INTAS POLIVET (2007) Vol. 8 No.
I : 11-19
Role of Vitamins in Immune Response
P. Kavitha, J.V Ramana and J. Rama Prasad
Department of Animal Nutrition, College of Veterinary Science
Tirupati - 517 502 (A.P.), India
Abstract
Vitamins play an important role in maintaining
immune response of the animals. The vitamin
deficiency causes specific pathologic changes,
the tissues affected become liable to secondary
infection. The paper reviews the role played by
various vitamins in immune response. Vitamin A
& E-carotene influence both specific & non-
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specific host defence mechanisms. It enhances
the lymphocyte proliferation, delayed type of hyper
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sensitivity& natural killer cell activity. It stimulates
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the production of IL-1 & IL-2. Vitamin A increases
serum antibody levels and enhances
phagocytosis & intracellular kill
polymorphonuclear cells & macrophages. The
defence mechanism of vitamin E is mainly
dependent on its antioxidant activity. It enhances
antibody production, cell proliferation, cytokine
production & neutrophil function. Vitamin D
enhances the phagocytic activity of macrophages,
T- cell differentiation & slows down the
spontaneous thymic involution. Vitamin C
stimulates the phagocytic activity of leukocytes,
function of reticulo endothelial system and the
formation of antibodies and has antiviral &
anticancer properties. Vitamin K influence the
level of serum complement. The B-complex
vitamins are associated with antibody production
& their deficiency causes decrease in complement
and reduction of leukocytes in peritoneal-induced
exudates & reduced cellular migration to areas of
inflammation. Thus the vitamins can reduce the
use of antibodies as feed additives.
Key words: Vitamins, Immune response
Introduction
Any foreign substance enters the body of an
organism, the organism reacts/responds to it and
this response is known as immune response. The
Review Article
ultimate aim of the immune response is to activate,
destroy and eliminate the antigen from the body
of the organism. The response is mainly of two
types. In the first type, the body fights against the
antigen by producing antibodies which are present
in the fluids (humors) of the body, hence it is called
as humoral immunity (or) antibody mediated
immunity. In the second type of response, the
body produces large number of activated
lymphocytes that are specially designed to destroy
the foreign organism, hence it is called the cellular
immunity (or) cell mediated immunity. This
immune response is affected by many factors.
by
The new frontiers of nutrition research lies in the
application of micronutrients-vitamins, minerals
and related cofactors to immune response.
A good deal of interest has been centered on the
possible influence of vitamins on susceptibility to
infectious disease. In general, vitamin deficiency
causes specific pathologic changes, the tissues
affected become liable to secondary infection.
This is probably a non specific consequence of
cellular damage, and occurs in several
deficiencies. There is some evidence that the
lack of certain vitamins may lower resistance in
specific ways, by interfering with known
mechanisms of defense, such as the phagocytic
cells, bactericidal enzymes, or the antibody
producing cells.
Although refinement in nutritional and
immunological techniques has allowed the
influence of vitamins on the immunological
response to be examined in greater depth, the
order of immunological impairment brought about
by most deficiencies had been recognized as
early as 1951. Since that time, attention has been
paid to those deficiencies most actively affecting
11
 Kavitha and others
the response, whereas others such as vitamin D
and K deficiencies have been relatively
neglected.
Role of Vitamin A in Immune response
The fat soluble vitamin retinol is crucial for immune
defense. Vitamin A has been called the anti
infective vitamin. Impairment of animals immune
system resulting from the vitamin deficiency may
account for increased susceptibility to infection.
Vitamin A & E carotene afford the protection
against infections by influencing both specific and
nonspecific host defense mechanisms. Specific
host defence includes cell-mediated and
antibody-mediated (humoral) immunity &
nonspecific host defence includes phagocytic
functions.
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The effects of vit A & E carotene on host defence
will be divided into 4 categories.
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1. Cellularity of lymphoid organs & lymphocyte
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trapping.
2. Cell mediated immunity.
3. Humoral immunity and
4. Non specific defence.
1. Cellularity of lymphoid organs & lymphocyte
trapping:
Lymphoid organs play a central role in the function
of the immune system. Both vitamin A and
E-carotene influence cellularity and function of the
lymphoid organs. Rats fed a diet deficient in
vitamin A showed decreased cellularity in the
bursal (B) cell germinal centers & Periarteriolar
thymal (T)-cell sheaths of the spleen and also
showed decreased cellularity in the regional
lymphnodes (Butera & Krakowka, 1986).
