new capillary beds in the area to increase blood flow

What does vasodilation result in?

heat and redness

What mediates vasodilation?

hisamine and NO

What occurs with you increase the permeability of the microvasculature?

there is an outpouring of protein-rich fluid into extravascular tissues (edema)

What is a consequence of the loss of fluid to the extravasculature space?

inc. conc of RBCs in small vessels, increased viscosity of blood, dilation of vessels, and slow blood flow

What is the hallmark of acute inflammation?

increased vascular permeability leading to edema

What are some ways the vascular permeability is increased?

- retraction of the endothelial cells
- direct endothelial cell injury
- delayed prolonged leakage
- leukocyte-mediated endothelial injury
- increased transcytosis
- leakage from new blood vessels

What is the most common mechanism of increasing vascular permeability?

retraction of the endothelial cells

What triggers the contraction of endothelial cells?

histamine, bradykinin, NO, leukotrienes, and neuropeptide substance-P

What does direct endothelial injury result in?

endothelial cell necrosis or platelet adhesion and thrombosis

What is delayed prolong leakage of the endothelium caused by?

mild to moderate injury:
- thermal, UV, radiaton, or certain bacterial toxins

Where does leukocyte-mediated endothelial injury normally occur?

venules, pulmonary capillaries, and glomerular capillaries

How does leukocyte-mediated endothelial injury normally occur?

by WBCs adhering to the endothelium for prolonged periods of time

What is a visiculovacular organelle?

channel in the cytoplasm of endothelial cells that is made up of vesicles and vacuoles in which transcytosis takes place

What is VEGF?

- vascular endothelial grwoth factor
- inc. vascular leakage by increasing the size of vesiculovacuolar channels

What is extravasation?

sequenced events of white blood cells from the vessel lumen to the interstitial tissue

What are the effector cells of the acute inflammatory response?

- vascular endothelial cells
- mast cells
- neutrophils
- eosinophils
- macrophages/ monocytes

What is the function of vascular endothelial cells?

- regulate hemostasis/coagulation, vascular pressure, angiogenesis during wound healing, carcinogenesis, leukocyte homing, and inflammation

Where are mast cells normally found?

in the interstitium:
- skin, mucous membranes

What do mast cells respond to?

foreign proteins and microbes

what antibody do mast cells have a high affinity for?

IgE

What is mast cell degranulation triggered by?

TNF-alpha, histamine

What is the first type of white blood cell in inflammatory exudate?

neutrophils

what are the main functions of neutrophils?

- kill or limit the growth of microbes
- to kill tumor cells
- to eliminate foreign materials via phagocytosis

What is the life span of a neutrophil?

1-4 days

what do neutrophil granules contain?

myeloperoxidase, defensins, cathelicidins, lactoferrin, elastases, and gelatinase

What is the function of myeloperoxidase when it is released by neutrophils?

degrades microbes

What is the function of defensin and cathelicidin when released by neutrophils?

degrade by forming pores in microbial membranes

what is the function of lactoferrin?

inhibits growth of phagocytosed bacteria be sequestering iron

what is the function of elastase?

hydrolyzes bacterial cell wall proteins and tissue elastin

What is the function of gelatinase and myeloperoxidase when they are release by neutrophils together?

kill extracellular microbes and degrades the ECM

What do eosinophil granules contain?

basic proteins
-degrade collagen

What types of pathological processes are eosinophils normally seen?

- helminthic infections and allergic diseases

How are monocytes recruited for circulation to sites of inflammation?

via chemokines

What do macrophages trigger?

trigger the adaptive immune response by presenting antigens to T cells

what is the function of macrophages?

phagocytosis and cytokine release

What does leukocyte activation result in?

increased Ca and activation of enzymes

What are the steps of extravasation?

- margination (cell accumulation)
- rolling
- adhesion
- transmigration
- migration

What are the mediators of margination?

selectins an cytokines/chemokines

What are the mediators of rolling?

selectins and integrins

what are the mediators of activation and adhesion?

integrins and chemokines

What are the mediators of transmigration?

P-CAM (CD31)

What is another word for transmigration?

diapedesis

Whate mediators stimulate the distribution of P-selectin on endothelial cells?

histamine, thrombin, and PAF

What is the predominant cell type in the first 6-24 hours of acute inflammation?

neutrophils

In viral infections, what cell type is the first to arive?

lymphocytes

How long do neutrophils predominate in pseudomonas infections?

2-4 days

In hypersensitivity reactions, what is the main type of cell?

eosinophils

What molecules are important in white blood cells to get rid of bacterial infections?

adhesion molecules

What is leukocyte adhesion deficiency?

- mutation in B2 integrins
- results in neutrophilia with impared transmigration bc they cannot adhere to the endothelium
- severe gingivitis, tooth loss, ulcers, abscesses lacking pus, pneumonia

Is there a treatment for leukocyte adhesion deficiency?

no

What is phagocytosis?

release of enzymes by neutrophils and macrophages to eliminate injurious agents

What are the steps in phagocytosis?

- recognition and attachment to antigen
- engulfment in vacuole
- killing or degradation of ingested material

What is phagocytosis dependent on?

polymerization of actin filaments and requires similar signals as in chemotaxis

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