innate defenses

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immune system

first line of defense

keratinized skin and mucosa
produce variety of chemicals
acidity of skin secretions (pH 3 to 5) inhibits bacterial growth
lipids in sebum & dermcidin in eccrine sweat are toxic to bacteria
vaginal secretions are also very acidic
stomach mucosa secretes concentrated HCl acid solution and protein-digesting enzymes to kill microorgs.; sticky mucus in digestive/respiratory passageways; mucus coated nose hairs and cilia in resp tract

If the skin/mucosa are penetrated, this second line of defense kicks in

internal; antimicrobial proteins, phagocytes, other cells
hallmark of 2nd line of defense: inflammation

when does a person develop the innate defense system?

it's in place at birth

Lysozyme

an enzyme that destroys bacteria; it is contained in saliva and lacrimal fluid of the eye.

Phagocytes

EAT! chief phagocyte = macrophages

Macrophages are derived from?

Monocytes (WBCs): Monocytes leave the bloodstream, enter the tissues, and develop into macrophages

Free Macrophages

Wander throughout the tissue spaces in search of cellular debris and foreign invaders; like alveoli in lungs

Fixed Macrophages

like Kupffer cells in liver & microglia of brain, are permanent residents of particular organs

Neutrophils!

-most abundant WBC type
-FIRST RESPONDERS
-become phagocytic on encountering infectious material in tissues

phagocytic steps

1) phagocyte adheres to pathogens/debris
2) phagocyte forms pseudopods that eventually engulf the particles forming a PHAGOSOME
3)lysosome fuses with the phagocytic vesicle, forming a PHAGOLYSOSOME
4) lysosomal enzymes digest the particles, leaving a residual body
5) Exocytosis of the vesicle removes indigestible & residual material

In order for a phagocyte to accomplish ingestion, what must occur?

Adherence; cling to the pathogen, which is made possible by recognizing the pathogen's Carbohydrate signature;
Adherence is more probable/efficient when complement proteins or antibodies coat foreign particles, called opsonization, the coating provides handles that the phagocyte receptors can bind to

What bacteria is hard to recognize because in has external capsules made of sugar?

Pneumococcus

Opsonization

the process of coating foreign particles with complement proteins or antibodies, that form handles for phagocyte receptors to bind to

Respiratory bursts

liberate a deluge of free radicals, including nitric oxide and super oxide, that have potent killing abilities.

killing of pathogens

-more killing is caused by oxidizing chemicals, which increase osmolarity and pH in the phagolysosome which then activates other protein-digesting enzymes that digest invaders
-neutrophils also produce antimicrobial chemicals, called DEFENSINS, that pierce the pathogen's membrane

Natural Killer (NK) cells

- "police" the body in blood & lymph
-defensive cells can lyse & kill cancer cells and virus-infected body cells before the adaptive immune system is activated.
-part of a group of large granular lymphocytes
-called the "pit bulls" of the defense system
- Not phagocytic, they kill by inducing the target cell to undergo apoptosis, uses same killing mechanism as cytotoxic T cells
-secrete potent chemicals that enhance inflammatory response

the inflammatory response & cardinal signs

-triggered when there's body tissue injuries from trauma, intense heat, irritating chemicals or infection by viruses, fungi, or bacteria
-cardinal signs: redness, heat, swelling, pain
*some consider, functional impairment to be a 5th

Beneficial effects of the inflammatory response

1) prevents the spread of damaging agents to nearby tissues
2) disposes of cell debris & pathogens
3) sets the stage for repair

Toll- like Receptors (TLRs)
-eleven types

-Surface membrane receptors on macrophages and certain cells of boundary tissues; role in triggering immune responses
-Triggers release of chemicals called Cytokines

Cytokines

promote inflammation and attract WBCs to the scene

Mast Cells

-Key component of the inflammatory response
-release histamine

Histamine

-potent inflammatory chemical

Sources of inflammatory mediators

injured tissue cells, phagocytes, lymphocytes, basophils, and blood proteins

inflammatory chemicals released other than the main histamine

prostaglandins, kinins, leukotrienes, and complement which all cause the arterioles to dilate

hyperemia

As more blood flows into the area, local hyperemia occurs
-Congestion with blood which accounts for redness and heat of inflamed region

Exudate

fluid-containing clotting factors and antibodies- seeps from the blood into tissue spaces

Edema

which is causes by exudate is local swelling that presses adjacent nerve endings, contributing to a sense of pain

ß-defensins

enter at inflammatory sites where an epithelial barrier has been breached

Leukocytosis

-an increase in WBCs that is characteristic of inflammation
- neutrophils enter blood from red bone marrow in response to chemicals called leukocytosis-inducing factors released by injured cells. within a few hours, the number of neutrophils in blood increases four to fivefold.