Therefore through their effects on growth and cell
differentiation vit A & E-carotene seem to influence
the cellularity & function of lymphoid organs.
Trapping of lymphocytes in lymphoid organs after
antigen challenge constitutes a very important
initial event leading to an immune response
(Sprent et al. 1971). The defect in lymphocyte
localization in vitamin A deficiency is due to
impaired lymphocyte surface membrane
glycoproteins, resulting in decreased antigen and
lymphocyte recognition and contact, because
vitamin A plays an important role in glycosylation.
12
2. Cell mediated immunity:
¾ Vitamin A & E carotene are immuno
stimulatory. They enhance the lymphocyte
proliferation (or) mitogen induced lymphocyte
transformation. They enhance the delayed
type of hyper sensitivity reactions (DHS),
transplant rejection, cell mediated cytotoxicity
& natural killer (NK) cell activity.
¾ Vitamin A stimulates the production of
Interlukin-2 (IL-2) by lymphocytes and IL-1
by macrophages. But suppresses the
production of IFN (interferon) by lymphocytes.
Interferon is an induced glycoprotein that
limits the replication of viruses within the host.
Vitamin A inhibits the antiviral activity of IFN
& potentiates the cytostatic action of IFN on
lymphoblastoid cells.
¾ E-Carotene behaves in opposition to vitamin
A in its effect on IFN action. It potentiates the
stimulatory action of IFN on monocyte F
cr-receptor and inhibits the cytostatic action
of IFN.
¾ Vitamin A appears to act in the induction
phase of immunity. It stimulates T-Killer cell
activity and possibly acts on proliferating
helper type T cells that participate in the
inductive phase of T-killer sensitization.
3. Humoral Immunity:
Vitamin A increases serum antibody levels,
number of spleenic antibody forming cells and
local immunity. Vitamin A may influence local
immunity by modulating the synthesis of transport
glycoprotein.
™ Vitamin A deficiency may alter the
glycoprotein surface properties of
lymphocytes and consequently may lead to
depressed differentiation and proliferation of
lymphocytes, there by decreased antibody
production.
™ Vitamin A is also capable of inhibiting the
immunosuppressive effects of
hydrocortisone. Vitamin A may counteract
the immuno-suppressive effect of
hydrocortisone by destabilizing lysosomal
membranes, because carticosteroids stablize
these membranes (Cohen and Elin, 1974).
 Kavitha and others
4. Non specific host defence:
The non specific cellular defence of the host
animal comprises phagocytic cells, which belong
to two complementary systems.
1. Myeloid system which is made up of rapidly
acting cells extremely efficient at
phagocytosis but incapable of sustained
effort, the predominant phagocytic cells in the
system includes polymorpho nuclear
leukocytes (PMN) that is neutrophils.
2. Mononuclear phagocytic system which
consists of phagocytic cells capable of
repeated phagocytosis and can process the
antigens in order to initiate an immune
response.
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Vitamin A enhances phagocytosis and
intracellular killing by PMN cells & macrophages.
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Macrophages from vitamin A supplemented mice
also showed increase ability to produce IL-1.
Which is a non antigen-specific monokine
produced by monocytes & macrophages and acts
on immature T-helper cells to promote their
differentiation & the release of IL-2.
In addition to IL-1 vitamin A supplementation also
helps in the production of transglutaminase in
mouse peritoneal macrophages & arginase by
Guinea Pig peritoneal macrophages (Rhodes and
Oliver 1980). Arginase is tumoricidal enzyme.
Mechanism of action:
Modulation of glycosylation: This model was
proposed by DeLuca (1977) suggested that
retinol, functioning as retinyl phosphate, is
involved in post translational transfer of
monosaccharides to an acceptor protein, resulting
in the synthesis of a specific glycoprotein.
Because glycoproteins are important components
of membranes, this mechanism may allow cell
differentiation by a non nuclear mechanism,
glycoproteins play important role in cell
communication and adherence.
In addition carotenoids can enhance immune
functions independently of any provitamin A
activity (Bendich, 1991).
13
E-carotene functions as an antioxidant (Bendich
and Olson, 1989) and it is an efficient quencher of
singlet oxygen. Vitamin A cannot quench singlet
oxygen and has less antioxidant activity than other
antioxidant nutrients.
