Effect of oral administration of kefir on serum proinflammatory cytokines on 5-FU induced oral mucositis in patients with colorectal cancer.

In order to investigate the effect of kefir consumption on mucositis induced by 5-FU based chemotherapy (CT), we monitored the systemic immune response by measurement of the serum proinflammatory cytokine levels and we evaluated the anti-microbial effect of kefir with an agar diffusion method. Forty patients with colorectal cancer were included in this randomized prospective study. On the first 5 days of each CT cycle, the study group received oral lavage with kefir and then swallowed 250 ml of kefir while control group received oral lavage with 0.09% NaCl twice a day. Before and after every cycle of CT, the oral mucosa was assessed. Serum proinflammatory cytokine levels were evaluated before the initiation and after the third and the sixth cycle. Kefir was administered in 99 out of 205 courses. Mucositis developed in 27.3% of the courses given with kefir administration and in 21.7% of the courses given with 0.9% NaCl oral rinses. The difference between the two groups was not statistically significant (p > 0.05). When we compared the serum proinflammatory cytokine levels of the two groups at the baseline and following the third and the sixth cycles, we again found no statistically significant difference (p > 0.05). Kefir consumption at the mentioned doses made no statistically significant effect on serum proinflammatory cytokine levels and on the incidence of mucositis development in cancer patients. Under in vitro conditions, kefir inhibits only Staphylococcus epidermidis.

Effect of the function of polymorphonuclear leukocytes and interleukin-1 beta on wound healing in patients with diabetic foot infections.

OBJECTIVES: This study was carried out prospectively to determine the effect on prognosis of phagocytic activity index (PAI) and intracellular killing activity (IKA) of polymorphonuclear leukocytes (PMNL), and the levels of interleukin-1 beta (IL-1beta) on prognosis in patients with diabetic foot infection (DFI). METHODS: The evaluation of PAI and IKA in PMNL and the levels of IL-1beta were performed at the beginning and in the second and fourth weeks of therapy in all diabetic patients, who were categorized into a healing group (HG) and a non-healing group (NHG) on the basis of therapy results. RESULTS: Sixty-six cases (38 diabetic patients and 28 non-diabetic controls) were included in the study. Full recovery was observed in 23 HG patients, whereas 15 (NHG) patients were unresponsive to treatment and nine patients were subjected to amputation at the end. At the baseline, PAI, IKA and IL-1beta levels in HG were not significantly different compared to those of NHG, but at weeks 2 and 4, PAI and IKA levels were significantly higher and IL-1beta levels were significantly lower than those in NHG. On the other hand, at the baseline, PAI and IKA values in HG were significantly lower and IL-1beta levels were significantly higher in comparison with the controls. However, no significant difference was observed at week 2 or 4. CONCLUSION: Our results suggest that the PMNL functions and IL-1beta regulation deteriorated in patients with DFI, and that such deteriorations might indicate inefficient therapeutic responses in patients with diabetes mellitus.

Effect of fluconazole on human polymorphonuclear leucocyte functions ex vivo against Candida albicans.

Polymorphonuclear leucocytes (PMNs) are important components of host defence against fungi. We investigated the ex vivo effect of fluconazole on chemotaxis, adherence, superoxide anion (O-2) generation and intracellular killing of Candida albicans blastoconidia after the administration of fluconazole (300 mg per os) to healthy volunteers. With regard to chemotaxis in response to zymosan-activated serum (ZAS), as measured using an agarose gel technique, fluconazole neither increased, nor decreased the chemotaxis of PMNs. The adherence was significantly enhanced after exposure of PMNs to fluconazole under ex vivo conditions, whereas, O-2 production after stimulation of PMNs with ZAS was not affected by fluconazole. The effect of fluconazole on intracellular killing of C. albicans blastoconidia by PMNs was determined by viable colony count, after release of yeast cells from disturbed neutrophils. Fluconazole under in vitro conditions, at a therapeutic concentration, significantly increased the intracellular killing of C. albicans by PMNs at 30 min when compared with the results obtained in ex vivo experiments (p < 0.001). During 90 min of exposure, no significant difference was found between in vitro and ex vivo conditions (p > 0.05).