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Background <p><i>Eimeria tenella</i>, one of the most virulent causative agents of coccidiosis, specifically colonizes the cecum and imposes substantial economic losses on the poultry industry. Toll-like receptors (TLRs), key mediators of the innate immune response, initiate rapid defense against invading parasites. However, their roles during <i>E. tenella</i> infection remain poorly defined.</p> Methods <p>In this study, coccidiosis infection parameters (cecal lesions, oocyst output, and clinical signs) were monitored, and the expression profiles of 10 chicken TLRs (chTLRs) and related immune genes in the cecum and spleen of <i>E. tenella</i>-infected chickens were characterized at multiple time points using quantitative real-time polymerase chain reaction (PCR) and histopathological analysis. Spearman correlation analysis was performed to evaluate associations between TLR expression and pathogenicity parameters.</p> Results <p>Infected chickens exhibited marked clinical signs, although no mortality occurred in either group. Cecal lesions became apparent by 96&#xa0;h post-infection (hpi), peaking at 144 hpi, and were accompanied by significant epithelial necrosis and extensive inflammatory cell infiltration. Most TLR genes showed distinct expression patterns between the cecum and spleen: cecal TLRs were upregulated during the middle phase (24–72 hpi) of infection, whereas splenic TLRs were downregulated in later stages (96–168 hpi). Key proinflammatory cytokines—interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ—were elevated in the cecum during early infection but declined in the spleen during later phases. Infection also induced dynamic expression changes in the downstream signaling molecules myeloid differentiation factor 88 (MyD88) and nuclear factor-kappa B (NF-κB) p65 in both tissues. Spearman correlation analysis revealed that, in the cecum, chTLR7 positively correlated with both oocyst output and lesion scores, whereas chTLR2a positively correlated with lesion scores. By contrast, chTLR1a, chTLR1b, chTLR15, and chTLR21 negatively correlated with oocyst output. In the spleen, chTLR15 and chTLR21 positively correlated with oocyst output, while chTLR5 uniquely and negatively correlated with lesion scores.</p> Conclusions <p>These findings identify both proinflammatory and potentially protective TLR pathways in subclinical coccidiosis.</p> Graphical abstract <p></p>

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Toll-like receptor-mediated innate immune response correlate with the pathogenicity of Eimeria tenella infection in SPF chickens

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月27日

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  • Huili Zhu,
  • Guijie Zheng,
  • Danni Wang,
  • Qian Zhang,
  • Yanhui Han,
  • Song Wang,
  • Qiangqiang Wang,
  • Hongxuan He,
  • Longxian Zhang,
  • Jianhe Hu

摘要

Background

Eimeria tenella, one of the most virulent causative agents of coccidiosis, specifically colonizes the cecum and imposes substantial economic losses on the poultry industry. Toll-like receptors (TLRs), key mediators of the innate immune response, initiate rapid defense against invading parasites. However, their roles during E. tenella infection remain poorly defined.

Methods

In this study, coccidiosis infection parameters (cecal lesions, oocyst output, and clinical signs) were monitored, and the expression profiles of 10 chicken TLRs (chTLRs) and related immune genes in the cecum and spleen of E. tenella-infected chickens were characterized at multiple time points using quantitative real-time polymerase chain reaction (PCR) and histopathological analysis. Spearman correlation analysis was performed to evaluate associations between TLR expression and pathogenicity parameters.

Results

Infected chickens exhibited marked clinical signs, although no mortality occurred in either group. Cecal lesions became apparent by 96 h post-infection (hpi), peaking at 144 hpi, and were accompanied by significant epithelial necrosis and extensive inflammatory cell infiltration. Most TLR genes showed distinct expression patterns between the cecum and spleen: cecal TLRs were upregulated during the middle phase (24–72 hpi) of infection, whereas splenic TLRs were downregulated in later stages (96–168 hpi). Key proinflammatory cytokines—interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ—were elevated in the cecum during early infection but declined in the spleen during later phases. Infection also induced dynamic expression changes in the downstream signaling molecules myeloid differentiation factor 88 (MyD88) and nuclear factor-kappa B (NF-κB) p65 in both tissues. Spearman correlation analysis revealed that, in the cecum, chTLR7 positively correlated with both oocyst output and lesion scores, whereas chTLR2a positively correlated with lesion scores. By contrast, chTLR1a, chTLR1b, chTLR15, and chTLR21 negatively correlated with oocyst output. In the spleen, chTLR15 and chTLR21 positively correlated with oocyst output, while chTLR5 uniquely and negatively correlated with lesion scores.

Conclusions

These findings identify both proinflammatory and potentially protective TLR pathways in subclinical coccidiosis.

Graphical abstract