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Purpose <p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease in which cytomegalovirus (CMV) reactivation has been linked to severe and steroid-refractory cases. However, the effect of CMV on cytokine regulation in UC remains unclear. This study investigated colonic and systemic cytokine profiles in CMV-positive and CMV-negative UC patients.</p> Methods <p>A total of 190 UC patients were enrolled, including 90 CMV-positive and 100 CMV-negative cases. CMV status was confirmed by molecular and histopathological tests. Colonic gene expression of cytokines (TNF-α, IL-1β, IL-6, IL-17&#xa0;A, IFN-γ, TGF-β, IL-8, IL-12, and RANTES) was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), and serum concentrations were assessed using enzyme-linked immunosorbent assay (ELISA).</p> Results <p>Demographic and clinical features were comparable between groups. CMV-positive patients showed higher colonic mRNA expression and serum concentrations of TNF-α, IL-1β, IL-6, and IL-17&#xa0;A compared to CMV-negative patients (all <i>p</i> &lt; 0.05). In contrast, IFN-γ, TGF-β, IL-8, IL-12, and RANTES did not differ significantly. Notably, CMV tissue viral load was significantly higher in patients with moderate to severe disease (Mayo score ≥ 6) and showed a positive correlation with plasma viral load (<i>r</i> = 0.664, <i>p</i> &lt; 0.01). Multivariable logistic regression analysis adjusted for Mayo score confirmed that elevated TNF-α, IL-1β, and IL-6 remained independently associated with CMV positivity. These findings indicate a selective pro-inflammatory cytokine pattern rather than generalized immune activation.</p> Conclusion <p>CMV infection in UC is associated with selective upregulation of pro-inflammatory cytokines at both mucosal and systemic levels. These findings highlight CMV as a potential driver of immune amplification in UC and support cytokine profiling as a tool for risk stratification and management of affected patients.</p>

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Cytomegalovirus infection drives a distinct mucosal and systemic cytokine signature in ulcerative colitis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月15日

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  • Nasim Izadi,
  • Masoud Shirmohammadi,
  • Nasser Ebrahimi Daryani,
  • Emad Behboudi,
  • Hossein Bannazadeh Baghi,
  • Mahin Ahangar Oskouee,
  • Shima Sadeghipoor,
  • Shaghayegh Yazdani,
  • Arezou Azadi,
  • Behrooz Naghili,
  • Mohammad Aghazadeh,
  • Vahdat Poortahmasebi

摘要

Purpose

Ulcerative colitis (UC) is a chronic inflammatory bowel disease in which cytomegalovirus (CMV) reactivation has been linked to severe and steroid-refractory cases. However, the effect of CMV on cytokine regulation in UC remains unclear. This study investigated colonic and systemic cytokine profiles in CMV-positive and CMV-negative UC patients.

Methods

A total of 190 UC patients were enrolled, including 90 CMV-positive and 100 CMV-negative cases. CMV status was confirmed by molecular and histopathological tests. Colonic gene expression of cytokines (TNF-α, IL-1β, IL-6, IL-17 A, IFN-γ, TGF-β, IL-8, IL-12, and RANTES) was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), and serum concentrations were assessed using enzyme-linked immunosorbent assay (ELISA).

Results

Demographic and clinical features were comparable between groups. CMV-positive patients showed higher colonic mRNA expression and serum concentrations of TNF-α, IL-1β, IL-6, and IL-17 A compared to CMV-negative patients (all p < 0.05). In contrast, IFN-γ, TGF-β, IL-8, IL-12, and RANTES did not differ significantly. Notably, CMV tissue viral load was significantly higher in patients with moderate to severe disease (Mayo score ≥ 6) and showed a positive correlation with plasma viral load (r = 0.664, p < 0.01). Multivariable logistic regression analysis adjusted for Mayo score confirmed that elevated TNF-α, IL-1β, and IL-6 remained independently associated with CMV positivity. These findings indicate a selective pro-inflammatory cytokine pattern rather than generalized immune activation.

Conclusion

CMV infection in UC is associated with selective upregulation of pro-inflammatory cytokines at both mucosal and systemic levels. These findings highlight CMV as a potential driver of immune amplification in UC and support cytokine profiling as a tool for risk stratification and management of affected patients.