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EN
INTRODUCTION: Cell adhesion molecules on neutrophils and monocytes play an important role in the immunity of newborns. MATERIAL AND METHODS: Eighty-two premature infants (47 with early-onset infection and 35 without infection, 37 male and 45 female, 40 delivered vaginally and 42 by Caesarean section) between the 3rd and 7th day of life were assessed for the expression rate of CD11a, CD11b, CD11c, CD18 CD54 and CD62L on granulocytes and monocytes using a Becton Dickinson FACS Canto II flow cytometer. Both groups were analysed for sex, body weight, gestational age, type of delivery and infection, and correlations between adhesion molecules were identified. RESULTS: Preterm infants with infection had a significantly higher mean CD62L level than preterm infants without infection. There was also a positive correlation between gestational age and CD11b and CD11c, as well as correlations between CD11b and CD11c, CD11b and CD54, and CD11c and CD54U. In preterm infants without infection, there was a significant correlation between body weight and CD11a level, and correlations between CD11a and CD18, as well as CD11a and CD54. The sex of the preterm infants and type of delivery in both groups had no significant effect on the mean levels of the analysed molecules. There was no significant relationship between the expression of the analysed molecules and the CRP concentration and platelet count in preterm infants with infection. CONCLUSIONS: 1. Early-onset infection in premature infants promotes increased expression of the CD62L molecule, which despite the lack of correlation with the CRP concentration and platelet count may prove useful in the diagnosis of infections. 2. CD11b expression in preterm infants with infections is affected by gestational age, while the expression of CD11a in preterm infants without infections is correlated with body weight. 3. Expression of the analysed molecules in premature neonates does not depend on sex or type of delivery.
PL
WSTĘP: Molekuły adhezji komórkowej na neutrofilach i monocytach odgrywają ważną rolę w odporności noworodków. MATERIAŁ I METODY: U 82 wcześniaków (47 z zakażeniem wczesnym i 35 bez zakażeń; 37 płci męskiej i 45 żeńskiej; 40 urodzonych siłami natury i 42 cięciem cesarskim) między 3 a 7 dobą życia dokonano oceny odsetka ekspresji CD11a, CD11b, CD11c, CD18, CD54 i CD62L na granulocytach i monocytach krwi cytometrem przepływowym Becton Dickinson FACS Canto II, z uwzględnieniem płci, masy ciała, wieku płodowego wcześniaków, typu porodu i zakażenia, oraz określono wzajemne korelacje między molekułami. WYNIKI: U wcześniaków z zakażeniem stwierdzono istotne statystycznie zwiększenie średniego odsetka CD62L niż u wcześniaków bez zakażeń, dodatnie korelacje między wiekiem płodowym a CD11b i CD11c oraz wzajemne korelacje między CD11b i CD11c, CD11b i CD54 oraz CD11c i CD54. U wcześniaków bez zakażeń wykazano znamienną zależność między masą ciała a CD11a oraz korelacje między CD11a i CD18 oraz CD11a i CD54. Płeć wcześniaków i typ porodu w obu grupach nie miały istotnego wpływu na średnie wartości badanych molekuł. Wykazano brak istotnych zależności między ekspresją badanych molekuł a stężeniem CRP i liczbą płytek krwi u chorych wcześniaków. WNIOSKI: 1. Wczesne zakażenia u wcześniaków sprzyjają zwiększeniu ekspresji molekuły CD62L, co mimo braku korelacji ze stężeniem CRP i liczbą płytek krwi może dowodzić przydatności oznaczania tej molekuły w diagnostyce zakażeń. 2. Na wartość ekspresji CD11b u wcześniaków z zakażeniem wpływa wiek płodowy, a na CD11a masa ciała u wcześniaków bez zakażeń. 3. Ekspresja badanych molekuł u wcześniaków nie zależy od ich płci i typu porodu.
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2002
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vol. 49
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issue 2
393-406
EN
Synthetic analogs of vitamin D for potential use in differentiation therapy should selectively regulate genes necessary for differentiation without inducing any perturbations in calcium homeostasis. PRI-1906, an analog of vitamin D2, and PRI-2191, an analog of vitamin D3 bind nuclear vitamin D receptor (nVDR) with substantially lower affinity than 1,25-dihydroxyvitamin D3 (1,25-D3), but have higher differentiation-inducing activity as estimated in HL-60 leukemia cell model. To examine how their increased differentiation-inducing activity is regulated we tested the hypothesis that membrane-mediated events, unrelated to nVDR, take part in the differentiation in response to PRI-1906 and PRI-2191. The induction of leukemia cell differentiation in response to the analogs of vitamin D was inhibited by LY294002 (phosphatidylinositol 3-kinase inhibitor), PD98059 (inhibitor of MEK1,2, an upstream regulator of extracellular-signal regulated kinase) and rapamycin (p70S6K inhibitor) pointing out that activation of signal transduction pathways unrelated to nVDR is necessary for differentiation. On the other hand, inhibition of cytosolic phospholipase A2 accelerated the differentiation of HL-60 cells induced by either 1,25-D3 or by the vitamin D analogs suggesting possible existence of a feedback loop between extracellular-signal regulated kinases and phospholipase A2.
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