Neisseria gonorrhoeae releases anhydro peptidoglycan monomers during growth through the action of two lytic transglycosylases encoded in the N. gonorrhoeae genome, LtgA and LtgD. Because peptidoglycan and peptidoglycan components activate innate immune signaling, we hypothesized that the activity of LtgA and LtgD would influence the host responses to gonococcal infection. N. gonorrhoeae lacking LtgA and LtgD caused increased host production of inflammatory cytokines IL-1β and TNF-α. Culture supernatants from ΔltgA/ΔltgDN. gonorrhoeae contain more shed outer membrane-associated proteins and multimeric peptidoglycan fragments rather than monomers. These culture supernatants were more potent activators of host TLR2 and NOD2 signaling when compared to supernatants from the isogenic parental N. gonorrhoeae strain. Purified peptidoglycan monomers containing anhydro muramic acid produced by LtgA were poor stimulators of NOD2, whereas peptidoglycan monomers containing reducing muramic acid produced by host lysozyme were potent stimulators of NOD2. These data indicate that LtgA and LtgD reduce recognition of N. gonorrhoeae by TLR2 and NOD2.

中文翻译：

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淋病奈瑟氏球菌溶菌转糖基酶LtgA和LtgD通过TLR2和NOD2降低宿主先天免疫信号

淋病奈瑟菌在生长过程中通过淋病奈瑟氏球菌基因组中编码的两种裂解转糖基酶LtgA和LtgD的作用释放脱水肽聚糖单体。因为肽聚糖和肽聚糖成分激活先天性免疫信号传导，所以我们假设LtgA和LtgD的活性会影响宿主对淋球菌感染的反应。缺乏LtgA和LtgD的淋病奈瑟氏球菌导致宿主细胞产生炎性细胞因子IL-1β和TNF-α。ΔltgA / ΔltgD淋病奈瑟氏球菌的培养上清液含有更多脱落的外膜相关蛋白和多聚肽聚糖片段，而不是单体。与来自同基因亲本淋病奈瑟氏球菌菌株的上清液相比，这些培养上清液是宿主TLR2和NOD2信号传导的更有效的激活剂。由LtgA产生的含有脱水尿酸的纯化肽聚糖单体是NOD2的弱刺激物，而由宿主溶菌酶产生的含有还原性尿酸的肽聚糖单体是NOD2的有效刺激物。这些数据表明LtgA和LtgD减少了TLR2和NOD2对淋病奈瑟氏球菌的识别。