Exposure to UV light directly increases the free
radical burden imposed on the body, decreases
immune responses especially cell mediated
responses and significantly increases the risk of
skin cancer (Donawho & Kripke, 1991). E-carotene
& certain other carotenoids can block the formation
of UV-induced singlet oxygen. Singlet oxygen
can initiate the generation of immuno suppressive
reactive free radical species containing oxygen.
Role of vitamin E & Selenium in host defence
Vitamin E & Se defence mechanism is related to
their antioxidant property. Antioxidants stabilize
highly reactive, potentially harmful molecules
called free radicals. These are produced during
normal cellular metabolism & result from the
metabolism of certain drugs or xenobiotics.
Exposure to UV light, cigarette smoke and other
environmental pollutants also increases the
body’s free radical burden. The ability of
antioxidants to destroy free radicals protects the
structural integrity of cells & tissues.
Free radicals and Immune cell function:
Many of the protective functions of immune cells
depend on the fluidity of the membranes of the
cell. As the concentration of polyunsaturated fatty
acids (PUFA) in the membranes increased, the
potential for membrane lipid peroxidation
mediated by free radicals also is increased. Lipid
peroxidation decreases the membrane fluidity,
which adversely affects immune responses. Loss
of membrane fluidity has been related directly to
the decreased ability of lymphocytes to respond
to challenges to the immune system (Bendich,
1990).
Vitamin E (a-tocopherol), the major lipid soluble
antioxidant present in all cellular membranes,
protect against lipid peroxidation and prevents
the loss of membrane fluidity. Vitamin E quenches
free radicals & singlet oxygen.
In old age there is decline in immune responses.
Delayed type of hypersensitivity to skin test
 Kavitha and others
antigens are diminished. Deficiency in adults
results in anergy; a complete loss of skin test
responses. Vitamin E supplementation (800 IU/
day) for 1 month significantly increased delayed
type of hypersensitivity (DTH) responses of healthy
adults (Meydani et al., 1990).
Vitamin E supplementation enhances host
defence mechanisms including antibody
production, cell proliferation, cytokine production,
prostaglandin metabolism and neutrophil function
(smith, 1986). Neutrophils are considered to be a
primary defense mechanism to bacterial infections
in mammals.
Vitamin E & selenium protects the neutrophils from
free radicals. Vitamin E protect against free
radicals at the membrane, glutathione peroxidase
activity is in the cytosol. It convert H2O2 to water
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and lipid peroxides to the corresponding alcohol
(Baker & Cohen, 1983).
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Role of Vitamin E & Selenium in host defence
against mastitis
Vitamin E & Selenium deficiency related to
increased incidence and severity of mastitis. Their
deficiency resulted in reduced neutrophil activity.
Vitamin E & glutathione peroxidase protects
neutrophils from the destructive action of toxic
oxygen molecules necessary for intracellular kill
of ingested pathogens. Dietary supplementation
of cattle with Se results in a more rapid influx of
neutrophils into milk following Intramammary
bacterial challenge & increased phagocytic
activity of neutrophils.
Dietary vitamin E & selenium supplementation of
dairy cows reduced the rates & duration of clinical
mastitis. The first controlled study on the effects
of vit E & Se supplementation on clinical mastitis
was reported by Smith et al. 1984.
Vitamin E & selenium are synergistic on duration
of clinical sings. Cows supplemented with both
vitamin E & selenium had shorter duration of
clinical signs than cows supplemented with either
micronutrient alone. Concentration of vit E in
neutrophils was related linearly to killing ability of
neutrophils.
Recommended dietary intake & blood levels: The
recommended and legal upper limit for selenium
14
concentration in dairy cow rations is 0.3 ppm
(NRC, 1988). Whole blood concentrations of
selenium should be at least 0.2 mg/ml but not
exceeding mg/ml. Requirement for dietary
vitamin E is 15 IU/kg of dry matter in take for both
dry and lactating cows. (NRC,1988). It is worthy
to note that megadoses of vitamin E may be
immunosuppressive.
Weiss et al., (1997) reported that cows receiving
vitamin E as dietary supplement at the rate of 1000
IU / d had 30 % less clinical mastitis than did cows
receiving a supplement of 100 IU / d of vitamin E
in first week of lactation and the reduction was
88% when cows were fed 4000 IU / d of vitamin E
during the last 14 days of the dry period.
