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Cross-reactivity between cow’s milk and central and enteric nervous system antigens in the context of experimental autoimmune encephalomyelitis

Maurer, H;

Objectives: Multiple sclerosis (MS) is a chronic inflammatory disease of the central
nervous system (CNS). Previous studies have revealed that not only the CNS
exhibits degeneration, but also the enteric nervous system (ENS), which is
apparently affected even prior to the CNS. Interestingly, MS patients often suffer from
intestinal dysfunction and have independently reported a worsening of symptoms
upon consumption of specific food, especially milk. Here we aimed to investigate any
effects of milk on the ENS and the CNS in mice.
Design and Methods: Four groups of eight-week-old female C57BL/6 mice (n = 6)
were immunized with different milk proteins, including milk powder, β-lactoglobulin,
α-lactalbumin and casein. The brain, spinal cord, and the myenteric plexus of the
ENS were examined and evaluated by means of electron microscopy (EM) and light
microscopy. The electron micrographs were evaluated using three different criteria.
The number of axons of a certain area in cross-section was counted, the rate of
axolytic axons was determined and the size of the mitochondria was measured to
estimate the degree of degeneration. By ELISA, antigen-antibody reactions between
milk and brain proteins could be detected.
Observation and Results: In the ENS, degeneration could be detected in all groups,
but the casein-immunized mice showed the strongest degeneration of the myenteric
plexus. In the CNS, immunization with casein resulted in a severe demyelination and
loss of axons in the lumbar spinal cord. In addition, the animals developed a spastic
movement pattern of the hind limbs. In no other group such degeneration could be
detected. Myelin-associated glycoprotein (MAG) was confirmed by ELISA as a
possible target antigen of casein-specific antibodies.
Conclusion: Excessive consumption of milk could lead to degeneration of the ENS
and CNS through antibody formation and cross-reactivity with myelin proteins under
appropriate inflammatory conditions.