Indoleamine 2,3-Dioxygenase Cannot Inhibit Chlamydia trachomatis Growth in HL-60 Human Neutrophil Granulocytes

• DOI: 10.3389/fimmu.2021.717311
• Publication Date: 2021-11-08T07:09:59Z
• Authors: Dezső P. Virok; Ferenc Tömösi; Anikó Keller-Pintér; Kitti Szabó; Anita Bogdanov; Szilárd Poliska; Zsolt Rázga; Bella Bruszel; Zsuzsanna Cseh; Dávid Kókai; Dóra Paróczai; Valéria Endrész; Tamás Janáky; Katalin Burián
• Keywords: Indoleamine 2,3-dioxygenase; Chlamydophila pneumoniae; Interferon-stimulated gene

Neutrophil granulocytes are the major cells involved in Chlamydia trachomatis (C. trachomatis)-mediated inflammation and histopathology. A key protein human intracellular antichlamydial defense is tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO) which limits growth of tryptophan auxotroph Chlamydia. Despite its importance, role IDO against neutrophils not well characterized.Global gene expression screen was used to evaluate effect C. serovar D infection on transcriptome neutrophil granulocytes. Tryptophan metabolite concentrations Chlamydia-infected and/or interferon-gamma (IFNG)-treated were measured by ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS).Our results indicate that had a impact expression, inducing 1,295 genes repressing 1,510 genes. bioinformatics analysis revealed important factors induction interferon-related transcription such as IRF1-5, IRF7-9, STAT2, ICSB, ISGF3. One upregulated ido1, known infection- interferon-induced host gene. The activity IDO1 induced significantly alone, but addition IFNG greatly increased activity. significant IFNG-treated cells, affected IFNG. This result contrast what we observed HeLa cervical epithelial where IFNG-mediated inhibition IFNG-induced correlated with inhibition.IDO able inhibit chlamydial neutrophils. Whether high enough for or other growth-promoting mechanisms infected interferon-treated needs be further investigated.