Host-pathogen interaction in invasive Salmonellosis.
Host-pathogen interaction in invasive Salmonellosis.
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DOI：
10.1371/journal.ppat.1002933
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发表时间：
2012
期刊：
影响因子：
6.7
通讯作者：
Wiersinga WJ
中科院分区：
文献类型：
--
作者：
de Jong HK;Parry CM;van der Poll T;Wiersinga WJ
肠道沙门氏菌感染会导致多种临床表现。由肠道沙门氏菌血清型伤寒杆菌（S. Typhi）和甲型副伤寒杆菌引起的伤寒是一种菌血症疾病，但其临床特征与其他革兰氏阴性菌血症不同。非伤寒沙门氏菌（NTS）血清型会引起自限性腹泻，偶尔会出现继发性菌血症。原发性NTS菌血症可能发生在撒哈拉以南非洲的免疫功能低下的宿主和婴儿身上。最近利用基因组测序、小鼠模型和患者研究对沙门氏菌病中宿主 - 病原体相互作用的研究提供了新的见解。许多肠道沙门氏菌血清型的全基因组序列已经确定。与鼠伤寒沙门氏菌的基因组相比，伤寒沙门氏菌的基因组含有许多失活或中断的基因。这可以部分解释这两种血清型进入宿主时所诱导的不同免疫反应。在与撒哈拉以南非洲侵袭性感染有关的鼠伤寒沙门氏菌ST313菌株中也观察到了类似的基因组退化。毒力因子，最显著的是III型分泌系统、Vi抗原、脂多糖和其他表面多糖、鞭毛以及肠道沙门氏菌细胞内生命周期所必需的各种因子已经被鉴定。这些因子的基因通常位于沙门氏菌致病岛（SPIs）上。质粒也携带假定的与毒力相关的基因以及那些导致抗菌药物耐药性的基因。沙门氏菌病原体相关分子模式（PAMPs）与Toll样受体（TLRs）和NOD样受体（NLRs）的相互作用导致炎症小体形成、中性粒细胞和巨噬细胞的激活和募集以及促炎细胞因子的产生，最显著的是白细胞介素（IL）-6、IL - 1β、肿瘤坏死因子（TNF）-α和干扰素 - γ（IFN - γ）。肠道微生物组可能是这种免疫反应的重要调节剂。鼠伤寒沙门氏菌通常引起局部肠道免疫反应，而伤寒沙门氏菌通过阻止由Toll样受体激活导致的中性粒细胞吸引，逃避局部反应并引起全身性感染。对感染发病机制的进一步了解可能会引出潜在的新治疗策略。
Salmonella enterica infections result in diverse clinical manifestations. Typhoid fever, caused by S. enterica serovar Typhi (S. Typhi) and S. Paratyphi A, is a bacteremic illness but whose clinical features differ from other Gram-negative bacteremias. Non-typhoidal Salmonella (NTS) serovars cause self-limiting diarrhea with occasional secondary bacteremia. Primary NTS bacteremia can occur in the immunocompromised host and infants in sub-Saharan Africa. Recent studies on host–pathogen interactions in Salmonellosis using genome sequencing, murine models, and patient studies have provided new insights. The full genome sequences of numerous S. enterica serovars have been determined. The S. Typhi genome, compared to that of S. Typhimurium, harbors many inactivated or disrupted genes. This can partly explain the different immune responses both serovars induce upon entering their host. Similar genome degradation is also observed in the ST313 S. Typhimurium strain implicated in invasive infection in sub-Saharan Africa. Virulence factors, most notably, type III secretion systems, Vi antigen, lipopolysaccharide and other surface polysaccharides, flagella, and various factors essential for the intracellular life cycle of S. enterica have been characterized. Genes for these factors are commonly carried on Salmonella Pathogenicity Islands (SPIs). Plasmids also carry putative virulence-associated genes as well as those responsible for antimicrobial resistance. The interaction of Salmonella pathogen-associated molecular patterns (PAMPs) with Toll-like receptors (TLRs) and NOD-like receptors (NLRs) leads to inflammasome formation, activation, and recruitment of neutrophils and macrophages and the production of pro-inflammatory cytokines, most notably interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and interferon-gamma (IFN)-γ. The gut microbiome may be an important modulator of this immune response. S. Typhimurium usually causes a local intestinal immune response, whereas S. Typhi, by preventing neutrophil attraction resulting from activation of TLRs, evades the local response and causes systemic infection. Potential new therapeutic strategies may lead from an increased understanding of infection pathogenesis.
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