In vitro neutralization of IL-6 receptor exacerbates damage to intestinal epithelial cells during Mycobacterium avium paratuberculosis infection Article Swipe
Ala’ Alhendi
,
Saleh A. Naser
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.3389/fimmu.2024.1412800
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.3389/fimmu.2024.1412800
Like TNFα, IL-6 is upregulated in Crohn’s disease (CD) especially in patients associated with Mycobacterium avium paratuberculosis (MAP) infection, and both cytokines have been targeted as a therapeutic option for the treatment of the disease despite the accepted partial response in some patients. Limited response to anti-IL-6 receptor-neutralizing antibodies therapy may be related to the homeostatic dual role of IL-6. In this study, we investigated the effects and the signaling mechanism of IL-6 involved in intestinal epithelial integrity and function during MAP infection using an in vitro model that consists of THP-1, HT-29 and Caco-2 cell lines. Clinically, we determined that plasma samples from MAP-infected CD patients have higher IL-6 levels compared to controls (P-value < 0.001). In CD-like macrophages, MAP infection has significantly upregulated the secretion of IL-6 and the shedding of (IL-6R) from THP-1 macrophages, P-value < 0.05. Intestinal cell lines (Caco-2 and HT-29) were treated with the supernatant of MAP-infected THP-1 macrophages with or without a neutralizing anti-IL-6R antibody. Treating intestinal Caco-2 cells with supernatant of MAP-infected macrophages resulted in significant upregulation of intestinal damage markers including claudin-2 and SERPINE1/PAI-1. Interestingly, blocking IL-6 signaling exacerbated that damage and further increased the levels of the damage markers. In HT-29 cells, MAP infection upregulated MUC2 expression, a protective response that was reversed when IL-6R was neutralized. More importantly, blocking IL-6 signaling during MAP infection rescued damaged Caco-2 cells from MAP-induced apoptosis. The data clearly supports a protective role of IL-6 in intestinal epithelia integrity and function especially in CD patients associated with MAP infection. The findings may explain the ineffective response to anti-IL6 based therapy and strongly support a therapeutic option that restores the physiologic level of IL-6 in patient’s plasma. A new treatment strategy based on attenuation of IL-6 expression and secretion in inflammatory diseases should be considered.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.3389/fimmu.2024.1412800
- https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1412800/pdf
- OA Status
- gold
- Cited By
- 2
- References
- 43
- Related Works
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- OpenAlex ID
- https://openalex.org/W4401405616
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4401405616Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.3389/fimmu.2024.1412800Digital Object Identifier
- Title
-
In vitro neutralization of IL-6 receptor exacerbates damage to intestinal epithelial cells during Mycobacterium avium paratuberculosis infectionWork title
- Type
-
articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
- Publication date
-
2024-08-07Full publication date if available
- Authors
-
Ala’ Alhendi, Saleh A. NaserList of authors in order
- Landing page
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https://doi.org/10.3389/fimmu.2024.1412800Publisher landing page
- PDF URL
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https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1412800/pdfDirect link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1412800/pdfDirect OA link when available
- Concepts
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Paratuberculosis, In vitro, Microbiology, Neutralization, Mycobacterium avium complex, Immunology, Mycobacterium, Biology, Virology, Antibody, Bacteria, Biochemistry, GeneticsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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2Total citation count in OpenAlex
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2025: 1, 2024: 1Per-year citation counts (last 5 years)
- References (count)
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43Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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