Neutropenia is a common and often dose limiting side effect of some chemotherapy regimens. The aim of this study was to investigate the ability of an immunomodulator, glycosaminylmuramyl dipeptide (GMDP, CAS 78113-36-7, romurtide) to reduce chemotherapy induced neutropenia. BALB/c mice were treated with 200 mg kg-1 cyclophosphamide (CY) to induce a reversible neutropenia lasting approximately 6-7 days. There was no change in the duration or depth of neutropenia in mice treated with GMDP for 3 consecutive days (2.5 or 25 mg kg-1) starting the day after CY injection. In addition, at the doses used, the time of administration of GMDP relative to CY did not alter this response. However, a marked neutrophilia compared to controls was consistently observed in all cases. Neutrophil counts of up to 14 times the baseline value were measured 6-7 days after the induction of neutropenia. GMDP had no effect in the absence of CY. Less variation was seen in white cell counts of older non-SPF mice treated with CY. When the activity of GMDP (5 mg kg-1) was compared with G-CSF (granulocyte colony stimulating factor, 100 micrograms kg-1) in these animals, GMDP showed a consistent trend to reduce the length of neutropenia, however, under the conditions tested only G-CSF treatment resulted in a significant reduction in the duration of neutropenia. In the 12-week-old mice, the neutrophilia seen with both G-CSF and GMDP was much smaller than in the 8-week-old mice, and was not significantly different from that in control mice treated with CY alone.
Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the
Caucasian race, generally leading to death in early adulthood.1 The
frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations,
1:2000 in African-Americans, and practically non-existent in Asian populations. The
disease occurs in about 1 in every 2500 life births of the white population. Mean
survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in
treatment. The genetic defect causes a pathological electrolyte transport through the
cell membranes by a defective chloride channel membrane transport protein [cystic
fibrosis transmembrane conductance regulator (CFTR)]. With respect to the function,
this affects mainly the exocrine glands of secretory cells, sinuses, lungs, pancreas,
liver, and the reproductive tract of the human body leading to a highly viscous,
water-depleted secretion. The secretion cannot leave the glands and in consequence
causes local inflammation and destruction of various organs. The main symptoms include
chronic inflammatory pulmonary disease with a progressive loss of lung function,
exocrine and sometimes endocrine pancreas insufficiency, and an excessive salt loss
through the sweat glands.1 A summary of the signs and symptoms of CF will
be given with a special emphasis on the effect of exercise performance and
capacity.
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