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寄生虫介导的肺外结核中系统性和分枝杆菌抗原刺激细胞因子谱的调节。

Helminth mediated modulation of the systemic and mycobacterial antigen - stimulated cytokine profiles in extra-pulmonary tuberculosis.

机构信息

National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.

National Institute for Research in Tuberculosis (NIRT), Chennai, India.

出版信息

PLoS Negl Trop Dis. 2019 Mar 21;13(3):e0007265. doi: 10.1371/journal.pntd.0007265. eCollection 2019 Mar.

Abstract

BACKGROUND

Helminth infections are known to regulate cytokine responses in both pulmonary and latent tuberculosis infection. Whether helminth infections also modulate cytokine responses in extra-pulmonary tuberculosis, specifically tuberculous lymphadenitis (TBL), has not been examined thus far.

METHODOLOGY

Hence, to determine the cytokine profile in helminth-TBL coinfection, we measured the systemic and mycobacterial (TB)-antigen stimulated levels of Type 1, Type 2, Type 17, regulatory and pro-inflammatory cytokines in TBL individuals coinfected with or without Strongyloides stercoralis (Ss) infection.

SIGNIFICANT FINDINGS

TBL-Ss+ individuals have significantly higher bacterial burdens in the affected lymph nodes in comparison to TBL-Ss- individuals. TBL-Ss+ individuals exhibit significantly enhanced plasma levels of Type 2 (IL-5 and IL-13), Type 17 (IL-17 and IL-22) and regulatory (IL-10) cytokines in comparison to TBL-Ss- individuals. In contrast, TBL-Ss+ individuals exhibit significantly diminished plasma levels of pro-inflammatory cytokines (IL-1α and GM-CSF) in comparison to TBL-Ss- individuals. TBL-Ss+ individuals also exhibit significantly diminished unstimulated or mycobacterial-antigen stimulated levels of Type 1, Type 17 or IL-1 family cytokines in comparison to TBL-Ss- individuals but no differences in mitogen stimulated cytokine levels.

CONCLUSION

Therefore, our data reveal a profound influence of Ss infection on the bacteriological profile of TBL and suggesting that the underlying modulation of cytokine responses might be a mechanism by which this helminth infection could impart a detrimental effect on the pathogenesis of TBL disease.

摘要

背景

已知寄生虫感染可调节肺部和潜伏性结核感染中的细胞因子反应。迄今为止,尚未研究寄生虫感染是否也调节肺外结核,特别是结核性淋巴结炎(TBL)中的细胞因子反应。

方法

因此,为了确定寄生虫-TBL 合并感染中的细胞因子谱,我们测量了合并感染或未感染 Strongyloides stercoralis(Ss)的 TBL 个体中系统性和分枝杆菌(TB)抗原刺激的 1 型、2 型、17 型、调节性和促炎细胞因子水平。

重要发现

与 TBL-Ss-个体相比,TBL-Ss+个体的受累淋巴结中的细菌负荷明显更高。与 TBL-Ss-个体相比,TBL-Ss+个体的血浆中 2 型(IL-5 和 IL-13)、17 型(IL-17 和 IL-22)和调节性(IL-10)细胞因子水平显著升高。相比之下,与 TBL-Ss-个体相比,TBL-Ss+个体的促炎细胞因子(IL-1α 和 GM-CSF)的血浆水平显著降低。与 TBL-Ss-个体相比,TBL-Ss+个体的未刺激或分枝杆菌抗原刺激的 1 型、17 型或 IL-1 家族细胞因子水平也显著降低,但促分裂原刺激的细胞因子水平没有差异。

结论

因此,我们的数据揭示了 Ss 感染对 TBL 细菌学特征的深远影响,并表明细胞因子反应的潜在调节可能是这种寄生虫感染对 TBL 疾病发病机制产生不利影响的一种机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9871/6445485/4ac0026b2c50/pntd.0007265.g001.jpg

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