We investigated the presence of factors in human milk that inhibit invasion of pathogenic bacteria. The effect of human milk fat globule membrane (HMFGM) components on adhesion of cloned S-fimbriated Escherichia coli to human buccal epithelial cells was analyzed. S fimbriae are a common feature of E. coli strains causing sepsis and meningitis in newborns and are bound to epithelia via sialyl-(a-2-3)galactoside structures. Human milk fat globules (HMFG) could be agglutinated by the above-mentioned bacteria. Agglutination could be inhibited by fetuin, human glycophorin, and al-acid glycoprotein. In addition, pretreatment of HMFG with Vibrio chokrae neuraminidase markedly reduced bacterium-induced agglutinations, indicating the involvement of neuraminic acid-containing glycoproteins. In contrast, lipid droplets of infant formula or artificial lipid emulsions (Intralipid) could not be agglutinated. HMFG were present in stools of breast-fed neonates as shown by indirect immunofluorescence staining with a monoclonal antibody directed against carbohydrate residues present on HMFGM. These HMFG could be agglutinated by bacteria. HMFG inhibited E. coli adhesion to buccal epithelial cells. To further characterize relevant E. coli binding structures, HMFGM components were separated by gel chromatography. The mucin fraction showed the most pronounced inhibitory effect on adhesion of S-fimbriated E. coli to human buccal epithelial cells. Our data suggest that HMFG inhibit bacterial adhesion in the entire intestine and thereby may provide protection against bacterial infection.
S-fimbriated Escherichia coli strains cause sepsis and meningitis in newborns and are known to recognize the carbohydrate sequence sialyl-(α2-3)-galactoside. We show that adhesion of cloned S-fimbriated E. coli to human epithelial cells is inhibited Fab independently by sialyloligosaccharides on secretory immunoglobulin A (s-IgA). This indicates an anti-infective function of s-IgA (Fc), particularly in early human milk.
The aim of o w studies is to identify genes involved in the pathogenesis of common variable immunodeficiency (CVI). One of our CVI patients with severely depressed mitogen response and defective B cell differentiation in response to T cell dependent and T cell independent stimulators, shows in addition a reduced CD 25 (IL 2 receptor) expression after T cell stimulation with mitogen. CD 25 expression is lacking on T cells and an EBV-immortalized B cell line (BCL) in response to stimulation with phorbol ester PMA, an activator of protein kinase C (PKC). Binding studies with phnrbol ester on patient's BCL show that PKC is expressed at slightly increased numbers and affinity. Inhibition studies of proliferative responses t o T cell mitogens with protein kinase inhibitors (H7, H8, HA1004) indicate that PKC is altered in patient's T cells. Om hypothesis is ,that immunodeficiency in this patient is causedby an alteration in a subspecies of PKC affecting activation of lymphocytes. This report synthesizes the updated results of a longitudinal study of chronic type B hepatitis including 87 untreated,antidelta negative children(46 with active,37 with persistent hepati tis and 4 with cirrhosis) followed for 2-13 years(mean 6+3 y.).-Of the 76 cases who were initially HBeAg and HBV DNA positive,59 (77X)terminated HBV replication and achieved sustained biochemical remission.0f 1 1 cases who were anti-HBe positive on entry, all 3 HBV DNA positive terminated replication,9 normalized ALT, while both cases with persistent liver damage had antibodies to hepatitis C virus(HCV).Overall 5 children eventually cleared HBs Ag,while liver histology was improved in all cases with previous active hepatitis or cirrhosis.During follow-up,however,routine alphafetoprotein testing made possible the diagnosis of hepatocellular carcinoma in an asymptomatic boy with cirrhosis. These data show that most children with chronic hepatitis B terminate HBV replication before reachins adulthood and become asymptomatic HBsAg carriers with normal ALT.Superinfection with HCV has to be considerad in patients with increased ALT after loss of HBV DNA.Periodica1 alphafetoprotein testing may help the early diagnosis of carcinoma. Universities of Padua,Genoa and Turin.Prodotti Roche, Nilan.Italy. To evaluate the effect of recombinant alpha 2a interFeron(1FN) in Italian children with HBeAg and HBV DNA positive chronic type B hepatitis,Cwo studies have been conducted:l)a multicentre randomized,controlled trial using 3?lU IFN thrice weekly for 6 months, 2) an observational study using 9YU thrice weekly for 6 months. The controlled study included 36 children,aged 3-14 years,vith active (12 cases),persistent (21 cases)or minimal hepatitis,that were randomly assigned to either treatment or control group (18 cases each).All patients completed the treatment schedule and a 6-months follow-up.At 12 months j ( 2 7 % ) treated patients and 3(lfX) controls were HBV DNA negative and 3(16%) and one patient,respeccively,had lost HBeAg.Only one patient had a significant .XT flare 4...
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