Pentanoate modulates B cells to suppress allergic contact hypersensitivity

Allergic contact dermatitis (ACD) is a common T cell-mediated hypersensitivity reaction affecting the skin after exposure to an allergen. ACD is managed by antihistamines or steroids and avoiding exposure to allergens. Pentanoate is a short chain fatty acid with a therapeutic potential to modulate lymphocytes to secrete interlukin-10 (IL-10). Although IL-10 producing B cells are known to reduce inflammatory response, their role in ACD remains poorly understood. This study aims to investigate how B cells respond during ACD and how pentanoate influences them. Trinitrochlorobenzen (TNCB) was used to develop an in vivo model of contact hypersensitivity (CHS) in mice. Ear swelling and cellular analysis were used to examine allergic inflammatory reactions. Using flow cytometry, the B and T cell subsets were examined. Data showed that the central memory T cell subset and total CD4 + T cells significantly increased during recurrent CHS responses. Concurrently, there was a significant decrease in regulatory T cell subsets, marginal reduction in regulatory B cells, and naïve T cells during recurrent CHS. In vitro stimulation of B cells with pentanoate lead to their activation to produce IL-10. Adoptive transfer of these pentanoate-stimulated B cells into CHS mouse model diminished inflammatory response significantly. These findings highlight the ability of pentanoate in modulation of CHS responses by enhancing IL-10-production by B cells, indicating its potential therapeutic relevance for allergic contact dermatitis.

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Publication Details

Journal
Scientific Reports
Published
2025-10-14
DOI
https://doi.org/10.1038/s41598-025-19886-8
Citations
2
Primary Topic
Asthma and respiratory diseases
Type
article
Field-Weighted Citation Impact
2.33

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article

Pentanoate modulates B cells to suppress allergic contact hypersensitivity

Sherif M. Karam, Subi Sugathan, Yasir Waheed, Khalid Muhammad et al.
2 citations
Scientific Reports
Asthma and respiratory diseases
2.33
article

Pentanoate modulates B cells to suppress allergic contact hypersensitivity

Sherif M. Karam, Subi Sugathan, Yasir Waheed, Khalid Muhammad, Hidaya Abdul Kader, Dhanya Saraswathiamma, Sadiya Sadiq Shiek, Sara Alhmoudi, Khushbakhat Alia, Yusra Al Dhaheri
article en
2 citations

Abstract

Allergic contact dermatitis (ACD) is a common T cell-mediated hypersensitivity reaction affecting the skin after exposure to an allergen. ACD is managed by antihistamines or steroids and avoiding exposure to allergens. Pentanoate is a short chain fatty acid with a therapeutic potential to modulate lymphocytes to secrete interlukin-10 (IL-10). Although IL-10 producing B cells are known to reduce inflammatory response, their role in ACD remains poorly understood. This study aims to investigate how B cells respond during ACD and how pentanoate influences them. Trinitrochlorobenzen (TNCB) was used to develop an in vivo model of contact hypersensitivity (CHS) in mice. Ear swelling and cellular analysis were used to examine allergic inflammatory reactions. Using flow cytometry, the B and T cell subsets were examined. Data showed that the central memory T cell subset and total CD4 + T cells significantly increased during recurrent CHS responses. Concurrently, there was a significant decrease in regulatory T cell subsets, marginal reduction in regulatory B cells, and naïve T cells during recurrent CHS. In vitro stimulation of B cells with pentanoate lead to their activation to produce IL-10. Adoptive transfer of these pentanoate-stimulated B cells into CHS mouse model diminished inflammatory response significantly. These findings highlight the ability of pentanoate in modulation of CHS responses by enhancing IL-10-production by B cells, indicating its potential therapeutic relevance for allergic contact dermatitis.

Scientific ReportsVol. 15(1)
United Arab Emirates University (AE), Near East University (CY), National University of Sciences and Technology (PK)
United Arab Emirates University
Openalex Percentile: Top 10%
Asthma and respiratory diseases
2.33
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