Biology Reference
In-Depth Information
1
The Brave New World of
Neuroimmune Biology
Istvan Berczi
1
, Andres Quintanar-Stephano
2
,
Kalman Kovacs
3
1
Department of Immunology, Faculty of Medicine, The University of
Manitoba, Winnipeg, Manitoba, Canada,
2
Department of Physiology,
Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico,
3
Department of Pathology, St. Michael's Hospital, University of Toronto,
Toronto, Ontario, Canada
1.1 Introduction
1.1.1 How Did It Begin?
Sporadic suggestions of neuroimmune interactions date back to the late nineteenth
century. The students and followers of Pavlov in Russia thoroughly investigated the
nature of immunoregulation by neuroimmune mechanisms and eventually concluded
that the hypothalamus is a likely center of immunoregulation
[1,2]
.
Using modern technology, Szentivanyi and colleagues observed that hypothalamic
lesions inhibited the development of anaphylactic shock in immunized animals
[3]
.
Tuber cinereum lesions (TBLs) in the hypothalamus inhibited anaphylaxis in preimmu-
nized guinea pigs and (in later experiments) also in rabbits. Anaphylaxis was induced
in immunized animals by intravenous (IV) injection of the immunizing antigen. TBLs
also inhibited antibody production if the lesions were created prior to immunization.
TBLs did not affect antigen-antibody reactions, nor did the release of tissue materials
mediating anaphylaxis. Hypothalamic lesions temporarily increased histamine resis-
tance and inhibited the anaphylactic reaction even when the animals were provided
with passively transferred antibodies, which elicited lethal shock in control animals.
The Schultz-Dale test, which was performed with small pieces of intestine
in vitro,
was also inhibited by TBLs. The Arthus reaction, turpentine-induced inflammation,
and the Sanarelli-Shwartzman phenomenon were unaffected. Lesions of other areas
of the hypothalamus or of the central nervous system (CNS) were ineffective in modu-
lating immune phenomena. Further, electrical stimulation of the mammillary region
of the hypothalamus had an inhibitory effect on the anaphylactic response and
increased the resistance of animals to histamine
[4-6]
. In 1964, Korneva and Khai
[7]
confirmed that hypothalamic lesions in rabbits, guinea pigs, and rats inhibited the pro-
duction of complement-fixing antibodies.
