Intestinal antilectin immunoglobulin A antibody response and immunity to Entamoeba dispar infection following cure of amebic liver abscess.
Intestinal antilectin immunoglobulin A antibody response and immunity to Entamoeba dispar infection following cure of amebic liver abscess.
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阿米巴肝脓肿治愈后肠抗凝集素免疫球蛋白 A 抗体反应和对内阿米巴迪帕感染的免疫力。
DOI：
10.1128/iai.71.12.6899-6905.2003
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发表时间：
2003
影响因子：
3.1
通讯作者：
Jackson,TerryFHG
中科院分区：
文献类型：
--
作者：
Ravdin,JonathanI;Abd-Alla,MohamedD;Welles,SethL;Reddy,Selvan;Jackson,TerryFHG
我们随访了93例阿米巴肝脓肿（ALA）患者和963例密切相关的对照者，间隔3个月，为期36个月，以表征对阿米巴半乳糖凝集素的肠道和体液抗体反应，并确定ALA治愈后是否产生了对溶组织内阿米巴的免疫力。结果发现，ALA患者肠道抗凝集素免疫球蛋白A（伊加）和血清抗LC 3（富含半胱氨酸的重组凝集素蛋白）伊加和IgG抗体的检出率和水平均显著高于对照组（P< 0.01和P < 0.05）。ALA受试者的肠道抗凝集素伊加抗体应答持续时间较长（18个月时71.8%保持阳性，36个月时52.6%保持阳性，P< 0.001，而对照组分别为17.6%和10.3%）。ALA受试者对E具有高度免疫力。在整个研究期间，感染率为0%（6个月和36个月时为0%，而对照组分别为6.5%和4.9%，P< 0.05）。入组研究时，6.3%的ALA受试者感染了E。组织溶解性;新大肠杆菌的发生率。对照组中的溶组织感染（通过培养确定）太低（1.4%），无法确定ALA受试者是否表现出对新感染的免疫力。我们发现每3个月进行一次粪便培养明显低估了新大肠杆菌的发生。在12个月的随访中，15.3%的对照组发生了血清转化。不幸的是，在南非德班的田间条件下，用于检测粪便中凝集素抗原的酶联免疫吸附试验产生了不可靠的结果。总之，ALA治愈的受试者表现出对阿米巴半乳糖凝集素的持续粘膜伊加抗体应答和对E的高水平免疫。肺部感染。对E. ALA的组织溶解性随访治疗将需要使用更敏感和可靠的诊断方法。
We followed 93 subjects with amebic liver abscess (ALA) and 963 close associate controls at 3-month intervals for 36 months to characterize intestinal and humoral antibody responses to the amebic galactose-inhibitable lectin and to determine whether immunity developed toEntamoeba histolyticaorEntamoeba disparinfection following cure of ALA. We found that ALA subjects had a higher prevalence and level of intestinal antilectin immunoglobulin A (IgA) and serum anti-LC3 (cysteine-rich recombinant lectin protein) IgA and IgG antibodies,P< 0.01 andP< 0.05, respectively, compared to controls. The intestinal antilectin IgA antibody response was sustained over a longer time period in ALA subjects (71.8% remained positive at 18 months and 52.6% at 36 months,P< 0.001 compared to 17.6% and 10.3% of controls, respectively). ALA subjects were highly immune toE. disparinfection throughout the study (0% infected at 6 and 36 months, compared to 6.5% and 4.9% of control subjects, respectively,P< 0.05). Upon entry into the study, 6.3% of ALA subjects were infected withE. histolytica;the incidence of newE. histolyticainfections in controls (as determined by culture) was too low (1.4%) to determine whether ALA subjects exhibited immunity to new infections. We found that stool cultures every 3 months markedly underestimated the occurrence of newE. histolyticainfections, as 15.3% of controls seroconverted after 12 months of follow-up. Unfortunately, under the field conditions present in Durban, South Africa, enzyme-linked immunosorbent assay for detection of lectin antigen in stool yielded unreliable results. In summary, subjects cured of ALA exhibited sustained mucosal IgA antibody responses to the amebic galactose-inhibitable lectin and a high level of immunity toE. disparinfection. Determination of immunity toE. histolyticafollowing cure of ALA will require the use of more sensitive and reliable diagnostic methods.