IMMUNOLOGY

WHY OUR BODY

DEVELOP FEVER

AFTER INFECTION?

GROUP MEMBERS LAILATUL JALILAH

ZUHAIDA

WAN IZZATI

SITI MARIAM

POIN T

OF

VIEW

Definition of feverMechanisms of fever

Development offever Pro and contra of

fever

DEFINITION:

Fever is a rise in our body's normal temperature, which on average, is 98.6 degrees Farenheit.

Fever is part of our body's defense mechanism.

FEVER

•Fever is a symptom of an infection.

•Fever is a good thing.

•Fever is our body's natural response to fighting germs.

•The cause of the fever is quite an intricate process.

CAUSES OF FEVER

• When infection occur, our blood and lymphatic system produce

white blood cell which are what fight off infection.

• As the white blood cells increase in number to fight and attack the

germs, this causes our body to heat up.

• The white blood cells that are produced to fight the germs,

has affected the hypothalamus in the brain which is the body’s

heat regulating mechanism.

• When the body is fighting an injury or infection, the

hypothalamus sets the body temperature at higher level.

• The body compensates for this by moving blood away from the

skin so the amount of heat lost through the skin is reduced.

• Therefore, the muscles might repeatedly contract to keep the

body warm, which causes shivering.

Mechanisms of fever

Pyrogens

Endogenous Exogenous

Endogenous

The cytokines like ( interleukin 1) are a part of The cytokines like ( interleukin 1) are a part of

the innate immune system, produced by the innate immune system, produced by

phagocytic cells, and cause the increase in the phagocytic cells, and cause the increase in the

thermoregulatory set-point in the thermoregulatory set-point in the

hypothalamus. Other examples is (IL-6) and hypothalamus. Other examples is (IL-6) and

tumor necrosis factor-alpha.tumor necrosis factor-alpha.

• These cytokine factors are released into These cytokine factors are released into

general circulation where they migrate to the general circulation where they migrate to the

circumventricular organs of the brain, where circumventricular organs of the brain, where

the blood-brain barrier is reduced. The cytokine the blood-brain barrier is reduced. The cytokine

factors bind with endothelial receptors on factors bind with endothelial receptors on

vessel walls, or interact with local microglial vessel walls, or interact with local microglial

cells. When these cytokine factors bind, they cells. When these cytokine factors bind, they

activate the arachidonic acid pathway. activate the arachidonic acid pathway.

Exogenous

One model for the mechanism of fever caused One model for the mechanism of fever caused

by exogenous pyrogens includes LPS, which is by exogenous pyrogens includes LPS, which is

a cell wall component of gram-negative a cell wall component of gram-negative

bacteria. An immunological protein called bacteria. An immunological protein called

lipopolysaccharide-binding protein (LBP) binds lipopolysaccharide-binding protein (LBP) binds

to LPS. The LBP–LPS complex then binds to to LPS. The LBP–LPS complex then binds to

the CD14 receptor of a nearby macrophage. the CD14 receptor of a nearby macrophage.

• This binding results in the synthesis and This binding results in the synthesis and

release of various endogenous cytokine release of various endogenous cytokine

factors, such as interleukin 1 (IL-1), interleukin factors, such as interleukin 1 (IL-1), interleukin

6 (IL-6), and the tumor necrosis factor-alpha. In 6 (IL-6), and the tumor necrosis factor-alpha. In

other words, exogenous factors cause release other words, exogenous factors cause release

of endogenous factors, which, in turn, activate of endogenous factors, which, in turn, activate

the arachidonic acid pathway. the arachidonic acid pathway.

HYPOTHALAMUS RESPONSE

• part of the brain called the hypothalamus controls body temperature.

• Fever results from an actual resetting of the hypothalamus's thermostat.

• The body raises its temperature to a higher level by moving (shunting) blood from the skin surface to the interior of the body, thus reducing heat loss.

• Shivering (chills) may occur to increase heat production through muscle contraction.

•The body's efforts to conserve and produce heat continue until blood reaches the hypothalamus at the new, higher temperature.

• The new, higher temperature is then maintained.

• Later, when the thermostat is reset to its normal level, the body eliminates excess heat through sweating and shunting of blood to the skin.

PGE2 RELEASE

•PGE2 release comes from the arachidonic acid pathway.

• This pathway (as it relates to fever), is mediated by the

enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-

2), and prostaglandin E2 synthase which will mediate the

synthesis and release of PGE2.

• PGE2 is the ultimate mediator of the febrile response. The

set-point temperature of the body will remain elevated until

PGE2 is no longer present.

causing an unbearable environment for some pathogens

white blood cells rapidly proliferate due to the

suitable environment

help fight off the harmful pathogens and

microbes that invaded the body

PRO AND CONTRA FEVERPRO AND CONTRA FEVER

Research has demonstrated that fever has several

important functions in the healing process:

increased mobility of leukocytes

enhanced leukocytes phagocytosis

endotoxin effects decreased

increased proliferation of T Cells

enhanced activity of interferon

However, if a fever goes too high, measures

must be taken to bring the fever down a bit.

Antipyretics are medications that lower fever,

such as tylenol, aspirin and so on.

Never give a child aspirin products if it is

believed they have chicken pox or the flu.

Lead to a condition called Reye's Syndrome that

is potentially fatal.

Above 105 degrees, damage can occur in the

nervous system.

THE END

Thank you for listening…