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. 2018 May 25;9:1105. doi: 10.3389/fmicb.2018.01105

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Copyright © 2018 Song, Zhang, Cai, Lv, Zhao, Wei and Zhu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Deletion of htsA decreased GAS resistance to phagocytosis. (A) Deletion of htsA decreased survival in blood. Wild type, ΔhtsA, and ΔhtsA-htsA strains were incubated with heparinized blood, and bacterial CFU were determined at 0 min, 30 min, 60 min, 120 min, and 180 min postincubation. After 60 min of incubation, the growth of ΔhtsA in human blood was significantly slower than that of wild type and ΔhtsA-htsA; (B) deletion of htsA decreased survival in rat neutrophils. Wild type, ΔhtsA, and ΔhtsA-htsA strains were incubated with purified rat neutrophils, and bacterial CFU values were determined at 0 min, 30 min, 60 min, 120 min, and 180 min postincubation. At 120 min and 180 min of incubation, the growth of ΔhtsA in rat neutrophils was significantly slower than that of wild type and ΔhtsA-htsA.