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Abstracts from 2009 NASPGHAN Meeting in National Harbor, MD Journal of Pediatric Gastroenterology and Nutrition 49:E1–E103 # 2009 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Abstracts North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Annual Meeting November 12–14, 2009 National Harbor, Maryland (6.9 mM), VHTAPK (9.0 mM) and PDENK (9.0 mM), the THURSDAY, NOVEMBER 12, 2009 inhibition rate is 20.4%, 14.76% and 34.93%, respectively. 4. Peptide NPSRQERR has 2 positive charges. If decrease its positive charge from 2 to 0, the inhibition activity lost 12%; if increase the positive from 2 to 3, the inhibition Poster Session I activity increase 16.5%. 5. Peptide PDENK has 1 negative Cellular/Molecular Biology charge, if increase its negative charge from 1 to 3, the inhibition activity increase 17.16%; if decrease its negative 5:00 PM–7:00 PM charge, instead by 2 positive charges, the inhibition activity lost 15.78%. 1 LACTOBACILLUS GG SECRETES SMALL Conclusions: Lactobacillus GG peptide NPSRQERR, PEPTIDES THAT INHIBIT THE GROWTH OF VHTAPK and PDENK can inhibit not only Gram- ANTIBIOTIC-RESISTANT BACTERIA negative and Gram-positive bacteria growth, but also Ruiliang Lu, Alessio Fasano. Mucosal Biology Research antibiotics resistant Gram-negative and Gram-positive Center, University of Maryland School of Medicine, bacteria growth. Baltimore, MD. Background and Aims: We previous reported that seven 2 STUDIES ON THE REGULATION OF A TYPE small peptides from Lactobacillus GG conditional media IV PILI OF ETEC that exert anti-Gram-negative and Gram-positive bac- Bharani Pandrangi, Oscar Gomez-Duarte. Pediatrics, tericidal activity. Among them, peptide NPSRQERR, University of Iowa, Iowa City, IA. VHTAPK and PDENK have more activities than others. This research is to further explore if these peptides work Enterotoxigenic Escherichia coli (ETEC) is a leading on antibiotics resistant Gram-negative bacteria and cause of diarrhea in developing countries and an import- Gram-positive bacteria. ant cause of traveler’s diarrhea. Longus, a recently Methods: Peptides were synthesized, purified, iden- identified type IV pili, is one of the most prevalent pili tified and dissolved in different media. LGGCM in ETEC and believed to be involved in colonization. (19.7 Â 1012 CFU/mL) was used as positive control and Longus is a 20-mm polymer, 22 kDa, major structural media only as negative control. A600 measurement was subunit designated LngA. Longus pilus is plasmid used to test antibacterial activity. encoded in a 16 gene cluster and highly conserved among Results: 1. Peptide NPSRQERR (2.76 mM), VHTAPK ETEC strains. A regulatory region has been identified in (3.25 mM) and PDENK (3.31 mM) can inhibit kanamy- the Longus DNA cluster based on homology to other cine-resistant E. coli SM10 lpir (2.6 Â 1013 CFU/mL) regulatory proteins composed of two genes, lngR and growth. The inhibition rate is 43.75%, 29.45% and lngS. To further evaluate the regulatory system of longus, 68.54%, respectively. 2. Peptide NPSRQERR lngR, lngS, and promoter sequences were studied. (2.76 mM), VHTAPK (3.25 mM) and PDENK The genetic diversity of regulatory longus genes were (3.31 mM) can inhibit Tetracycline-resistant E. coli analyzed by DNA sequencing of multiple lngA positive TOPO10 (8.7 Â 1013 CFU/mL) growth. The inhibition rate ETEC strains. DNA sequence analysis with alignments is 69.08%, 48.53% and 81.4% respectively. 3. Methicillin- showed more similarity between lngR than lngS. At the resistant Staphylococcus aureus (MRSA) (2.89 Â protein level for Lng R only 1 out of 14 sequences 1014 CFU/mL) growth can be inhibited by NPSEQERR analyzed had multiple non-synonymous mutations. All E1 E2 of the lngR gene differences were within the animal to 46.7-fold ULN. LDL and HDL cholesterol were derived ETEC strain versus the human derived ETEC reduced. Mean CHT, ACE, HDL cholesterol and LDL strains. LngS had 37 nucleotide differences with respect cholesterol were correlated with severity of hepatome- to the E9034A published sequence which resulted in 19 galy. Pearson correlation coefficient 0.694 (P < 0.001), residue changes. 7 of the 19 residue changes were among 0.494 (P < 0.001), -0.319 (P ¼ 0.01) and -0.322 the animal versus human derived ETEC strains. LngS (P ¼ 0.01). Similar correlations were obtained using genes had multiple synonymous and nonsynonymous extent of splenomegaly and overall severity score index. mutations. Phylogenetic trees were then created for each ERT resulted in marked reduction of CHT and ACE and gene at the DNA and protein levels. Restriction analysis rise of HDL and LDL cholesterol. and ligation was performed for detection of promotor Conclusions: CHT is a promising biomarker for GD1 for regions within the longus cluster by cloning of the further validation in large patient population. Biomarkers promoters P1, P2, and P1-P1 inserts into the pcr2.1 are needed to track disease progression before irrevers- plasmid vector. Subsequent cloning into the vector ible complications arise. This could