This febrile response is in part dependent on the local action of interleukin-1beta within the pouch.

Response correlated with prior exposure to BCG vaccine or tuberculosis, and with a febrile response to vaccine administration.

Here, using mice of both sexes, we examined the role of local versus generalized PGE 2 production in the brain for the febrile response.

These data imply that the febrile response is dependent on the local release of PGE 2 onto its target neurons, possibly by a paracrine mechanism.

As opposed to observations on STAT3 or NFkB, the percentage of NF-IL6-reactive cells increased in parallel to late phases of the febrile response.

In contrast, PGE 2 production in other brain areas and the overall PGE 2 level in the brain do not influence the febrile response.

There was no significant difference among groups in febrile responses to switching their cages.

Febrile responses up to 40 degrees C may play a beneficial role in host defense.

Conclusions: C5a is crucial for the development of febrile responses to LPS in mice; its site of action is peripheral, not central.