Dataset Information

Recent advances in understanding and treating scabies.

ABSTRACT: Scabies is an infestation of the skin caused by the mite Sarcoptes scabiei. In 2017, scabies was recognised by the World Health Organisation as a disease of public importance and was consequently added to the list of neglected tropical diseases. An estimated 200 million people currently have scabies worldwide. Scabies is endemic in many developing countries, with the highest prevalence being in hot, humid climates such as the Pacific and Latin American regions. Scabies causes a host immune response which is intensely itchy. Scratching of the lesions can lead to secondary bacterial infections of the skin, such as impetigo, most commonly caused by Streptococcus pyogenes or Staphylococcus aureus. This can have fatal consequences, such as septicaemia, glomerulonephritis, and rheumatic heart disease. Advances over the past 5 years indicate that mass drug administration is an effective strategy to treat scabies. This review will outline advances in the mite biology, epidemiological understanding, diagnosis, and treatment of scabies.

SUBMITTER: Welch E

PROVIDER: S-EPMC8009191 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Vitiligo, an acquired depigmentation disorder, manifests as white macules on the skin and can cause significant psychological stress and stigmatization. Recent advances have shed light on key components that drive disease onset and progression as well as therapeutic approaches. Vitiligo can be triggered by stress to the melanin pigment-producing cells of the skin, the melanocytes. The triggers, which range from sunburn to mechanical trauma and chemical exposures, ultimately cause an autoimmune response that targets melanocytes, driving progressive skin depigmentation. The most significant progress in our understanding of disease etiology has been made on three fronts: (1) identifying cellular responses to stress, including antioxidant pathways and the unfolded protein response (UPR), as key players in disease onset, (2) characterizing immune responses that target melanocytes and drive disease progression, and (3) identifying major susceptibility genes. The current model for vitiligo pathogenesis postulates that oxidative stress causes cellular disruptions, including interruption of protein maturation in the endoplasmic reticulum (ER), leading to the activation of the UPR and expression of UPR-regulated chemokines such as interleukin 6 (IL-6) and IL-8. These chemokines recruit immune components to the skin, causing melanocytes to be targeted for destruction. Oxidative stress can further increase melanocyte targeting by promoting antigen presentation. Two key components of the autoimmune response that promote disease progression are the interferon (IFN)-?/CXCL10 axis and IL-17-mediated responses. Several genome-wide association studies support a role for these pathways, with the antioxidant gene NRF2, UPR gene XBP1, and numerous immune-related genes including class I and class II major histocompatibility genes associated with a risk for developing vitiligo. Novel approaches to promote repigmentation in vitiligo are being investigated and may yield effective, long-lasting therapies.

Dataset Information

Recent advances in understanding and treating scabies.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets