Dermal Infection
Dermal Infection - Related Videos
03:32
Generating Neurons by Reprogramming Human Dermal Fibroblast Cells
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2025
The video demonstrates the generation of neurons from adult human dermal fibroblasts (aHDFs). The aHDFs are reprogrammed using a lentiviral vector carrying genes for neuronal transcription factors and short hairpin RNAs (shRNAs). The shRNAs inhibit the expression of a neuronal transcriptional repressor, and the neuronal transcription factors activate genes to differentiate aHDFs into neurons. These reprogrammed aHDFs are cultured in an early and a late neuronal conversion medium to generate...
06:04
Murine Dermal Fibroblast Isolation by FACS
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Cited by 28 •
2016
Fibroblast behavior underlies a spectrum of clinical entities, but they remain poorly characterized, largely due to their inherent heterogeneity. Traditional fibroblast research relies upon in vitro manipulation, masking in vivo fibroblast behavior. We describe a FACS-based protocol for the isolation of mouse skin fibroblasts that does not require cell culture.
10:45
Deep Dermal Injection As a Model of Candida albicans Skin Infection for Histological Analyses
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Cited by 9 •
2018
Here we describe a protocol that allows histological and molecular analysis of skin samples after Candida albicans intradermal injection. This protocol maintains the structural integrity of the skin and allows for the localization of tissue-resident or newly recruited immune cells as well as the pathogen distribution.
05:52
Murine Dermal Lymphatic Endothelial Cell Isolation
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Cited by 1 •
2023
This paper describes a method for magnetic bead-based isolation of murine endothelial cells from dermal lymphatic capillaries. The isolated lymphatic endothelial cells can be used for downstream in vitro experiments and protein expression analysis.
11:40
Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature
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Cited by 7 •
2014
Neisseria meningitidis is a human specific pathogen that infects blood vessels. In this protocol human microvessels are introduced into a mouse by grafting human skin onto immunocompromised mice. Bacteria adhere extensively to the human vessels, leading to vascular damage and development of the purpuric rash typically observed in human cases.
FAQs
Entry through a wound or hair follicle creates a route past the skin’s protective barrier, allowing microorganisms to reach and multiply within tissue. The resulting interaction can remain localized or contribute to systemic disease. Comparing these entry points helps biology connect barrier integrity with infection risk and clinical severity.
Immune recognition initiates inflammation rather than serving as a passive response. Cytokine release helps coordinate the recruitment of defensive cells to the affected skin, creating a local biological response to invading microbes. Examining this sequence clarifies how host defenses shape tissue changes and may influence whether disease remains localized or becomes systemic.
Severity depends on more than the presence of a microorganism. Barrier disruption can permit continued interaction between microbes and tissue, while immune recognition can amplify inflammation through cytokine release and defensive-cell recruitment. This biology explains how a process beginning in skin may produce broader disease and why severity is an important research question.
These infections provide a setting for examining two linked processes: host–microbe interaction and restoration of damaged tissue. Microbial invasion challenges the barrier, while inflammation and defensive-cell recruitment alter the local environment in which repair occurs. Studying both processes helps biologists relate immune activity to tissue recovery rather than viewing infection as an isolated event.
Research connects the observable condition of infected skin with its biological causes, including bacterial, fungal, viral, or parasitic involvement, and with the host response. That connection supports more accurate diagnosis and better-informed wound management. It also helps investigators consider how barrier damage, inflammation, and whether disease remains localized or becomes systemic affect the problem being managed.
It is particularly valuable when infections are drug-resistant or recurrent, because those cases motivate the search for therapies beyond routine antimicrobial treatment. Understanding the responsible microorganism together with host inflammation and barrier disruption gives researchers biological targets to investigate. The same knowledge can also support infection prevention by identifying how disease develops.