The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.
If you have any questions or comments, please contact us.
In high-income countries, the leading causes of death are noncommunicable diseases (NCDs), such as obesity, cancer, and cardiovascular disease. An important feature of most NCDs is inflammation-induced gut dysbiosis characterized by a shift in the microbial community structure from obligate to facultative anaerobes such as This microbial imbalance can contribute to disease pathogenesis by either a depletion in or the production of microbiota-derived metabolites. However, little is known about the mechanism by which inflammation-mediated changes in host physiology disrupt the microbial ecosystem in our large intestine leading to disease. Recent work by our group suggests that during gut homeostasis, epithelial hypoxia derived from peroxisome proliferator-activated receptor γ (PPAR-γ)-dependent β-oxidation of microbiota-derived short-chain fatty acids limits oxygen availability in the colon, thereby maintaining a balanced microbial community. During inflammation, disruption in gut anaerobiosis drives expansion of facultative anaerobic , regardless of their pathogenic potential. Therefore, our research group is currently exploring the concept that dysbiosis-associated expansion of can be viewed as a microbial signature of epithelial dysfunction and may play a greater role in different models of NCDs, including diet-induced obesity, atherosclerosis, and inflammation-associated colorectal cancer.
Copyright © 2020 American Society for Microbiology.
Vaccines have been incredibly successful at stemming the morbidity and mortality of infectious diseases worldwide. However, there are still no effective vaccines for many serious and potentially preventable infectious diseases. Advances in vaccine technology, including new delivery methods and adjuvants, as well as progress in systems biology and an increased understanding of the human immune system, hold the potential to address these issues. In addition, maternal immunization has opened an avenue to address infectious diseases in neonates and very young infants. This report summarizes the presentations from a 1-day symposium at the New York Academy of Sciences entitled "Innovative Vaccines against Resistant Infectious Diseases and Emerging Threats," held on May 20, 2019.
© 2019 New York Academy of Sciences.
Gut dysbiosis is associated with many non-communicable human diseases, but the mechanisms maintaining homeostasis remain incompletely understood. Recent insights suggest that during homeostasis, epithelial hypoxia limits oxygen availability in the colon, thereby maintaining a balanced microbiota that functions as a microbial organ, producing metabolites contributing to host nutrition, immune education and niche protection. Dysbiosis is characterized by a shift in the microbial community structure from obligate to facultative anaerobes, suggesting oxygen as an important ecological driver of microbial organ dysfunction. The ensuing disruption of gut homeostasis can lead to non- communicable disease because microbiota-derived metabolites are either depleted or generated at harmful concentrations. This Opinion article describes the concept that host control over the microbial ecosystem in the colon is critical for the composition and function of our microbial organ, which provides a theoretical framework for linking microorganisms to non-communicable diseases.
Cancer prevalence and mortality are high in developing nations, where resources for cancer control are inadequate. Nearly one-quarter of cancers in resource-limited nations are infection related, and molecular assays can capitalize on this relationship by detecting pertinent pathogen genomes and human gene variants to identify those at highest risk for progression to cancer, to classify lesions, to predict effective therapy, and to monitor tumor burden over time. Prime examples are human papillomavirus in cervical neoplasia, Helicobacter pylori and Epstein-Barr virus in gastric adenocarcinoma and lymphoma, and hepatitis B or C virus in hepatocellular cancer. Research is underway to engineer devices that overcome social, economic, and technical barriers limiting effective laboratory support. Additional challenges include an educated workforce, infrastructure for quality metrics and record keeping, and funds to sustain molecular test services. The combination of well-designed interfaces, novel and robust electrochemical technology, and telemedicine tools will promote adoption by frontline providers. Fast turnaround is crucial for surmounting loss to follow-up, although increased use of cell phones, even in rural areas, enhances options for patient education and engagement. Links to a broadband network facilitate consultation and centralized storage of medical data. Molecular technology shows promise to address gaps in health care through rapid, user-friendly, and cost-effective devices reflecting clinical priorities in resource-poor areas.
Copyright © 2014 American Society for Investigative Pathology and the Association for Molecular Pathology. Published by Elsevier Inc. All rights reserved.