Role of Vitamin D in the Immune System
Metabolism & Mechanism of action:
UV irradiation of skin converts 7-dehydro
cholesterol to pre vitamin D3. At body temperature,
pre vitamin D3 rapidly isomerizes to vitamin D3
which then enters the blood. Dietary vitamin D2
and D3 are absorbed in the small intestine where
they enter the lymphatic circulation. Vitamin D is
then taken up by the liver & hydroxylated to form
25-hydroxy vitamin D. This is the major circulating
form of vitamin D & it is transported in the blood
primarly associated with vitamin D binding protein.
25 (OH) vit D is then taken up by the kidney where
it is further hydroxylated to form the steroid
hormone 1,25 (OH)2 vitamin D.1,25 (OH)2 vitamin
D circulates bound to plasma proteins primarly vit
D-binding protein. A small portion of the hormone
circulates in the free state and readily enters cells
due to its lipophilic nature. Binding of 1,25
dihydroxy cholicalciferol to its intracellular
receptor results in the transformation of the
receptor-hormone complex to a form which has
increased affinity for nuclear components.
Specific DNA domain binding or acceptor site
binding by the receptor-hormone complex results
in the induction or repression of mRNA
transcription. These events lead to specific
alterations in protein synthesis, which modulate
cell function.
Calf thymus glands & lymphnodes, tonsils possess
1,25 (OH)2 vit D receptors indistinguishable from
those described for classical target tissues of 1,25
 Kavitha and others
(OH)2 vitamin D. The concentration of receptors
for this vitamin in thymus & lymphatic tissue was
about 10-20% of that found in intestine. Large,
mitotically active medullary thymocytes have these
receptors. Peripheral blood monocytes also
possess receptors, but peripheral blood T & B
lymphocytes do not have these receptors.
Receptors for vitamin D also present on
malignant cell lines.
Effect on Monocyte & Macrophage functions:
Physiological doses of 1,25 (OH)2 vit D promotes
differentiation of several mono & promonocyte cell
lines toward a macrophage phenotype. 1, 25
(OH)2 vitamin D mediated cell differentiation is
receptor dependent. Cells that contain less than
400 receptors per cell are resistant to the actions
of 1,25 (OH)2 vit D. It increases the phagocytic
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activity of 1,25 (OH)2 D3 enhances the cytotoxicity
of pulmonary macrophages (Abe, et al., 1984). It
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also enhances the competence for H2O2 secretion
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in monocytes. In normal monocytes 1,25 (OH)2
vitamin D induces morphological changes as well
as accelerated differentiation, increase in
lysosomal enzymes, enhances adherence,
accelerates cell fusion, increases synthesis of heat
shock proteins and controls the proliferation of
intracellular Mycobacterium tuberculosis in
monocytes (Polla et al., 1986).
Effect on thymocyte function:
Enhance T cell differentiation & slows down
spontaneous thymic involution.
Effect on lymphocyte function:
Activated lymphocytes express large amounts of
1,25 (OH)2 vitmain D receptors. 1,25(OH)2 vitamin
D is a potent inhibitor of IL-2 production by
peripheral lymphocytes. Vitamin D inhibits
mitogen stimulated lymphocyte proliferation.
Vitamin D decreases the development of
cytotoxic, helper and inducer T-cells (Limire et
al., 1984).
In vitamin D deficiency, rickets often accompanied
by increased rates & severity of infections (stroder,
1975). In rickets, neutrophils have defective
motility. In vitamin D deficiency there is impaired
macrophage function and decrease in bone
marrow cellularity.
15
Bone resorption & cells of Immune system:
Cells of monocyte & macrophage serve as
precursors to bone resorbing cells, osteoclasts
and lymphocytes or monocytes produce
osteoclast activating factor (OAF) which is
important in bone resorption. Osteoclasts are of
hemopoietic origin (Loutit and Nisbet, 1982).
Macrophages possess calcitonin receptors as
osteoclasts.
Monocytes regulate production of IL-1 and
lymphokine, OAF two potent mediators of bone
resorption (Mundy 1983).
Role of Vitamin C in Immune Response
Vitamin C is necessary for the proper formation
and maintenance of intercellular material, such
as collagen of all fibrous tissues, the cement
substance of endothelial tissues and especially
that of the capillaries, and the matrix of bone and
cartilage.
