Antigen-Specific Memory B-Cell Responses to Vibrio cholerae O1 Infection in Bangladesh
Antigen-Specific Memory B-Cell Responses to Vibrio cholerae O1 Infection in Bangladesh
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DOI：
10.1128/iai.00369-09
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发表时间：
2009-09-01
影响因子：
3.1
通讯作者：
Harris, Jason B.
中科院分区：
文献类型：
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作者：
Harris, Aaron M.;Bhuiyan, M. Saruar;Harris, Jason B.
霍乱由霍乱弧菌引起，是一种非侵入性的脱水性肠道疾病，如果不治疗，死亡率很高。在霍乱流行的国家，感染霍乱弧菌可长期预防随后的疾病。尽管这种保护性免疫的机制尚不清楚，但已假设肠道相关淋巴组织中记忆B细胞的回忆应答可能介导了对霍乱弧菌感染的保护性粘膜应答。为了表征记忆B细胞对霍乱的反应，我们招募了一组39例经培养确诊的霍乱住院患者，并在随后的1年中频繁评估他们的免疫反应。记忆B细胞对霍乱抗原，包括脂多糖（LPS），蛋白抗原霍乱毒素B亚单位（CT B）和毒素共调节菌毛主要亚单位A（TcpA）进行了计数，使用的方法是多克隆刺激外周血单核细胞，然后通过标准的酶联免疫斑点程序。到第90天，所有患者均表现出CTB、TcpA和LPS特异性免疫球蛋白G（IgG）和伊加记忆反应。此外，这些记忆性B细胞反应持续长达1年，比其他传统的霍乱弧菌感染免疫学标志物长得多。虽然LPS特异性IgG记忆B细胞应答的幅度在感染后1年减弱，但CTB和TcpA特异性IgG记忆B细胞在感染后1年仍显著升高，表明T细胞帮助可能导致对霍乱弧菌蛋白抗原的更持久的记忆B细胞应答。这种记忆B细胞可以介导再次暴露于霍乱弧菌时的回忆反应。
Cholera, caused by Vibrio cholerae, is a noninvasive dehydrating enteric disease with a high mortality rate if untreated. Infection with V. cholerae elicits long-term protection against subsequent disease in countries where the disease is endemic. Although the mechanism of this protective immunity is unknown, it has been hypothesized that a protective mucosal response to V. cholerae infection may be mediated by anamnestic responses of memory B cells in the gut-associated lymphoid tissue. To characterize memory B-cell responses to cholera, we enrolled a cohort of 39 hospitalized patients with culture-confirmed cholera and evaluated their immunologic responses at frequent intervals over the subsequent 1 year. Memory B cells to cholera antigens, including lipopolysaccharide (LPS), and the protein antigens cholera toxin B subunit (CTB) and toxin-coregulated pilus major subunit A ( TcpA) were enumerated using a method of polyclonal stimulation of peripheral blood mononuclear cells followed by a standard enzyme-linked immunospot procedure. All patients demonstrated CTB, TcpA, and LPS-specific immunoglobulin G (IgG) and IgA memory responses by day 90. In addition, these memory B-cell responses persisted up to 1 year, substantially longer than other traditional immunologic markers of infection with V. cholerae. While the magnitude of the LPS-specific IgG memory B-cell response waned at 1 year, CTB- and TcpA-specific IgG memory B cells remained significantly elevated at 1 year after infection, suggesting that T-cell help may result in a more durable memory B-cell response to V. cholerae protein antigens. Such memory B cells could mediate anamnestic responses on reexposure to V. cholerae.