Cancer survivors are at an elevated risk for infection because of immune suppression associated with prior cancer treatments, and they are at increased risk of complications from vaccine-preventable diseases. This section of the NCCN Guidelines for Survivorship provides recommendations for the prevention of infections in survivors through education, antimicrobial prophylaxis, and the judicious use of vaccines. These guidelines provide information about travel and gardening precautions and safe pet care/avoidance of zoonosis, and include detailed recommendations regarding vaccinations that should be considered and encouraged in cancer and transplant survivors.
Copyright © 2014 by the National Comprehensive Cancer Network.
Iron is an essential nutrient for both humans and pathogenic microbes. Because of its ability to exist in one of two oxidation states, iron is an ideal redox catalyst for diverse cellular processes including respiration and DNA replication. However, the redox potential of iron also contributes to its toxicity; thus, iron concentration and distribution must be carefully controlled. Given the absolute requirement for iron by virtually all human pathogens, an important facet of the innate immune system is to limit iron availability to invading microbes in a process termed nutritional immunity. Successful human pathogens must therefore possess mechanisms to circumvent nutritional immunity in order to cause disease. In this review, we discuss regulation of iron metabolism in the setting of infection and delineate strategies used by human pathogens to overcome iron-withholding defenses.
Copyright © 2013 Elsevier Inc. All rights reserved.
Whooping cough, due to Bordetella pertussis and Bordetella parapertussis, is an important cause of childhood morbidity and mortality. Despite widespread pertussis immunization in childhood, there are an estimated 50 million cases and 300,000 deaths due to pertussis globally each year. Infants who are too young to be vaccinated, children who are partially vaccinated and fully-vaccinated persons with waning immunity are especially vulnerable to disease. Since pertussis is one of the vaccine-preventable diseases on the rise, additional vaccine approaches are needed. These approaches include vaccination of newborns, additional booster doses for older adolescents and adults, and immunization of pregnant women with existing vaccines. Innovative new vaccines are also being studied. Each of these options will be discussed and their potential impact on pertussis control assessed.
OBJECTIVES - To examine whether prenatal exposure to perfluorooctanesulfonate (PFOS) or perfluorooctanoate (PFOA) is associated with the occurrence of hospitalization for infectious diseases during early childhood.
METHODS - We randomly selected 1400 pregnant women and their offspring from the Danish National Birth Cohort (1996-2002) and measured PFOS and PFOA levels in maternal blood during early pregnancy. Hospitalizations for infection of the offspring were identified by the linkage to the National Hospital Discharge Register through 2008.
RESULTS - Hospitalizations due to infections were not associated with prenatal exposure to PFOA and PFOS. On the contrary, the relative risks of hospitalizations ranged from 0.71 to 0.84 for the three higher quartiles of maternal PFOA levels compared with the lowest, but no dose-response pattern was found. No clear pattern was observed when results were stratified by child's age at infection, with the exception of an inverse association between maternal PFC levels and risk of hospitalization during the child's first year of life.
CONCLUSIONS - These findings suggest that prenatal exposure to PFOA or PFOS is not associated with increased risk of infectious diseases leading to hospitalization in early childhood.
Copyright © 2010 Elsevier Inc. All rights reserved.
Co-infections contribute to HIV-related pathogenesis and often increase viral load in HIV-infected people. We did a systematic review to assess the effect of treating key co-infections on plasma HIV-1-RNA concentrations in low-income countries. We identified 18 eligible studies for review: two on tuberculosis, two on malaria, six on helminths, and eight on sexually transmitted infections, excluding untreatable or non-pathogenic infections. Standardised mean plasma viral load decreased after the treatment of co-infecting pathogens in all 18 studies. The standardised mean HIV viral-load difference ranged from -0.04 log(10) copies per mL (95% CI -0.24 to 0.16) after syphilis treatment to -3.47 log(10) copies per mL (95% CI -3.78 to -3.16) after tuberculosis treatment. Of 14 studies with variance data available, 12 reported significant HIV viral-load differences before and after treatment. Although many of the viral-load reductions were 1.0 log(10) copies per mL or less, even small changes in plasma HIV-RNA concentrations have been shown to slow HIV progression and could translate into population-level benefits in lowering HIV transmission risk.
Copyright (c) 2010 Elsevier Ltd. All rights reserved.