Vitamin C is having an antiviral and anticancer
activity. It is an antioxidant and quench free
radicals and singlet oxygen. White blood cells
use vitamin C to combat infections, and in the
face of inflammation or microbial challenge, levels
of vitamin C are depleted. In vitamin C deficiency
there is marked increase in fragility and an
impairment of phagocytosis of leukocytes. In some
infections, of which tuberculosis is an outstanding
example, the ascorbic acid requirement may be
considerably greater in infected than in normal
individuals. Enhanced immunity by dietary
ascorbic acid (ASA) appears to be T-lymphocyte
dependent.
Vitamin C is reported to have a stimulating effect
on phagocytic activity of leukocytes, on function
of the reticulo endothelial system and on the
formation of antibodies. Some of the most
controversial topics regarding the interactions of
vitamin C with immune functions have been the
reduction of common cold symptoms and
favourable responses to cancer treatment.
In calves stress associated with confinement
decreased the immune response to a specific
antigen and decrease the concentration of
ascorbic acid in plasma (Cummins & Brunner
1991). Supplementation of vitamin C increased
 Kavitha and others
the concentration of IgG in plasma of calves
deprived of colostrum (Blair and Cummins 1984).
But in normal calves supplemented with ascorbic
acid had lower plasma concentrations of IgG and
reduced antibody titres (Cummins and Brunner,
1989).
Dietary supplementation of calves with ascorbic
acid has shown to increase plasma ascorbate
concentrations and concurrently improve antibody
responses to an antigen (Cummins and Brunner,
1990).
Carol et al., (1987) reported that guinea pigs fed
100 times the amount of vitamin C needed for
growth and for prevention of scurvy have elevated
levels of complement C1q which is a plasma
protein rich in hydroxy proline. Hydroxy proline is
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an amino acid whose biosynthesis requires
ascorbate which is essential for host defense
against pathogens, both as a component of the
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classical complement pathway and as an opsonin
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in the phagocytosis process.
Ascorbate has been shown to restore polymorpho
nuclear leukocyte function in Scorbutic rhesus
monkeys by restoring normal phenotype and
improving phagocytosis which help in killing of
bacteria (Goldshmidt, 1991).
Ascorbic acid has a positive effect on cattle
neutrophils following injection of dexamethasone
by reversing decrease in neutrophil random
migration, oxidative metabolism and antibody
dependent cell-mediated cytotoxicity (Roth and
Kaeberle, 1985).
Tyler and Cummins (2003) reported that cells of
the immune system do appear to respond to
differing ascorbate concentrations but the effects
are often negative as well as positive. They also
reported that dietary Ascorbyl-2-phosphate
magnesium decreased the mononuclear
lymphocyte proliferation following stimulation with
a mitogen in vitro.
Supplementation of vitamin C, E & A or E-carotene
increased the activation of cells involved in tumor
immunity in the elderly.
Role of Vitamin K in Immune Response
Vitamin K deficiency can lead to a reduced level
16
of serum complement in chickens (Werber et al.,
1963).
There is a slow resynthesis when vitamin K is
restored to the diet, normal complement activity
returning more slowly than prothrombin activity.
Role of Vitamin B Complex Group on Immunity
Deficiencies of vitamins of this group have long
been associated with reduction of antibody
production to antigenic stimuli.
1. Thiamin: Thiamin deficiency in mouse
increases its susceptibility to Cryptococcus
neoformans. But there is no good evidence that
antibody formation or acquired resistance to
infection itself is affected in any direction by
thiamin deficiency.
2. Pantothenic acid: Deficiency may in some
cases increase native susceptibility to
experimental infections, in others decrease it. In
man deficiency of Pantothenic acid results in
increased susceptibility to upper respiratory tract
infections.
3. Riboflavin: Riboflavin deficiency is usually
associated with greater susceptibility to infections.
There are few studies dealing with the effect of
riboflavin deficiency upon antibody formation, and
these suggest that this is decreased. Although
deficiency of this vitamin is accompanied by a
decrease in lymphocytes, this cytologic change
has not been correlated with the impairment of
antibody manufacture.
