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首页> 外文期刊>Infection and immunity >Antigen-Specific Memory B-Cell Responses to Vibrio cholerae O1 Infection in Bangladesh
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Antigen-Specific Memory B-Cell Responses to Vibrio cholerae O1 Infection in Bangladesh

机译：孟加拉国霍乱弧菌O1感染的抗原特异性记忆B细胞反应

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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.
机译：霍乱弧菌是由霍乱弧菌引起的霍乱，是一种非侵入性脱水肠疾病，如果不及时治疗，其死亡率很高。感染 V。霍乱可在该病流行的国家/地区长期预防继发性疾病。尽管这种保护性免疫的机制尚不清楚，但据推测对 V具有保护性粘膜反应。肠道相关淋巴组织中记忆B细胞的记忆消除可能介导了霍乱感染。为了表征记忆性B细胞对霍乱的反应，我们招募了39例经培养证实为霍乱的住院患者，并在随后的1年中定期评估其免疫学反应。使用多克隆刺激外周血单核细胞的方法，列举了针对霍乱抗原的记忆B细胞，包括脂多糖（LPS）和蛋白抗原霍乱毒素B亚基（CTB）和毒素核心的菌毛主要亚基A（TcpA）标准的酶联免疫斑点法。所有患者在第90天时均表现出CTB，TcpA和LPS特异性免疫球蛋白G（IgG）和IgA记忆反应。此外，这些记忆B细胞反应持续长达1年，大大长于其他传统的免疫学标记物，其感染< em> V。霍乱。虽然LPS特异性IgG记忆B细胞反应的强度在1年时减弱，但CTB和TcpA特异性IgG记忆B细胞在感染后1年仍显着升高，这表明T细胞的帮助可能导致更持久记忆B细胞对 V的反应。霍乱蛋白抗原。此类记忆B细胞在暴露于 V时可以介导记忆消除反应。霍乱。

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