Francisella tularensis, the causative agent of tularemia, is transmitted by arthropod vectors within mammalian hosts. The detailed mechanisms contributing to growth and survival of Francisella within arthropod remain poorly understood. To identify novel factors supporting growth and survival of Francisella within arthropods, a transposon mutant library of F. tularensis subsp. novicida (F. novicida) was screened using an F. novicida–silkworm infection model. Among 750 transposon mutants screened, the mltA-encoding membrane-bound lytic murein transglycosylase A (MltA) was identified as a novel growth factor of F. novicida in silkworms. Silkworms infection with an mltA deletion mutant (ΔmltA) resulted in a reduction in the number of bacteria and prolonged survival. The ΔmltA strain exhibited limited intracellular growth and cytotoxicity in BmN4 silkworm ovary cells. Moreover, the ΔmltA strain induced higher expression of the antimicrobial peptide in silkworms compared to the wild-type strain. These results suggest that F. novicida MltA contributes to the survival of F. novicida in silkworms via immune suppression-related mechanisms. Intracellular growth of the ΔmltA strain was also reduced in human monocyte THP-1 cells. These results also suggest the contribution of MltA to pathogenicity in humans and utility of the F. novicida–silkworm infection model to explore Francisella infection.

图拉弗朗西斯菌节律性疾病的致病因子，是节肢动物媒介在哺乳动物宿主内传播的。促进金枪鱼生长和存活的详细机制弗朗西斯拉在节肢动物中仍然知之甚少。找出新的因素来支持其生长和存活弗朗西斯拉 在节肢动物中，转座子突变体文库 图莱树 亚种 诺维达 （F.novicida）已使用 F.novicida–蚕感染模型。在筛选的750个转座子突变体中，毫升编码膜结合的溶质murein转糖基化酶A（MltA）被确定为一种新的生长因子 F.novicida在蚕中。蚕感染毫升 缺失突变体（Δ毫升）可减少细菌数量并延长生存期。Δ毫升该菌株在BmN4蚕卵巢细胞中显示出有限的细胞内生长和细胞毒性。而且，Δ毫升与野生型菌株相比，该菌株诱导了家蚕中抗菌肽的更高表达。这些结果表明F.novicida MltA有助于生存 F.novicida 在蚕中 通过免疫抑制相关机制。细胞内Δ的生长毫升人单核细胞THP-1细胞中的菌株也减少了。这些结果还表明MltA对人类致病性的贡献和F.novicida–蚕感染模型的探索 弗朗西斯拉 感染。