4. Vitamin B6: Pyridoxine, deficiency produces a
much more complete inhibition of the immune
response. Some experiments showed that in
pyridoxine deficient rats there was a poor
production of antibody to sheep red cells (Stoerk
and Eisen, 1946) and this was associated with a
reduction of lymphoid tissue mass. In later studies
the pyridoxine deficient animals were shown to
have impaired responses to antigenic stimuli such
as human red cells, diphtheria toxoid & influenza
virus. Hypersensitivity reactions also reduced in
this vitamin deficiency.
Delayed type hypersensitivity in vitamin B6
deficiency was also shown to be depressed in
 Kavitha and others
experiments with skin grafts; vitamin deficient mice
did not reject grafts as readily as control mice on
a normal diet. Vit B6 deficiency also involves in
the tumor suppression.
Three groups of observations have been made
on cellular metabolism during pyridoxine
deficiency which were thought to be related to
this responses. First there was reduction in the
synthesis of nucleic acid (DNA and RNA) in liver
& spleen. There is also a decreased protein
synthesis in the polysomes of these organs
(Axelrod and Trakatellis 1964). And there is
severe reduction in the number of antibody
forming cells.
The poor antibody response may indeed be part
of the generalized depression of protein
metabolism in liver and spleen. The vitamin acts
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as an apoenzyme and affects many enzyme
systems in protein and amino acid metabolism.
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Urinary tract infections occurs frequently in people
deficient in this vitamin. Acute pyridoxine
deficiency is deleterious to lymphoid cells.
Pyridoxine deficiency has been indicated recently
as permitting animals to accept homografts during
the intervals of the deficient state but efforts to
take advantage of this in man have failed.
5. Nicotinic Acid: Nicotinamide is the functional
group in coenzymes which act as hydrogen
carriers in the body. A deficiency of this substance
leads to pellagra. Among the symptoms
traditionally associated with pellagra are
inflammation of the tongue, gums and membranes
of the mouth and pharynx. The organisms of
vincent’s angina become very abundant
wherever the mucous membranes are involved
and several reports indicate that they disappear
following treatment with the vitamin. There is some
impairment of antibody formation in nicotinamide
deficiency.
6. Folic Acid: Folic acid deficiency reduces
antibody production in various animals to a
number of stimuli (Axelrod and Prozansky 1955).
It is needed to maintain the immune system. The
functioning of the immune system is severely
inhibited by folic acid deficiency and this is
probably mediated through a reduction in DNA
17
synthesis, resulting in impaired nuclear division.
Pteroylglutamic or folic acid is related chiefly to
the macrocytic anemias and pernicious anemia.
It is essential for the conversion of megaloblasts
into erythrocytes. In certain animals, including
the monkey and the rat, a deficiency of this
substance also depresses granulopoiesis, so that
only a small number of leukocytes are
manufactured. It might be imagine that the
depression of leukocyte formation would favour
susceptibility to a variety of microbes.
7. Biotin: Lack of this vitamin causes increased
susceptibility of rats and mice to salmonella & may
also depress the formation of antibodies.
8. Vitamin B12 (cyanacobalamine): In untreated
animals there was a correlation between the
serum concentration of vitamin B 12 and the
antibody concentration, whereas animals treated
with the vitamin B12 did not show this response.
In small intestine dietary vitamin B12 bound to an
intrinsic factor, a soluble receptor that participates
in the transport of vitamin across mucosa. In
autoimmune status associated with chronic
gastritis antibodies are found against the intrinsic
factor which effects the absorption of vitamin &
results in pernicious anemia.
9. Choline: The choline improves cellular immune
response. The choline supplementation at the
highest level (2000 mg/kg) increases the cellular
immune response which is measured as
lymphocyte migration inhibition (LMI). The choline
requirement for better health & immunity is more
than that required for optimum growth (Swain and
Johri, 2000).
10. Para Amino Benzoic Acid (PABA): This is
exceptional to all vitamins. Excessive amounts
are beneficial in rickettsial infections of animals &
man. This effect may be the result of stimulation
of the metabolism of the host’s cells, for rickettsiae
propagation, optimally when cellular respiration
is at a low level. A deficiency in this vitamin is
said to decrease susceptibility to malaria.
The deficiency of the B complex vitamins cause
1. Decrease in complement. 2. reduction of
leukocytes in peritoneal-induced exudates &
 Kavitha and others
reduced cellular migration to areas of
inflammation.
Thus all of vitamins function in the body in
improving the immune status. They can be used
as alternatives to antibiotic feeding to animals.
So that livestock products from Indian sub-
continent can compete with international market.
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