allow for optimizing pMLB1034, which contains a promoter-less beta-galac- of dosing of current medications as well as evaluating tosidase gene, tested for promoter expression. In sum- future medications in therapeutic trials. mary, lngR gene is conserved among human ETEC isolates while lngS is less conserved among animal 4 SODIUM BUTYRATE DOWNREGULATES and human ETECs, suggesting that differences in the INTESTINAL CFTR EXPRESSION longus gene regulation are likely mediated by lngS C. Alexander1,2, F. Ding1, N. Leleiko1,2,T.Paul1,2. regulation. Transcriptional fusion data shows that the 1Rhode Island Hospital, Providence, RI; 2Warren Alpert longus P2 DNA region has promoter activity and it School of Medicine, Brown University, Providence, RI. may drive expression of longus genes. Background and Aims: Butyrate (NaBu) decreases 3 AN EVALUATION OF SERUM BIOMAKERS intestinal chloride (Cl) and fluid secretion but the under- OF DISEASE BURDEN IN TYPE 1 GAUCHER lying mechanism is unknown. CFTR is a major regulator DISEASE of epithelial Cl and fluid secretion. NaBu can induce Philip B. Stein1, Hannah Yu2, Ruhua Yang1, Pramod K. activation and repression of target genes by different Mistry1. 1Pediatric GI, Yale New Haven Hospital, New mechanisms, including histone acetylation. Histone Haven, CT; 2Yale School of Medicine, New Haven, CT. acetylation can induce CFTR expression in intestinal epithelial cells. NaBu is known to downregulate CFTR Background and Aims: Gaucher disease (GD1) is an expression and associated anion and fluid secretion in inherited deficiency of lysosomal glucocerebrosidase airway epithelial cells. However, CFTR expression is (GBA1) that results in systemic accumulation of macro- tissue specific. The effect of NaBu on intestinal CFTR phages engorged with glucosylceramide-laden lyso- expression is unclear. The aim of this study was to somes. A complex phenotype results comprising determine the effect of NaBu treatment on CFTR expres- hepatosplenomegaly, failure to thrive, cytopenia, bone sion in HT29 colonic epithelial cells. involvement, and occasional cirrhosis. The standard of Methods: HT29 cells were treated with 2 mM and 5 mM care for GD1 is enzyme replacement therapy (ERT). NaBu for 24 and 48 hours. CFTR mRNA levels relative to Longitudinal follow-up of individual patients is challen- untreated controls were quantified by RT-PCR, normal- ging because of extreme heterogeneity. This limitation ized to 18s. Protein levels were evaluated by Western hinders determining optimal therapy. Availability of blot. Intestinal alkaline phosphatase (IAP) mRNA levels serum biomarkers of disease burden would address this were used as positive control for butyrate activity. Cell limitation. Aim- We examined the candidacy of several count and viability after treatment were evaluated. serum analytes as biomarkers of GD1. We searched for Results: NaBu treatment resulted in significant down- correlation of these analytes with indicators of disease regulation of CFTR mRNA, with the greatest decrease severity and response to ERT. noted with 5 mM at 24 hours. The Relative Quantities Methods: Baseline and post-ERT serum levels of chit- (RQ dRn) of CFTR mRNA relative to controls were 0.36 otriosidase (CHT), angiotensin converting enzyme (0.15-0.55) in 2 mM and 0.13 (0.02 to 0.24) in 5 mM (ACE), HDL, LDL, total cholesterol, and triglycerides samples at 24 h and 0.4 in 2 mM and 0.6 (0.4 to .88) in were measured in 75 GD1 patients. Markers of GD1 5 mM samples at 48 h. IAP mRNA levels were increased severity were assessed including liver and spleen size by in all NaBu treated samples. RQ dRn values were 29 MRI and bone disease by radiologic assessment. Based (21 to 39). There was no significant change in cell count on these results, a severity score was calculated. The or viability after NaBu treatment. serum markers were correlated with these measures. Conclusions: This is the first report of significant inhi- Results: Mean serum ACE levels were increased by 3- bition of intestinal CFTR expression by NaBu. The fold upper limit of normal (ULN). CHT was increased mechanisms by which this occurs may be complex. J Pediatr Gastroenterol Nutr, Vol. 49, Suppl 1, 2009 E3 Butyrate is a known HDAC inhibitor. However, HDAC 6 PHENOTYPIC CHARACTERIZATION OF inhibition by TSA results in upregulation of intestinal HUMAN PLACENTAL IMMUNE CELLS CFTR. Therefore, it is possible that other mediators of Christine E. Waasdorp Hurtado1, Michael Narkewicz1, butyrate activity such as PPARg activation may be Lucy Golden1, Mona Krull2, Hugo Rosen1. 1Gastroen- involved. Our future studies will aim to clarify further terology and Hepatology, University of Colorado, the complex transcriptional activity of NaBu. Denver, CO; 2OB, Denver Health, Denver, CO. Background and Aims: The placenta is vital to protec- 5 SECRETED PROBIOTIC FACTORS REDUCE tion of the fetus from infection. Placental membranes ENTEROCYTE INFLAMMATORY RESPONSE IN contain a maternal region (decidua), and a fetal region THE NEONATE (placenta).
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