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<p>Immunocompromised inflammatory bowel disease (IBD) patients may develop life-threatening pneumonia and bronchiolitis upon HCoV-NL63 infection. However, little is known whether these patients will be more susceptible to HCoV-NL63 infection. We compared the expression of ACE2 in different tissues and cell lines. Besides, the susceptibility of colonic cells to HCoV-NL63 was assessed. We then examined the expression of ACE2 in the colonic mucosa from IBD patients and animal models, and in the inflammatory colonic cells. The susceptibility of inflammatory colonic cells to HCoV-NL63 was detected using a pseudovirus-based system. Pseudovirus based neutralization assay was used to quantify the neutralizing antibodies to HCoV-NL63 in patients with IBD and healthy controls. ACE2 was abundantly expressed in the colonic tissue and cells. And colonic cells were susceptible to pseudotyped HCoV-NL63. The expression of ACE2 was increased in the colonic mucosa from IBD patients and animal models, and in inflammatory colonic cells. Inflammatory colonic cells were more susceptible to pseudotyped HCoV-NL63. Besides, reduced protective neutralizing antibody titers were seen in patients with IBD, especially for male or older IBD patients. These results suggest IBD patients may be particularly susceptible to infection with HCoV-NL63 and thus extra precautions should be taken to prevent them from infection. Further mechanistic studies are needed to support our findings.</p>

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Patients with inflammatory bowel disease exhibit increased susceptibility to HCoV-NL63

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月23日

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  • Tingting Ning,
  • Nianchen Liu,
  • Qi Jiang,
  • Nan Zhang,
  • Shengtao Zhu

摘要

Immunocompromised inflammatory bowel disease (IBD) patients may develop life-threatening pneumonia and bronchiolitis upon HCoV-NL63 infection. However, little is known whether these patients will be more susceptible to HCoV-NL63 infection. We compared the expression of ACE2 in different tissues and cell lines. Besides, the susceptibility of colonic cells to HCoV-NL63 was assessed. We then examined the expression of ACE2 in the colonic mucosa from IBD patients and animal models, and in the inflammatory colonic cells. The susceptibility of inflammatory colonic cells to HCoV-NL63 was detected using a pseudovirus-based system. Pseudovirus based neutralization assay was used to quantify the neutralizing antibodies to HCoV-NL63 in patients with IBD and healthy controls. ACE2 was abundantly expressed in the colonic tissue and cells. And colonic cells were susceptible to pseudotyped HCoV-NL63. The expression of ACE2 was increased in the colonic mucosa from IBD patients and animal models, and in inflammatory colonic cells. Inflammatory colonic cells were more susceptible to pseudotyped HCoV-NL63. Besides, reduced protective neutralizing antibody titers were seen in patients with IBD, especially for male or older IBD patients. These results suggest IBD patients may be particularly susceptible to infection with HCoV-NL63 and thus extra precautions should be taken to prevent them from infection. Further mechanistic studies are needed to support our findings.