Distinctive Craniofacial and Oral Anomalies in MN1 C-terminal Truncation Syndrome.

MN1 C-terminal truncation (MCTT) syndrome was first reported in 2020 and only 28 patients have been recorded to date. Since MCTT syndrome is a newly defined and rare syndrome with many clinical features, the present study reviewed the manifestations and management of oral and dental anomalies. Gene variants of MCTT syndrome and their positive phenotypes were summarised. The phenotypes of variants in two exons differed from each other mainly in the craniomaxillofacial region, including brain MRI abnormalities and palatal morphology. Pathogenic mechanisms, especially in craniofacial and oral anomalies, were discussed. Appropriate treatments in the stomatology and respiratory departments could improve the symptoms of MCTT syndrome. The different sites of MN1 gene variants may influence the clinical symptoms and there may be racial differences in MCTT syndrome. We recommend oral and pulmonary evaluations for the multidisciplinary treatment of MCTT syndrome.

Monoclonal antibody against l-lectin module of SraP blocks adhesion and protects mice against Staphylococcus aureus challenge.

BACKGROUND/PURPOSE: SraP is a serine-rich repeat protein (SRRP) from Staphylococcus aureus that binds to sialylated receptors to promote bacterial adhesion to and invasion into host epithelial cells, mediated by the l-lectin module of its ligand-binding region. METHODS: The sequence encoding the L-lectin module of SraP was inserted into pET28a plasmid, and the recombinant protein was purified by His label affinity chromatography. A monoclonal antibody (mAb) against the l-lectin module was obtained and confirmed by enzyme-linked immunosorbent assay and western blotting. The effect of the mAb on S. aureus adhesion and invasion was assessed in A549 cells and mice subjected to S. aureus challenge. RESULTS: We successfully obtained a mAb against the l-lectin module of SraP. Pre-incubation with the mAb dramatically inhibited the bacteria's ability to adhere to and invade A549 cells. Moreover, mice administered mAb through tail vein injection had significantly fewer bacteria in the blood. CONCLUSION: The anti-SraPL-Lectin mAb significantly reduced the adherence and invasion of S. aureus to host cells. This study lays the foundation for the future development of the l-lectin module of SraP as a target for the prevention and treatment of S. aureus infection. Our findings suggest that specific subdomains of SRRPs may represent potential antibacterial drug targets for intervention.