Margination

*clinging of phagocytes to the inner walls of the capillaries and postcapillary venules
-inflamed endothelial cells sprout cell adhesion molecules (CAMs) that signal "this is the place!" As neutrophils encounter these CAMs, they slow and roll along the surface, achieving an initial foothold. When activated by inflammatory chemicals, CAMs on neutrophils bind tightly to endothelial cells

Diapedesis

Continued chemical signaling prompts the neutrophils to flatten and squeeze through the capillary walls which is called diapedesis

chemotaxis

inflammatory chemicals act as homing devices or more precisely chemotactic agent. neutrophils and other WBCs migrate up the gradient of chemotactic agents to the cite of injury (positive chemotaxis). within an hour after the inflam response has been, neutrophils have collected at the site and are devouring any foreign materials

monocytes

replace neutrophils on the battlefield, they are late responders

Pus

Mixture of dead or dying neutrophils, broken-down tissue cells and living and dead pathogens can accumulate in the wound. An abscess, sac of pus that may be walled off by collagen fibers, can form if the inflammatory response fails to clear the area of debris.

tuberculosis bacilli

resistant to digestion by the macrophages that engulf them. Being in the macrophages, protects them from prescription antibiotics and infectious granulomas form (tumor-like growth)

Antimicrobial proteins

enhance the innate defenses by attacking microorganisms directly or by hindering their ability to reproduce.
- most important of these are interferons and complement proteins

interferons (IFNs)

-small proteins secreted by virus infected cells to alert and protect nearby cells that have not been infected yet
-they diffuse to nearby cells, where they stimulate synthesis of proteins that "interfere" with viral replication in the still- healthy cells by blocking protein synthesis and degrading viral RNA
-not virus specific
-also activate macrophages and mobilize NK cells, which act directly against malignant cells

Lymphocytes Secrete this type of interferon

gamma (γ) or immune interferon

other leukocytes (beside lymphocytes) secrete this type of interferon

alpha interferon

Fibroblasts secrete this type of interferon

Beta (ß) interferon

IFN-beta and IFN- alpha have what effect and what is each one used to treat?

Both reduce inflammation, and keep it in control
- IFN- beta is used to treat patients with multiple sclerosis, a devastating demyelinating disease
-IFN- alpha is used to treat genital warts and hepatitis-C

Complement System (or simply complement) is what?

- a nonspecific defensive mechanism that "complements" or enhances the effectiveness of BOTH innate and adaptive defenses
- it provides a major mechanism for destroying foreign substances in the body; it unleashes chemical mediators that amplify all aspects of the inflammatory process;

Complement System includes ?

- a group of at least 20 plasma proteins that normally circulate in the blood in an inactive state
-C1 through C9, factors B, D, P and several regulatory proteins
- activated by two pathways

classical pathway of complement

- depends on the binding of antibodies to the invading organisms and the subsequent binding of C1 to the microorganism-antibody complexes, step called complement fixation
-antibodies coating the surface of a pathogen activate complement proteins C1, C4, and C2, which in turn activates C3

alternative pathway of complement

- C3 spontaneously activates and attaches to pathogen membranes.
-Factors B, D, and P stabilize spontaneously activate C3.

The two pathways of complement converge at C3 , then what?

It splits C3 into two pieces, C3a and C3b.
-C3a promotes inflammation (with the help of C5a)
-C3b enhances phagocytosis by acting as an opsonin. In certain target cells (mostly bacteria), C3b also activates other complement proteins that can form a membrane attack complex (MAC)

Membrane Attack Complex (MAC)

- MACs form from activated complement components (C5b to C6 to C9) that insert into the target cell membrane, creating funnel-shaped pores that can lyse the target cell. This ensures lysis of the target cell by inducing massive influx of water

C3b opsonization

C3b molecules provide handles that receptors on macrophages and neutrophils can adhere to, so engulfing can occur more rapidly

C3a & other cleavage products form during complement fixation amplify the inflammatory response how?

- by stimulating mast cells and basophils to release histamine and by attracting neutrophils and other inflam cells to the area

Fever

is an abnormally high body temperature (normal is 98.6ºF or 37ºC); it's a systemic response to invading microorganisms
-body temp is regulated by the cluster of neurons in the hypothalamus, "thermostat"
-the thermostat is reset upward in response to chemicals called PYROGENS secreted by leukocytes and macrophages exposed to foreign substances in the body.

Mild to moderate fevers vs high fevers

-high fevers are dangerous because they denature enzymes
-mild/moderate fevers seem to benefit the body; fever increases metabolic rate of tissue cells in general, to speed up the repair process

What role do iron and zinc play in the immune response?

Iron and zinc are needed for bacteria to multiply, during an attack though the spleen and liver sequester these nutrients to lessen their availability

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