Tsaplina Olga, Khmel Inessa, Zaitseva Yulia, Khaitlina Sofia
Institute of Cytology, Russian Academy of Sciences, Tikhoretsky av. 4, 194064 St Petersburg, Russia.
Institute of Molecular Genetics of National Research Center "Kurchatov Institute", Kurchatov sq. 2, 123182 Moscow, Russia.
Microorganisms. 2021 Oct 2;9(10):2082. doi: 10.3390/microorganisms9102082.
The bacteria 94 have a LuxI/LuxR type QS system consisting of AHL synthase SprI and the regulatory receptor SprR. We have previously shown that inactivation of the AHL synthase gene resulted in an increase in the invasive activity of correlated with an increased bacterial adhesion. In the present work, the effects of inactivation of the receptor SprR are studied. Our results show that inactivation of the receptor gene leads to an increase in bacterial invasion without any increase in their adhesion. On the other hand, inactivation of the gene increases the activity of the extracellular protease serralysin. Inactivation of the QS system does not affect the activity of the pore-forming toxin ShlA and prevents the ShlA activation under conditions of a limited concentration of iron ions typical of the human body. While the wild type strain shows increased invasion in the iron-depleted medium, deletion of its QS system leads to a decrease in host cell invasion, which is nevertheless similar to the level of the wild type grown in the iron-rich medium. Thus, inactivation of either of the two component of the LuxI/LuxR-type QS system leads to an increase in the invasive activity of these bacteria through different mechanisms and prevents invasion under the iron-limited conditions.
细菌94具有由AHL合酶SprI和调节受体SprR组成的LuxI/LuxR型群体感应（QS）系统。我们之前已经表明，AHL合酶基因的失活导致侵袭活性增加，这与细菌黏附增加相关。在本研究中，我们研究了受体SprR失活的影响。我们的结果表明，受体基因的失活导致细菌侵袭增加，但其黏附没有任何增加。另一方面，该基因的失活增加了细胞外蛋白酶serratysin的活性。QS系统的失活不影响成孔毒素ShlA的活性，并在人体典型的铁离子浓度有限的条件下阻止ShlA的激活。虽然野生型菌株在缺铁培养基中侵袭增加，但其QS系统的缺失导致宿主细胞侵袭减少，不过这与在富铁培养基中生长的野生型水平相似。因此，LuxI/LuxR型QS系统的两个组分中的任何一个失活都会通过不同机制导致这些细菌的侵袭活性增加，并在铁限制条件下阻止侵袭。
