TY - JOUR
T1 - Investigating the release of inflammatory cytokines in a human model of incontinence-associated dermatitis
AU - Sofoklis Koudounas
AU - Dan L Bader
AU - Voegeli, David
N1 - Funding Information:
We would like to express our gratitude to all the participants involved in this study. This work was supported by a PhD studentship (SK) provided by the School of Health Sciences, Faculty of Environmental and Life Sciences, University of Southampton .
Funding Information:
This work was supported by a PhD studentship (SK) provided by the School of Health Sciences, Faculty of Environmental and Life Sciences, University of Southampton .
Publisher Copyright:
© 2021 Tissue Viability Society
PY - 2021/8/1
Y1 - 2021/8/1
N2 - Incontinence-associated dermatitis (IAD) is a painful complication in elderly patients, leading to reduced quality of life. Despite recent attention, its underlying inflammatory mechanisms remain poorly understood. This study was designed to quantify the release of inflammatory cytokines in a human model of IAD. The left volar forearm of ten healthy volunteers was exposed to synthetic urine and synthetic faeces for 2 h, simulating the effects of urinary and faecal incontinence, respectively, and the subsequent cytokine response compared to that of an untreated control site. Inflammatory cytokines were collected using both the Sebutape® absorption method and dermal microdialysis and quantified using immunoassays. Results from the former demonstrated an upregulation in IL-1α, IL-1RA and TNF-α. Synthetic urine caused a higher median increase in IL-1α from baseline compared to synthetic faeces, whereas synthetic faeces were associated with significantly higher median TNF-α levels compared to synthetic urine (p = 0.01). An increase in IL-1α/IL-1RA ratio was also observed with significant differences evident following exposure to synthetic urine (p = 0.047). Additionally, microdialysis revealed a time-dependent increase in IL-1β and IL-8 following exposure of up to 120 min to synthetic urine and synthetic faeces, respectively. This study demonstrated the suitability of both sampling approaches to recover quantifiable cytokine levels in biofluids for the assessment of skin status following exposure to synthetic fluids associated with incontinence. Findings suggest some differences in the inflammatory mechanisms of IAD, depending on moisture source, and the potential of the cytokines, IL-1α and TNF-α, as responsive markers of early skin damage caused by incontinence.
AB - Incontinence-associated dermatitis (IAD) is a painful complication in elderly patients, leading to reduced quality of life. Despite recent attention, its underlying inflammatory mechanisms remain poorly understood. This study was designed to quantify the release of inflammatory cytokines in a human model of IAD. The left volar forearm of ten healthy volunteers was exposed to synthetic urine and synthetic faeces for 2 h, simulating the effects of urinary and faecal incontinence, respectively, and the subsequent cytokine response compared to that of an untreated control site. Inflammatory cytokines were collected using both the Sebutape® absorption method and dermal microdialysis and quantified using immunoassays. Results from the former demonstrated an upregulation in IL-1α, IL-1RA and TNF-α. Synthetic urine caused a higher median increase in IL-1α from baseline compared to synthetic faeces, whereas synthetic faeces were associated with significantly higher median TNF-α levels compared to synthetic urine (p = 0.01). An increase in IL-1α/IL-1RA ratio was also observed with significant differences evident following exposure to synthetic urine (p = 0.047). Additionally, microdialysis revealed a time-dependent increase in IL-1β and IL-8 following exposure of up to 120 min to synthetic urine and synthetic faeces, respectively. This study demonstrated the suitability of both sampling approaches to recover quantifiable cytokine levels in biofluids for the assessment of skin status following exposure to synthetic fluids associated with incontinence. Findings suggest some differences in the inflammatory mechanisms of IAD, depending on moisture source, and the potential of the cytokines, IL-1α and TNF-α, as responsive markers of early skin damage caused by incontinence.
KW - Cytokines
KW - Incontinence
KW - Incontinence-associated dermatitis
KW - Inflammation
KW - Skin health
UR - http://www.scopus.com/inward/record.url?scp=85108056865&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/32c15985-4a5a-334a-becd-ff06c4fff30a/
U2 - 10.1016/j.jtv.2021.06.005
DO - 10.1016/j.jtv.2021.06.005
M3 - Article
VL - 30
SP - 427
EP - 433
JO - Journal of Tissue Viability
JF - Journal of Tissue Viability
SN - 0965-206X
IS - 3
ER -