Although it seems obvious that fever has some important general adapti
ve value, it is still not clear by what means this function is manifes
ted. One postulate is that febrile conditions result in the sequestrat
ion of soluble iron, effectively starving some pathogens of that essen
tial nutrient. On the basis of our recent experiments, we propose a ne
w mechanism for how fever serves to restrict a wide range of Gram-nega
tive bacteria. The elevated temperature prevents the bacteria from syn
thesizing their protective LPS, thereby enabling serum complement to p
erforate and kill the invading pathogens even prior to the production
of host antibodies.