Urinary tract infections (UTIs) are among the most common inflammatory diseases. Acute UTIs are typically caused by type 1-piliated Escherichia coli and result in urothelial apoptosis, local cytokine release, and neutrophil infiltration. To examine the urothelial apoptotic response, a human urothelial cell line was incubated with various E. coli isolates and was then characterized by flow cytometry. Uropathogenic E. coli (UPEC) induced rapid urothelial apoptosis that was strictly dependent upon interactions mediated by type 1 pili. Interestingly, nonpathogenic HB101 E. coli expressing type 1 pili induced apoptosis at approximately 50% of the level induced by UPEC, suggesting that pathogenic strains contribute to apoptosis by pilus-independent mechanisms. Consistent with this possibility, UPEC blocked activity of an NF-B-dependent reporter in response to inflammatory stimuli, yet this effect was independent of functional type 1 pili and was not mediated by laboratory strains of E. coli. UPEC suppressed NF-B by stabilizing IB␣, and UPEC rapidly altered cellular signaling pathways. Finally, blocking NF-B activity increased the level of piliated HB101-induced apoptosis to the level of apoptosis induced by UPEC. These results suggest that UPEC blocks NF-B and thereby enhances type 1 pili-induced apoptosis as a component of the uropathogenic program.Urinary tract infections (UTIs) are among the most common infectious diseases, resulting in over 7 million clinic visits annually in the United States alone (7) and causing significant morbidity and mortality. The majority of UTIs are due to ascending infections of the urinary bladder (cystitis) by Escherichia coli that expresses type 1 pili, fibrous organelles that mediate attachment to mannosylated host cell proteins (reviewed in reference 19). The infection process results in bladder inflammation that causes symptoms such as pain and frequent or urgent voiding. Given the emergence of antibiotic-resistant strains of uropathogenic E. coli (UPEC) (A. J. Schaeffer, Editorial, Curr. Opin. Urol. 10:23-24, 2000), a more thorough understanding of pathogenic mechanisms is necessary to identify novel therapeutic targets for the treatment and prevention of UTIs.A key feature of inflammation during UTIs is a disruption of the urothelial integrity due to the exfoliation and subsequent excretion of superficial urothelial cells (4). Studies with mice have shown that UPEC induces a rapid loss of superficial urothelial cells, and the sloughing of superficial cells is due to the induction of apoptosis (12). This apoptotic process is dependent upon the expression of intact type 1 pili, since fimH mutant UPEC strains lacking the adhesin subunit FimH that forms the pilus tip fail to induce apoptosis, yet laboratory strains of E. coli induce apoptosis if they express intact type 1 pili. As a result of the urothelial apoptotic response, clearance of a majority of UPEC from the bladder occurs during voiding of urine. Thus, urothelial apoptosis is considered to be an important host defense in r...

While adults' energy intake misreporting is a well-documented phenomenon, relatively little is known about the nature and extent of misreporting among children and adolescents. Children's and adolescents' dietary reporting patterns are likely to be distinct because of their ongoing cognitive and social development. These developmental differences present unique challenges to aspects of dietary reporting, such as food knowledge, portion size estimation and response editing. This review of 28 articles describes energy intake misreporting among children and adolescents. Like adults, children and adolescents tended to underreport energy, with the largest biases observed with food records. Even when mean reported energy intake was close to its expected value, approximately half of all individuals were classified as misreporters, and overreporting appeared to be more common than it is among adults. Associations between numerous characteristics and misreporting were explored in the literature, with the most consistent findings for age and adiposity. Two predictors for adults, gender and social desirability, were not consistent factors among children and adolescents. The review concludes by highlighting knowledge gaps and recommendations for future research and practice.

Uropathogenic Escherichia coli (UPEC), the most frequent cause of urinary tract infection (UTI), is associated with an inflammatory response which includes the induction of cytokine/chemokine secretion by urothelial cells and neutrophil recruitment to the bladder. Recent studies indicate, however, that UPEC can evade the early activation of urothelial innate immune response in vitro. In this study, we report that infection with the prototypic UPEC strain NU14 suppresses tumor necrosis factor alpha (TNF-␣)-mediated interleukin-8 (CXCL-8) and interleukin-6 (CXCL-6) secretion from urothelial cell cultures compared to infection with a type 1 piliated E. coli K-12 strain. Furthermore, examination of a panel of clinical E. coli isolates revealed that 15 of 17 strains also possessed the ability to suppress cytokine secretion. In a murine model of UTI, NU14 infection resulted in diminished levels of mRNAs encoding keratinocyte-derived chemokine, macrophage inflammatory peptide 2, and CXCL-6 in the bladder relative to infection with an E. coli K-12 strain. Furthermore, reduced stimulation of inflammatory chemokine production during NU14 infection correlated with decreased levels of bladder and urine myeloperoxidase and increased bacterial colonization. These data indicate that a broad phylogenetic range of clinical E. coli isolates, including UPEC, may evade the activation of innate immune response in the urinary tract, thereby providing a pathogenic advantage.Urinary tract infections (UTI) are most frequently caused by an ascending colonization of the bladder and/or kidneys by Escherichia coli (9, 33). Infection of the urinary tract results in an inflammatory response characterized by increased levels of urinary cytokines and neutrophil influx (1, 13-15). The innate immune response to infection by uropathogenic E. coli (UPEC) depends upon activation of host pattern recognition receptors of the Toll-like receptor pathway, including Toll-like receptor 4 (TLR4) (5,16,(37)(38)(39). Recognition of E. coli lipopolysaccharide (LPS) by urothelial cells that express TLR4 results in activation of the proinflammatory and prosurvival NF-B pathway and secretion of chemokines/cytokines, including CXCL-6 and CXCL-8 (2). The resulting accumulation of inflammatory chemokines in the bladder mucosa and urine during UTI induces the recruitment of neutrophils, which leads to the clearance of bacteria and resolution of infection. Infection of the urinary tract by UPEC also induces adaptive immune responses characterized by humoral and cell-mediated responses which protect against future infection (42).Many pathogenic bacterial species possess the ability to modulate the innate immune response to evade host defenses and promote colonization, including several that block the activation of the NF-B pathway (7,31,32,35,36). We previously reported that UPEC strain NU14 blocks activation of the NF-B pathway and thereby promotes apoptosis (26,27). Insertional mutation of the genes encoding the periplasmic chaperone SurA or the LPS biosynthetic oper...

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The Healthy, Hunger-Free Kids Act of 2010 updated the nutrition standards in the National School Lunch and School Breakfast Programs (NSLP and SBP) and expanded universal free meals’ availability in low-income schools. Past studies have shown that school meals are an important resource for children in food-insecure households. This analysis used data from the School Nutrition and Meal Cost Study to classify students as food insecure (FI), marginally secure (MS), or food secure (FS). Diet quality from school and nonschool foods that students consumed was assessed using Healthy Eating Index (HEI)-2010 scores. Chi-squared and two-tailed t-tests were conducted to compare school meal participation, students’ energy intakes, and diet quality across food security groups. FI and MS students were significantly more likely to participate in NSLP than FS students (79%, 71%, and 49%, respectively). SBP participation followed a similar pattern but was lower (38% FI, 33% MS, and 16% FS). Compared to FS students, FI and MS students more likely attended schools offering SBP, universal free meals, or afterschool snacks and suppers. School meals contributed significantly more energy to FI and MS students’ diets than to FS students (22%, 20%, and 13%, respectively). All groups’ dietary intakes from school foods were of higher quality than non-school foods. These findings highlight the role of school meals in meeting the energy and diet quality needs of FI and MS students.