SignificanceTo avoid the mucosal barrier and attach to the intestinal epithelium, enteric pathogens have evolved a unique proteinaceous fiber called type IVb pilus (T4bP). Despite its importance for bacterial pathogenesis, little is known about the adhesion mechanisms of T4bP, especially regarding the role of the minor pilin subunit located at its tip. Here, we show that the type IVb minor pilin CofB of CFA/III from enterotoxigenic Escherichia coli (ETEC) plays a role not only in T4bP assembly by forming a trimeric initiator complex, but also in bacterial adhesion by anchoring a secreted protein, CofJ, at the trimerization interface of H-type lectin domain. These findings expand our knowledge of T4P biology and provide important insights for developing therapeutics against ETEC infection.

Colonization of the host intestine is the most important step in Vibrio cholerae infection. The toxin-coregulated pilus (TCP), an operon-encoded type IVb pilus (T4bP), plays a crucial role in this process, which requires an additional secreted protein, TcpF, encoded on the same TCP operon; however, its mechanisms of secretion and function remain elusive. Here, we demonstrated that TcpF interacts with the minor pilin, TcpB, of TCP and elucidated the crystal structures of TcpB alone and in complex with TcpF. The structural analyses reveal how TCP recognizes TcpF and its secretory mechanism via TcpB-dependent pilus elongation and retraction. Upon binding to TCP, TcpF forms a flower-shaped homotrimer with its flexible N terminus hooked onto the trimeric interface of TcpB. Thus, the interaction between the minor pilin and the N terminus of the secreted protein, namely, the T4bP secretion signal, is key for V. cholerae colonization and is a new potential therapeutic target.

The most common genetic Creutzfeldt-Jakob disease (gCJD) in Japan is caused by a point mutation in which isoleucine replaces valine at codon 180 of the prion protein ( PrP ) gene (V180I gCJD). Evidence suggests that cerebral cortex swelling, which appears as abnormal hyperintensities on diffusion-weighted imaging (DWI), is a characteristic magnetic resonance imaging (MRI) finding of V180I gCJD. However, no study has directly compared the MRI findings between V180I gCJD and sporadic CJD (sCJD). The current study, therefore, aims to clarify the imaging features of V180I gCJD, which would lead to prompt genetic counselling and analysis of the PrP gene, particularly focusing on cerebral cortex swelling. We included 35 patients with sCJD ( n = 23) or V180I gCJD ( n = 12). Cerebral cortex swelling on T2-weighted imaging (T2WI) or fluid-attenuated inversion recovery (FLAIR) wherein abnormal cortical hyperintensities were observed on DWI, and the distribution of grey matter hyperintensities on DWI were visually evaluated. V180I gCJD patients had significantly more cerebral cortex swelling (100% vs. 13.0%, p < 0.001), an overall correct classification of 91.4%, and parahippocampal gyrus hyperintensities on DWI (100% vs. 39.1%, q = 0.019) than sCJD patients. Cerebral cortical hyperintensities on DWI with swelling on T2WI or FLAIR are characteristic imaging findings of V180I gCJD and are useful for differentiating it from sCJD.