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What happens during fever?

F. Frank LeFever flefever at ix.netcom.com
Mon Feb 3 00:21:01 EST 1997

In <01bc10df$7f7ed060$5cc31ec2 at slirp.hol.gr> "Stavros P. Zanos"
<stavrosz at med.auth.gr> writes: 
>Recent views on the role of interleukin-1beta (IL1b) during fever,
>1) IL1b is the predominant pyrogen, at least during poxvirus
infection. See
>the elegant study of Alcami et al., [PNAS 93: 11029-11034, 1996],
>resolved a long-standing puzzle.
>2) ILs, and cytokines in general, do not cross the blood brain barrier
>(BBB), so how does IL1b signal the brain to cause fever? This could be
>accomplished by either of four possible routes (reviewed in Licinio &
>Sternberg, [Handbook of Endocrinology, eds: Kaplan & Gass, CRC Press,
>Florida, pp. 261-269]):
>	a) by slowly crossing the BBB via specific transport systems
>	b) by entering the brain through regions lacking BBB protection
>	c) by transmitting a signal to the brain through the vagus nerve
>	d) by activating brain vasculature, and causing informational
>such as NO or 	prostaglandins to act on brain parenchyma.
>It seems that each of the above possibilities plays a role, according
>the conditions (ie mild inflammation vs. sepsis etc.)
>3) The above do not preclude a possible role of cytokines like
>TNF-alpha, IL-6 and interferons, possibly under different conditions.
>Stavros P. Zanos
>Medical Student
>Aristotle Univ. School of Medicine
>Thessaloniki, Greece
I don't know if I made it explicit in my earlier posting (#16908), but
IL-1 is produced IN the brain, on the basis of various stimuli--e.g.
peripheral IL-1, peripheral LPS (a bacterial product), OR
"psychological" stimuli (conspecific fighting, immobilization stress,
etc.)  All the routes Stavros lists may be involved at one point or
another, but the extreme rapidity of some of the reactions suggests to
me that the neural route(s) (vagus, and---??) may be most important.

The inhibition of exploratory behavior by peripheral IL-1 or LPS can be
abolished by cutting the vagus.

I hopw to provid a more precise reference than "Neuroimmmunology, 1996
or 1995" for a review of IL-1 effects on classical neurotransmitters,
which to me raises the possibility of an explanation (if indeed the
phenomenon of fever amelioration of ADD exists) in terms of
noradrenaline activity.

Frank LeFever
New York Neuropsychology Group

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