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Background <p><i>Helicobacter pylori (H. pylori)</i> is known to modulate host immunity and sustain chronic inflammation, yet most data come from HIV-negative populations. In people living with HIV, whose T cell compartments are already dysregulated, the way <i>H. pylori</i> shapes peripheral T cell phenotypes, and how those profiles change after eradication therapy, is still unclear. Because both infections are common in Central Ethiopia, we examined peripheral T cell phenotypes in adults with and without HIV according to <i>H. pylori</i> status and assessed the immunologic effects of antibiotic eradication.</p> Materials and methods <p>We conducted a prospective study in people with and without HIV infection from Ethiopia. <i>H. pylori</i> status was determined by stool-antigen testing; a subset received standard triple therapy and was followed for 12&#xa0;months. Multiparameter flow cytometry quantified T cell activation, proliferation, exhaustion, and regulatory T cells (T<sub>regs</sub>) at baseline and after therapy.</p> Results <p>T cell analyses showed that participants with HIV had consistently higher proliferation (Ki67), exhaustion (PD‐1, TIM3), and Th17 (CCR6⁺CD161⁺) markers than those without HIV. <i>H. pylori</i>-positive individuals exhibited&#xa0;higher T<sub>reg</sub> levels&#xa0;irrespective of HIV status (HIV-negative: median 2% vs 1.08%, <i>p</i> &lt; 0.0001; HIV-positive: median 2.9% vs 1.62%, <i>p</i> = 0.009). Successful eradication therapy led to a significant reduction in T<sub>regs</sub> in both HIV-positive (median 3.04% → 0.70%, <i>p</i> = 0.031) and HIV-negative (median 2.96% → 1.46%, <i>p</i> = 0.040) groups. A similar decline was also observed in HIV-negative individuals with unsuccessful therapy (median 2.85% vs 1.29%, <i>p</i> = 0.0039).</p> Conclusions <p><i>H. pylori</i> infection was linked to significant differences in T cell profiles in both HIV-negative and HIV-positive individuals. Eradication therapy was followed by a reduction in Tregs—significant in HIV-negative participants irrespective of outcome and in PLWH with successful eradication—with subgroup-specific shifts in activation and differentiation/exhaustion markers, highlighting potential therapeutic avenues for mitigating immune dysregulation in co-infected populations.</p>

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Effects of Helicobacter pylori infection on T cell activation markers and regulatory T cells in people with and without HIV infection in Central Ethiopia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月11日

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  • Smaranda Gliga,
  • Million Getachew Mesfun,
  • Tafese Beyene Tufa,
  • Andre Fuchs,
  • Hans Martin Orth,
  • Edmund Osei Kuffour,
  • Philipp A. Lang,
  • Tom Luedde,
  • Torsten Feldt

摘要

Background

Helicobacter pylori (H. pylori) is known to modulate host immunity and sustain chronic inflammation, yet most data come from HIV-negative populations. In people living with HIV, whose T cell compartments are already dysregulated, the way H. pylori shapes peripheral T cell phenotypes, and how those profiles change after eradication therapy, is still unclear. Because both infections are common in Central Ethiopia, we examined peripheral T cell phenotypes in adults with and without HIV according to H. pylori status and assessed the immunologic effects of antibiotic eradication.

Materials and methods

We conducted a prospective study in people with and without HIV infection from Ethiopia. H. pylori status was determined by stool-antigen testing; a subset received standard triple therapy and was followed for 12 months. Multiparameter flow cytometry quantified T cell activation, proliferation, exhaustion, and regulatory T cells (Tregs) at baseline and after therapy.

Results

T cell analyses showed that participants with HIV had consistently higher proliferation (Ki67), exhaustion (PD‐1, TIM3), and Th17 (CCR6⁺CD161⁺) markers than those without HIV. H. pylori-positive individuals exhibited higher Treg levels irrespective of HIV status (HIV-negative: median 2% vs 1.08%, p < 0.0001; HIV-positive: median 2.9% vs 1.62%, p = 0.009). Successful eradication therapy led to a significant reduction in Tregs in both HIV-positive (median 3.04% → 0.70%, p = 0.031) and HIV-negative (median 2.96% → 1.46%, p = 0.040) groups. A similar decline was also observed in HIV-negative individuals with unsuccessful therapy (median 2.85% vs 1.29%, p = 0.0039).

Conclusions

H. pylori infection was linked to significant differences in T cell profiles in both HIV-negative and HIV-positive individuals. Eradication therapy was followed by a reduction in Tregs—significant in HIV-negative participants irrespective of outcome and in PLWH with successful eradication—with subgroup-specific shifts in activation and differentiation/exhaustion markers, highlighting potential therapeutic avenues for mitigating immune dysregulation in co-infected populations.