<<snip>>
Lactoferrin may be a useful agent to accelerate restoration of immune
responsiveness
<<snip>>

Stem Cells and Development
Lactoferrin Accelerates Reconstitution of the Humoral and Cellular
Immune Response During Chemotherapy-induced Immunosuppression and Bone
Marrow Transplant in Mice
Oct 2005, Vol. 14, No. 5: 548-555

J. Artym
Department of Experimental Therapy, Institute of Immunology and
Experimental Therapy of the Polish Academy of Sciences, Wroclaw,
Poland.
M. Zimecki
Department of Experimental Therapy, Institute of Immunology and
Experimental Therapy of the Polish Academy of Sciences, Wroclaw,
Poland.
J. Kuryszko
Department of Histology and Embriology, Wroclaw Agriculture University,
Wroclaw, Poland.
Dr. M.L. Kruzel
Department of Integrative Biology and Pharmacology, University of
Texas, Health Science Center at Houston, TX 77030.
Experimental evidence from previous studies supports the conclusion
that orally administered lactoferrin (LF) restores the immune response
in mice treated with a sublethal dose of cyclophosphamide (CP). The aim
of this study was to elucidate potential benefit of LF in mice
undergoing chemotherapy with busulfan (BU) and CP, followed by
intravenous (i.v.) injection of bone marrow cells. CBA mice were
treated orally with busulfan (4 mg/kg) for 4 consecutive days, followed
by two daily doses of CP delivered intraperitoneally (i.p.) at a dose
of 100 mg/kg and reconstituted next day with i.v. injection of 107
syngeneic bone marrow cells. One group of these mice was given LF in
drinking water (0.5% solution). After treatment, mice were immunized
with ovalbumin (OVA) to subsequently measure delayed type
hypersensitivity responsiveness and with sheep red blood cells to
determine humoral immunity by evaluation of splenic antibody-forming
cells. As expected, both humoral and cellular immune responses of mice
that were treated with these chemotherapeutic agents was markedly
impaired. Here we report that this impairment was remarkably attenuated
by oral administration of LF. Humoral immunity fell to levels that were
66-88% lower than that of untreated animals. Humoral immunity of
LF-treated animals was equivalent to that of untreated mice within 1
month. Cellular immune responses were inhibited by chemotherapy
treatment to a lesser degree, reaching levels that were approximately
50% lower than those of untreated animals. Again, LF mitigated this
decrease, resulting in responses that were only slightly lower than
those observed in untreated animals. Furthermore, when mice were given
a lethal dose of BU (4 × 25 mg daily doses, i.p.) followed by a bone
marrow transplant, LF caused enhanced lympho-, erythro-, and
myelopoiesis in the bone marrow and appearance of transforming splenic
lymphoblasts, similar to effects caused by administration of
recombinant human granulocyte-macrophage colony-stimulating factor
(GM-CSF). In summary, our study suggests that LF may be a useful agent
to accelerate restoration of immune responsiveness induced by
chemotherapy in bone marrow transplant recipients

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