Recent views on the role of interleukin-1beta (IL1b) during fever, include:
1) IL1b is the predominant pyrogen, at least during poxvirus infection. See
the elegant study of Alcami et al., [PNAS 93: 11029-11034, 1996], which
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 molecules
such as NO or prostaglandins to act on brain parenchyma.
It seems that each of the above possibilities plays a role, according to
the conditions (ie mild inflammation vs. sepsis etc.)
3) The above do not preclude a possible role of cytokines like IL1alpha,
TNF-alpha, IL-6 and interferons, possibly under different conditions.
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Stavros P. Zanos
Medical Student
Aristotle Univ. School of Medicine
Thessaloniki, Greece
