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New Insights into the Use of Mouse Models for the Study of Skin Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 2015

Special Issue Editor

Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
Interests: mouse models; skin disorders; epithelia; sensory nerve; immune cell; ion channel; GPCR; cytokines; neurotransmitters

Special Issue Information

Dear Colleagues,

The skin is the largest organ of the body. The skin and its derivatives (hair, nails, sweat and oil glands), as well as numerous cell types (epithelial keratinocytes, innate and adaptive immune cells, melanocytes, and sensory nerves), make up the integumentary system, which maintains the skin barrier, interplays between the host and the external environment and protects the body from external nocious stimuli. Although recent studies have begun to elucidate the molecular, cellular and signling pathways that underlie physiological functions and the development of pathological conditions in the skin, the lack of critical mouse models for mechanistical studies has severely limited the development of new therapies for effectively treating skin disorders. In this Special Issue, we invite authors to submit original research and review articles that will contribute to a better understanding of the following topics: newly developed mouse models of various skin disorders, skin lesions, skin cancer, sensory disorders (pain and itch), sensitive skin, immune disregulation in the skin, skin infection, skin neuroendocrinology, skin hypertrophy and skin pigmentation.

Dr. Jing Feng
Guest Editor

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Keywords

  • pain
  • itch
  • inflammation
  • endocrine
  • infection
  • hypertrophy
  • aging
  • hair loss
  • wound healing

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Published Papers (1 paper)

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Research

16 pages, 2916 KiB  
Article
Chronic Morphine Treatment and Antiretroviral Therapy Exacerbate HIV-Distal Sensory Peripheral Neuropathy and Induce Distinct Microbial Alterations in the HIV Tg26 Mouse Model
by Danielle Antoine, Irina Chupikova, Richa Jalodia, Praveen Kumar Singh and Sabita Roy
Int. J. Mol. Sci. 2024, 25(3), 1569; https://doi.org/10.3390/ijms25031569 - 26 Jan 2024
Cited by 2 | Viewed by 1515
Abstract
Distal Sensory Peripheral Neuropathy (DSP) is a common complication in HIV-infected individuals, leading to chronic pain and reduced quality of life. Even with antiretroviral therapy (ART), DSP persists, often prompting the use of opioid analgesics, which can paradoxically worsen symptoms through opioid-induced microbial [...] Read more.
Distal Sensory Peripheral Neuropathy (DSP) is a common complication in HIV-infected individuals, leading to chronic pain and reduced quality of life. Even with antiretroviral therapy (ART), DSP persists, often prompting the use of opioid analgesics, which can paradoxically worsen symptoms through opioid-induced microbial dysbiosis. This study employs the HIV Tg26 mouse model to investigate HIV-DSP development and assess gut microbiome changes in response to chronic morphine treatment and ART using 16S rRNA sequencing. Our results reveal that chronic morphine and ART exacerbate HIV-DSP in Tg26 mice, primarily through mechanical pain pathways. As the gut microbiome may be involved in chronic pain persistence, microbiome analysis indicated distinct bacterial community changes between WT and Tg26 mice as well as morphine- and ART-induced microbial changes in the Tg26 mice. This study reveals the Tg26 mouse model to be a relevant system that can help elucidate the pathogenic mechanisms of the opioid- and ART-induced exacerbation of HIV-associated pain. Our results shed light on the intricate interplay between HIV infection, ART, opioid use, and the gut microbiome in chronic pain development. They hold implications for understanding the mechanisms underlying HIV-associated pain and microbial dysbiosis, with potential for future research focused on prevention and treatment strategies. Full article
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