The immune response to infection in the bladder
NATURE REVIEWS UROLOGY
Authors: Lacerda Mariano, Livia; Ingersoll, Molly A.
Abstract
The bladder is continuously protected by passive defences such as a mucus layer, antimicrobial peptides and secretory immunoglobulins; however, these defences are occasionally overcome by invading bacteria that can induce a strong host inflammatory response in the bladder. The urothelium and resident immune cells produce additional defence molecules, cytokines and chemokines, which recruit inflammatory cells to the infected tissue. Resident and recruited immune cells act together to eradicate bacteria from the bladder and to develop lasting immune memory against infection. However, urinary tract infection (UTI) is commonly recurrent, suggesting that the induction of a memory response in the bladder is inadequate to prevent reinfection. Additionally, infection seems to induce long-lasting changes in the urothelium, which can render the tissue more susceptible to future infection. The innate immune response is well-studied in the field of UTI, but considerably less is known about how adaptive immunity develops and how repair mechanisms restore bladder homeostasis following infection. Furthermore, data demonstrate that sex-based differences in immunity affect resolution and infection can lead to tissue remodelling in the bladder following resolution of UTI. To combat the rise in antimicrobial resistance, innovative therapeutic approaches to bladder infection are currently in development. Improving our understanding of how the bladder responds to infection will support the development of improved treatments for UTI, particularly for those at risk of recurrent infection. Lacerda Mariano and Ingersoll discuss how bacterial urinary tract infection affects the bladder, focusing on the development of immune responses and the cells and pathways that mediate immunity. They also highlight therapeutic approaches to bladder infection that are currently under development.
Iranian Registry of Infective Endocarditis (IRIE): Time to relook at the guideline, regarding to regional differences
IJC HEART & VASCULATURE
Authors: Sadeghpour, Anita; Maleki, Majid; Movassaghi, Massoud; Rezvani, Leila; Noohi, Feridoun; Boudagh, Shabnam; Ghadrdoost, Behshid; Bakhshandeh, Hooman; Alizadehasl, Azin; Naderi, Nasim; Kamali, Monireh; Ghavidel, Alireza A.; Peighambari, Mohammad Mahdi; Kyavar, Majid; Pasha, Hamidreza
Abstract
Aims: Infective endocarditis (IE) remained a potentially fatal disease with high rate of mortality and morbidity. The epidemiology and global burden of IE are largely different between the countries. We aimed to address the epidemiological aspects of IE in a tertiary hospital in Tehran, Iran. Methods and Results: Between 2006-2018, all adults patients with diagnosis of IE were enrolled in the Iranian Registry of Infective Endocarditis (IRIE). The data were analyzed using the chi(2), Kolmogorov-Smirnov, and Mann-Whitney U tests. Overall, 602 patients, 407 (67.6%) men, mean age 46 +/- 16 years were recruited. Positive blood culture found in 49%.The most common underlying heart diseases were: Congenital heart diseases (CHD) particularly bicuspid aortic valves (BAV) and ventricular septal defects (VSD) in 37%, followed by degenerative heart diseases : flail and mitral valve prolapse ( 16.3%), intravenous drug user in 12.6%, prosthetic valves in 11.1%, previous IE (8.9%), rheumatic heart diseases (RHD) in 8.4%. The most causative microorganisms were Staphylococcus aureus, Enterococci, coagulase-negative staphylococci and Streptococcus viridans. Cardiac or extra cardiac complications occurred in 56.6% of the patients. Conclusions: Based on IRIE, IE occurs in the younger population in Iran with high rates of blood culture-negative IE. RHD are not the main cause of IE in Iran, CHD including BAV and VSDs, followed by prolaptic or flail mitral valve were the most common. These 2 groups can be considered a high-risk group for IE. More than half of the patients with IE had cardiac or extra cardiac complications. (C) 2019 The Authors. Published by Elsevier B.V.