Animal studies for Vitamin B6

Kumar & Axelrod (1968) reported a lowered level of
circulating antibodies and a dramatic reduction in
the number of antibody-forming cells in the spleens
of vitamin B6-defi cient rats immunized with sheep
erythrocytes. This decreased cellular immune response
was independent of the inanition associated
with the defi ciency and was restored to normal by the
administration of PN shortly before immunization.
Robson & Schwarz (1975) reported a dramatic
85–95% reduction in the number of thoracic duct
lymphocytes and a signifi cant reduction in cellular
immunocompetence in vitamin B6-defi cient rats.
These conclusions were based on the results of two
tests: (1) the in vitro mixed lymphocyte reaction
(MLR) and (2) the in vivo normal lymphocyte transfer
reaction (NLT). In the MLR, lymphocytes from test
Lewis strain rats (in this case, vitamin B6-defi cient and
control rats) are cultured with genetically dissimilar
lymphocytes taken from normally nourished F1 hybrid
rats. If the lymphocytes are immunocompetent,
they will become activated and then they will proliferate
and transform into the larger lymphoblasts. The
extent of blastogenesis is quantitated by exposing
the cultures to [3H]thymidine and then measuring
the incorporation of the radioactivity into DNA. In
the NLT, lymphocytes from donor Lewis rats (the test
rats) are injected into the ventral abdominal wall of F1
hybrid rats. Immunologically competent donor cells
produce a graft-versus-host reaction in the skin of the
F1 rat. The impaired proliferation of lymphocytes and
loss of cellular immunocompetence may perhaps be
attributed to a cessation of T-lymphocyte development
within the thymus of the vitamin B6-defi cient
animal.
The development of functional T lymphocytes
depends on humoral factors secreted by thymic epithelial
(TE) cells. To investigate the effects of dietary
vitamin B6 defi ciency on TE cell function, Willis-Carr
& St. Pierre (1978) used three groups of Lewis strain
rats as cell donors: (1) normal (control) rats, (2) rats
maintained for 2 weeks on a vitamin B6-defi cient diet
and (3) rats whose thymus glands had been surgically
removed 24 hours after birth (neonatally thymectomized
rats). Spleen, bone marrow and mesenteric
lymph nodes were removed from each donor and
washed cells from these lymphoid tissues were exposed
to monolayers of TE cells. The TE monolayers
were made from (1) normal, (2) vitamin B6-defi cient
and (3) ‘post B6’ rats, i.e. rats placed back on a regular
diet for 3 weeks after the original 2-week B6-defi cient
diet. Exposure of T-lymphocyte precursors from
B6-defi cient or neonatally thymectomized donors to
normal TE monolayers resulted in their conversion to
functional T lymphocytes, as measured by their response
in MLR and to mitogens. However, TE monolayers
from B6-defi cient rats were unable to effect such
a maturation of T lymphocytes. When the defi cient
rats were returned to a normal diet, TE cell function
was restored. The authors suggested that the cause
of defective cellular immunocompetence following
vitamin B6 deprivation is the inability of TE cells to
effect the differentiation of T-lymphocyte precursors
to functional T lymphocytes. Vitamin B6 defi ciency
did not impair T-lymphocyte precursors, which could
be stimulated to differentiate by exposure to normal
TE cell monolayers. Presumably, the observed effect
of vitamin B6 defi ciency is due to a blocking of the
biosynthesis and/or release of a humoral factor that is
produced by TE cells. Chandra & Puri (1985) found
signifi cantly reduced serum thymic factor activity in
rats fed diets restricted in vitamin B6 and given 4-deoxypyridoxine
hydrochloride in their drinking water.
Vitamin B6-defi cient mice exhibited impaired
production and reduced activity of cytotoxic T lymphocytes
(Sergeev et al., 1978; Ha et al., 1984). Antibody-
mediated cytotoxicity, macrophage phagocytosis
and natural killer cell activity were not affected by
the level of vitamin B6 intake (Ha et al., 1984).