Epidemiologic reports routinely indicate that the high rate of HIV-1 transmission via mucosal exposure has been relatively stable since the epidemic began. Unfortunately, research on mucosal immune responses to HIV-1 has not been done in proportion to its importance. Most knowledge about immune responses against HIV-1 in humans comes from studies limited to the use of peripheral blood cells and plasma. Consequently, T-cell-based HIV-1 vaccines have long been considered a primary end point of preventive therapeutic strategies. The interest in HIV-1 exposed uninfected individuals has intensified because of the lessons to be learned about a natural immunologic response that promotes opposition to the infection. Such information has useful applications in the clinical setting. This review describes the current status of research on mucosal immune responses to HIV-1 from examining mucosal fluids and tissues of sexually exposed uninfected adults.
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http://dx.doi.org/10.1615/critrevimmunol.v29.i5.10 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Center for Nutritional Sciences, Food Science and Human Nutrition Department, College of Agricultural and Life Sciences, University of Florida, Gainesville, FL 32611.
Documented worldwide, impaired immunity is a cardinal signature resulting from loss of dietary zinc, an essential micronutrient. A steady supply of zinc to meet cellular requirements is regulated by an array of zinc transporters. Deletion of the transporter Zip14 (Slc39a14) in mice produced intestinal inflammation.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Institute of Medical Microbiology, Rheinisch-Westfälische Technische Hochschule Aachen University Hospital, Aachen 52074, Germany.
Postnatal establishment of enteric metabolic, host-microbial and immune homeostasis is the result of precisely timed and tightly regulated developmental and adaptive processes. Here, we show that infection with the invasive enteropathogen Typhimurium results in accelerated maturation of the neonatal epithelium with premature appearance of antimicrobial, metabolic, developmental, and regenerative features of the adult tissue. Using conditional Myd88-deficient mice, we identify the critical contribution of immune cell-derived mediators.
View Article and Find Full Text PDFVet Med Sci
January 2025
Department of Virology, Faculty of Veterinary Medicine, Van Yuzuncu Yil University, Van, Turkey.
Background: Bovine viral diarrhoea virus (BVDV) infection, caused by Pestiviruses A and B, with various clinical findings and causes significant economic losses. This disease is common in Turkey as well as in other countries, especially in European countries.
Objective: This study was designed to determine the genotypes of BVDVs and their variability among cattle in eastern Turkey.
Curr Gastroenterol Rep
December 2025
Division of Pulmonary, Critical Care, and Sleep Medicine, Medical College of Wisconsin, 8701 West Watertown Plank Road, 8th Floor: HUB for Collaborative Medicine, Milwaukee, WI, 53226, USA.
Purpose Of Review: The purpose of this narrative review is to describe the mechanisms for gut dysfunction during critical illness, outline hypotheses of gut-derived inflammation, and identify nutrition and non-nutritional therapies that have direct and indirect effects on preserving both epithelial barrier function and gut microbiota during critical illness.
Recent Findings: Clinical and animal model studies have demonstrated that critical illness pathophysiology and interventions breach epithelial barrier function and convert a normally commensal gut microbiome into a pathobiome. As a result, the gut has been postulated to be the "motor" of critical illness and numerous hypotheses have been put forward to explain how it contributes to systemic inflammation and drives multiple organ failure.
Ecotoxicol Environ Saf
January 2025
Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Pusan National University, Yangsan, Republic of Korea; Biomedical Research Institute, Pusan National University, Busan, Republic of Korea; Graduate Program of Genomic Data Sciences, Pusan National University, Yangsan, Republic of Korea; Program of Total Foodtech and PNU-Korea Maritime Institute (KMI) Collaborative Research Center, Busan, Republic of Korea. Electronic address:
Deoxynivalenol (DON), a prevalent mycotoxin produced by Fusarium species, contaminates global agricultural products and poses significant health risks, particularly to the gastrointestinal (GI) system. DON exposure disrupts ribosomal function, inducing stress responses linked to various inflammatory diseases, including inflammatory bowel disease (IBD). In this study, we elucidate a novel regulatory mechanism involving ribosomal proteins (RPs) RPL13A and RPS3, which mediate proinflammatory chemokine production in DON-exposed gut epithelial cells.
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