Levels of Cytokines in Leptospirosis Patients with Different Serovars and rfb Locus.

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Interferon and Cytokine Research Pub Date : 2024-02-01 DOI:10.1089/jir.2023.0091
Indika Senavirathna, Dinesha Jayasundara, Janith Warnasekara, Chamila Kappagoda, Suneth Agampodi
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Abstract

Leptospirosis has a wide spectrum of clinical manifestations ranging from mild to severe disease. The cytokine response is considered one of the key drivers for this varying manifestation. The different cytokine response observed in patients with leptospirosis could be due to the variation of infecting serovars. Since the rfb locus codes for the lipopolysaccharide synthesis of the bacterial cell wall, which also determines the serovar, this locus may play a role in driving a specific cytokine response in the host. We investigated 12 commonly used cytokine profiles in serum samples of culture, microscopic agglutination test (MAT), or polymerase chain reaction (PCR)-positive patients with leptospirosis. The sequences of the rfb locus in culture-positive samples were generated from whole genome sequencing and serovar status was drawn from original data published. Isolated cultures were subjected to whole genome sequencing using the PacBio RS II system, and the resulting data were used to determine the species. The recovered genomic data were annotated with the Rapid Annotation using Subsystem Technology (RAST) subsystem, and the rfb locus was extracted. The cytokine analysis was carried out using the Qiagen human ELISA kit. Eighteen samples were found to be positive by culture, while the other 7 samples were positive by PCR or MAT. Infections from Leptospira interrogans serovar Autumnalis (5), Pyrogens (3), Icterohaemorrhagiae (1) Leptospira borgpetersenii (all 7 samples clustered in same clonal group with serovar status not determined), Leptospira weilii (1 with serovar status not determined), and Leptospira kirschneri serovar Grippotyphosa (1) were included in the analysis. Three patients [infected with Leptospira interrogansserovar Autumnalis (2) and Pyrogens (1)] and 2 MAT-positive patients (highest titer against serovar Bratislava of L.interrognas) were reported to have severe clinical manifestations, while the rest had mild to moderate symptoms. Although the serum cytokine concentration of patients with severe clinical manifestation was comparatively higher, a statistically significant difference was observed only for interleukin (IL)-1β (P < 0.05). IL-10/tumor necrosis factor-alpha (TNF-α) ratio was high in patients with severe complications. In general, patients infected with L. interrogans showed higher concentration of cytokines compared to L. borgpetersenii.

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不同血清型和 rfb 基因座的钩端螺旋体病患者体内的细胞因子水平
钩端螺旋体病的临床表现范围很广,从轻微到严重不等。细胞因子反应被认为是导致这种不同表现的关键因素之一。在钩端螺旋体病患者身上观察到的不同细胞因子反应可能是由于感染的血清型不同造成的。由于 rfb 基因座编码细菌细胞壁脂多糖的合成,这也决定了血清型,因此该基因座可能在驱动宿主的特定细胞因子反应中发挥作用。我们研究了培养、显微凝集试验(MAT)或聚合酶链反应(PCR)阳性钩端螺旋体病患者血清样本中的 12 种常用细胞因子谱。培养阳性样本中 rfb 基因座的序列来自全基因组测序,血清型状态来自已发表的原始数据。使用 PacBio RS II 系统对分离培养物进行全基因组测序,并根据测序结果确定物种。利用子系统技术快速注释(RAST)子系统对恢复的基因组数据进行注释,并提取 rfb 基因座。细胞因子分析使用 Qiagen 人类 ELISA 试剂盒进行。通过培养发现 18 个样本呈阳性,另外 7 个样本通过 PCR 或 MAT 呈阳性。分析中包括的感染病原体有:审讯钩端螺旋体(Leptospira interrogans serovar Autumnalis)(5 例)、Pyrogens(3 例)、Icterohaemorrhagiae(1 例)、Leptospira borgpetersenii(所有 7 例样本均聚集在同一克隆组,血清型尚未确定)、Leptospira weilii(1 例,血清型尚未确定)和 Leptospira kirschneri serovar Grippotyphosa(1 例)。据报告,3 名患者(感染了 Leptospira interrogansserovar Autumnalis (2) 和 Pyrogens (1))和 2 名 MAT 阳性患者(对 L.interrognas 的血清菌株 Bratislava 的滴度最高)有严重的临床表现,其余患者的症状为轻度至中度。虽然临床表现严重的患者血清细胞因子浓度相对较高,但只有白细胞介素(IL)-1β(P. L. interrogans 的细胞因子浓度高于 L. borgpetersenii)有显著统计学差异。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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