Lactoferrin ameliorates symptoms of experimental encephalomyelitis in Lewis rats.

Lactoferrin (LF) is a multifunctional protein present in secretory fluids of mammals and circulating neutrophils. Beside anti-inflammatory properties, LF was found to inhibit some autoimmune disorders. In this investigation we studied effects of oral administration of LF on experimental autoimmune encephalomyelitis (EAE) in Lewis rats. LF was given in drinking water as 0.25% solution beginning the day of elicitation of EAE or with a seven-day delay. The effects of LF were evaluated by the following criteria: clinical score, lymph node cell number, serum cytokine levels and histopathological changes. We found that LF treatment led to a significant acceleration of the recovery process, particularly on days 16-18 following elicitation of EAE. The delayed administration of LF was less effective in reducing the score of EAE. In addition, cell number of the inguinal lymph nodes of untreated EAE rats, almost 3 times higher as compared with control, naïve rats, was normalized by LF treatment. Furthermore, LF decreased elevated serum concentrations of tumor necrosis factor alpha and transforming growth factor beta. The histological analysis of the spinal cord revealed reduction in the number and size of inflammatory foci in LF-treated rats. In summary, treatment of EAE Lewis rats with LF reduced the clinical symptoms and accelerated the recovery of animals.