As locomotive organelles, flagella allow bacteria to move toward favorable environments. A flagellum consists of three parts: the basal structure (rotary motor), the hook (universal joint), and the filament (helical propeller). For ages, flagella have been generally regarded as important virulence factors, mainly because of their motility property. However, flagella are getting recognized to play multiple roles with more functions besides motility and chemotaxis. Recent evidence has pinpointed that the bacterial flagella participate in many additional processes including adhesion, biofilm formation, virulence factor secretion, and modulation of the immune system of eukaryotic cells. This mini-review summarizes data from recent studies that elucidated how flagella, as a virulence factor, contribute to bacterial pathogenicity.

Influenza A (H1N1) virus, a high-risk infectious pathogen, can cause severe acute lung injury leading to significant morbidity and mortality. Angiotensin-converting enzyme 2 (ACE2), a negative regulator of the renin-angiotensin system (RAS), plays a protective role in pathogenesis of acute lung injury. Here, we showed that ACE2 protein levels were significantly downregulated after infection with H1N1 viruses but was dispensable for viral replication. ACE2 protein downregulation was most likely related to ACE2 protein degradation by proteasome pathway rather than ACE2 shedding. Finally, we found that ACE2 cleavage could be regulated by influenza neuraminidase (NA), which was fundamentally different from the classically sheddase-induced proteolytic cleavage of ACE2.

Accumulating data have suggested exosome-delivered microRNAs (miRNAs) play critical role in carcinogenesis and cancer progression. However, little is known about the influence of exosomal miR-6803-5p on the development and prognosis of colorectal cancer (CRC). Levels of serum exosomal miR-6803-5p were determined by microarray analysis and verified by quantitative real-time PCR (qRT-PCR). Outcomes of overall survival (OS) and disease-free survival (DFS) of CRC patients were estimated by Kaplan-Meier analysis. We used cox regression analysis to investigate the association between exosomes-encapsulated miR-6803-5p and the clinicopathological factors of CRC patients. The exosomal miR-6803-5p was significantly increased in serum samples from patients with CRC in contrast to healthy controls. Significantly higher levels of serum exosomal miR-6803-5p were observed in CRC patients at later TNM stage or with lymph node metastasis as well as liver metastasis. Patients with elevated levels of serum exosomal miR-6803-5p had much poorer OS and DFS. Cox regression analysis revealed high levels of exosomal miR-6803-5p was associated with poor prognosis in CRC independent of other confounding factors. Thus, exosomal miR-6803-5p is a potential diagnostic and prognostic biomarker for patients with CRC.

Heat-labile toxin (LT) is a well-characterized powerful enterotoxin produced by enterotoxigenic Escherichia coli (ETEC). This toxin is known to contribute to diarrhea in young children in developing countries, international travelers, as well as many different species of young animals. Interestingly, it has also been revealed that LT is involved in other activities in addition to its role in enterotoxicity. Recent studies have indicated that LT toxin enhances enteric pathogen adherence and subsequent intestinal colonization. LT has also been shown to act as a powerful adjuvant capable of upregulating vaccine antigenicity; it also serves as a protein or antigenic peptide display platform for new vaccine development, and can be used as a naturally derived cell targeting and protein delivery tool. This review summarizes the epidemiology, secretion, delivery, and mechanisms of action of LT, while also highlighting new functions revealed by recent studies.

Psoriasis is a chronic inflammatory skin disease characterized by abnormal proliferation of epidermal keratinocytes and infiltration of inflammatory cells. CRNN is a major component of the cornified cell envelope and implicated in several epithelial malignancies. Here, we show that CRNN expression was increased in the lesioned epidermis from the patients with psoriasis vulgaris and skin lesions from the imiquimod (IMQ)-treated mice. Expression of CRNN in cultured keratinocytes (HEKa and HaCaT) was also induced by M5, a mixture of five pro-inflammatory cytokines (i.e., IL-17A, IL-22, IL-1a, oncostatin M, and TNF-a). Lentiviral expression of CRNN increased cell proliferation by inducing cyclin D1. Conversely, knockdown of CRNN by small interfering RNA suppressed G1/S transition and attenuated the M5-induced proliferation. In addition, CRNN overexpression increased the phosphorylation and activation of phosphoinositide 3-kinase and Akt. Inactivation of the phosphoinositide 3-kinase and Akt pathways using small interfering RNA or selective inhibitors (LY294002 and MK2206) reduced the proliferative effects of CRNN. Furthermore, topical use of anti-psoriatic calcipotriol effectively decreased expression of CRNN, inhibited the Akt activation and improved the IMQ-stimulated psoriasis-like pathologies. Taken together, these results suggest that induced expression of CRNN may contribute to the pathogenesis of psoriasis.