Untreated and Enzyme-Modified Bovine Whey Products Reduce Association of Salmonella Typhimurium, Escherichia coli O157:H7 and Cronobacter malonaticus (formerly Enterobacter sakazakii) to CaCo-2 Cells

Adhesion of a micro-organism to a cell surface is often considered to be the first step in pathogenesis. Inhibiting this process may have therapeutic effects in vivo. This study investigates the inhibitory effects of various bovine whey products on the association of Salm. Typhimurium, E. coli O157:H7 and C. malonaticus (formerly Enterobacter sakazakii) to the human CaCo-2 cell line. Invasion of CaCo-2 cells by Salm. Typhimurium and C. malonaticus was also examined

The Effect of Untreated and Enzyme-Treated Commercial Dairy Powders on the Growth and Adhesion of Streptococcus mutans

Dental caries is a common bacterial infection, but the progression of this disease can be delayed by preventing initial attachment of cariogenic bacteria such as Streptococcus mutans to tooth surfaces. This study firstly compares the effect of untreated (UT) and enzyme-treated (ET) dairy powders on the adherence of S. mutans to hydroxylapatite (HA), an analogue of tooth enamel. A fluorescence-based method was used to quantify adherence of S. mutans to HA both in the presence (S-HA) and absence (PBS-HA) of saliva. Secondly, binding of proteins present in the test materials to HA was quantified using bicinchonic acid assays and SDS-PAGE. In addition, the effect of UT and ET dairy powders on growth of S. mutans was examined using an optical-density based assay. UT acid whey protein concentrate (WPC) 80, sweet WPC80, buttermilk powder (BMP) and cream powder (CP) significantly (P < 0.05) inhibited adhesion of S. mutans at ≥31.25 μg mL−1 in the presence and absence of saliva. ET dairy powders were less effective inhibitors of adhesion, but ET sweet WPC80 significantly (P < 0.05) inhibited growth of S. mutans at ≥0.6 mg mL−1. Therefore, due to their adherence- and growth-inhibitory properties, dairy powders may be beneficial in the treatment of dental caries

Determination of the Effect of Dairy Powders on Adherence of Streptococcus sobrinus and Streptococcus salivarius to Hydroxylapatite and Growth of these Bacteria

Dental caries is a highly prevalent disease caused by colonisation of tooth surfaces by cariogenic bacteria, such as Streptococcus sobrinus and Streptococcus salivarius. Reducing initial adherence of such bacteria to teeth may delay onset of caries. Many foods, such as milk, can inhibit microbial adherence. In this investigation, the effect of untreated (UT) and enzyme-treated (ET) dairy powders on adherence of S. sobrinus and S. salivarius to hydroxylapatite (HA), an analogue of tooth enamel, was examined. Untreated (UT) acid whey protein concentrate (AWPC) 80 inhibited streptococcal adherence to phosphate-buffered saline-coated HA (PBS-HA) and saliva-coated HA (S-HA) by >80% at ⩾31.25 μg mL−1. UT sweet WPC80, buttermilk powder and cream powder also significantly reduced adherence (P < 0.05). Enzyme-treatment of all dairy powders reduced their anti-adhesion activity. However, ET sweet WPC80 significantly inhibited growth of these streptococci (P < 0.05) at ⩾0.6 mg mL−1. Therefore, dairy powders may reduce progression of dental caries by their anti-adhesion and/or antibacterial activity

Adeno-associated virus 2 infection in children with non-A–E hepatitis

An outbreak of acute hepatitis of unknown aetiology in children was reported in Scotland1 in April 2022 and has now been identified in 35 countries2. Several recent studies have suggested an association with human adenovirus with this outbreak, a virus not commonly associated with hepatitis. Here we report a detailed case–control investigation and find an association between adeno-associated virus 2 (AAV2) infection and host genetics in disease susceptibility. Using next-generation sequencing, PCR with reverse transcription, serology and in situ hybridization, we detected recent infection with AAV2 in plasma and liver samples in 26 out of 32 (81%) cases of hepatitis compared with 5 out of 74 (7%) of samples from unaffected individuals. Furthermore, AAV2 was detected within ballooned hepatocytes alongside a prominent T cell infiltrate in liver biopsy samples. In keeping with a CD4+ T-cell-mediated immune pathology, the human leukocyte antigen (HLA) class II HLA-DRB1*04:01 allele was identified in 25 out of 27 cases (93%) compared with a background frequency of 10 out of 64 (16%; P = 5.49 × 10−12). In summary, we report an outbreak of acute paediatric hepatitis associated with AAV2 infection (most likely acquired as a co-infection with human adenovirus that is usually required as a ‘helper virus’ to support AAV2 replication) and disease susceptibility related to HLA class II status. © 2023, The Author(s), under exclusive licence to Springer Nature Limited

Genomic investigations of unexplained acute hepatitis in children

Since its first identification in Scotland, over 1,000 cases of unexplained paediatric hepatitis in children have been reported worldwide, including 278 cases in the UK1. Here we report an investigation of 38 cases, 66 age-matched immunocompetent controls and 21 immunocompromised comparator participants, using a combination of genomic, transcriptomic, proteomic and immunohistochemical methods. We detected high levels of adeno-associated virus 2 (AAV2) DNA in the liver, blood, plasma or stool from 27 of 28 cases. We found low levels of adenovirus (HAdV) and human herpesvirus 6B (HHV-6B) in 23 of 31 and 16 of 23, respectively, of the cases tested. By contrast, AAV2 was infrequently detected and at low titre in the blood or the liver from control children with HAdV, even when profoundly immunosuppressed. AAV2, HAdV and HHV-6 phylogeny excluded the emergence of novel strains in cases. Histological analyses of explanted livers showed enrichment for T cells and B lineage cells. Proteomic comparison of liver tissue from cases and healthy controls identified increased expression of HLA class 2, immunoglobulin variable regions and complement proteins. HAdV and AAV2 proteins were not detected in the livers. Instead, we identified AAV2 DNA complexes reflecting both HAdV-mediated and HHV-6B-mediated replication. We hypothesize that high levels of abnormal AAV2 replication products aided by HAdV and, in severe cases, HHV-6B may have triggered immune-mediated hepatic disease in genetically and immunologically predisposed children. © 2023, The Author(s)