ABSTRACT
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a complex systemic autoimmune disease characterized by small vessel vasculitis. Typically, the relapse rate is lower in patients with end-stage kidney disease (ESKD) than in those with chronic kidney disease, prior to dialysis. Here, we report a rare case of multi-organ relapse in a patient with myeloperoxidase (MPO)-AAV who underwent hemodialysis following coronavirus disease 2019 (COVID-19). A man in his 70s with type 2 diabetes and hypertension was undergoing maintenance hemodialysis for ESKD resulting from MPO-AAV glomerulonephritis. Following severe acute respiratory syndrome coronavirus 2 infection, the patient was hospitalized for persistent nausea and vomiting. No significant findings were observed, including in endoscopy. However, the patient experienced severe symptoms that hindered oral intake and was refractory to pharmacological therapy. Additionally, despite receiving antibiotics and antituberculosis treatment, the patient experienced persistent unexplained pleural effusion. Moreover, the patient's level of consciousness rapidly deteriorated during hospitalization. Although C-reactive protein levels and MPO-ANCA titers were elevated, no evidence of infection was detected on brain imaging or cerebrospinal fluid analysis. Therefore, we diagnosed this case as a relapse of AAV and promptly administered methylprednisolone pulse therapy and rituximab. Subsequently, all aforementioned symptoms in the patient improved, and the current ANCA levels remain negative. Thus, the relapse of AAV after COVID-19 is rare; however, it can present in several ways in patients undergoing dialysis. Therefore, clinicians should closely monitor ANCA titers and subtle symptoms, even in patients with dialysis-dependent AAV.
ABSTRACT
[This corrects the article DOI: 10.3389/fmicb.2018.02810.].
ABSTRACT
Outer membrane vesicles (OMVs) are spherical membranous structures released by Gram-negative bacteria. Several bacterial pathogens utilize OMVs as vehicles for the delivery of virulence factors into host cells. Results of our previous study on proteomic analysis revealed that OMVs isolated from Salmonella enterica serovar Typhimurium had virulence effectors that are known to be translocated by Salmonella pathogenicity island 1 (SPI-1)-encoded type III secretion system (T3SS1) into the host cell. In the present study, immunoblot analysis confirmed the secretion of the six T3SS1 effector proteins, namely SipB and SipC (translocators of T3SS1), and SipA, SopA, SopB, and SopE2 (effectors translocated by T3SS1), by OMVs. Results of proteinase K treatment revealed the localization of these T3SS1 effector proteins on the outer surface of OMVs. SipC and SopE2 were secreted by OMVs independent of the three secretion systems T3SS1, T3SS2, and flagella, signifying OMVs to be an alternative delivery system to T3SSs. T3SS1 effectors SipA, SipC, and SopE2 were internalized into the cytoplasm of the host cell by OMVs independent of cellular Salmonella-host cell contact. In epithelial cells, addition of OMVs harboring T3SS1 effectors stimulated the production of F-actin, thereby complementing the attenuated invasion of ΔsopE2 into host cells. These results suggest that S. Typhimurium might exploit OMVs as a long-distance vehicle to deliver T3SS1 effectors into the cytoplasm of the host cell independent of bacteria-host cell interaction.
