ACCUMULATION OF PLASMA-CELLS IN INFLAMED SITES - EFFECTS OF ANTIGEN, NONSPECIFIC MICROBIAL ACTIVATORS, AND CHRONIC INFLAMMATION
ACCUMULATION OF PLASMA-CELLS IN INFLAMED SITES - EFFECTS OF ANTIGEN, NONSPECIFIC MICROBIAL ACTIVATORS, AND CHRONIC INFLAMMATION
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DOI：
10.1128/iai.59.11.4019-4025.1991
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发表时间：
1991-11-01
影响因子：
3.1
通讯作者：
TEW, JG
中科院分区：
文献类型：
--
作者：
MALLISON, SM;SMITH, JP;TEW, JG
浆细胞常见于慢性炎症部位，包括牙周病变。 本研究的目的是确定哪些因素有助于浆细胞的局部积累。 具体而言，我们试图评估与慢性炎症相关的感染因子（具核梭杆菌，一种在慢性牙周病变中突出的生物体）的特异性抗原和非特异性激活剂的作用以及慢性炎症本身的作用。 在辣根过氧化物酶（HRP）免疫家兔的背部几个部位皮下注射50 μ l无菌明矾，诱导慢性炎症（14至17天）。 对照包括注射盐水的部位或在明矾炎症3天后检查的更急性部位。 用HRP（抗原）激发位点，超声处理F。nucleatum（非特异性激活剂），或两者一起，看看是否F。具核质具有佐剂作用。 激发后3天，过氧化物酶组织化学后计数HRP特异性抗体形成细胞（AFC）。 在非炎症部位或急性炎症部位，几乎没有明显的HRP特异性AFC。 相比之下，慢性炎症本身足以引起特异性AFC反应（相当于10个细胞/mm 2）。 添加F. nucleatum或HRP对慢性病变的HRP特异性AFC的数量增加了一倍左右。 然而，在用抗原和活化剂一起攻击的慢性炎症部位中观察到显著的8至15倍（80至150/mm 2）增加。 有趣的是，活化剂在急性部位或正常皮肤中没有这种佐剂作用。 简而言之，浆细胞在发炎部位的积累是由慢性炎症、微生物来源的活化剂和特异性抗原促进的。 预计这种环境会在某些牙周病变中发展，并且可以帮助解释为什么某些部位的牙龈沟液可能含有极高水平的局部产生的针对某些抗原的特异性抗体。
Plasma cells are common in chronically inflamed sites, including periodontal lesions. The aim of this study was to determine which factors contribute to this local accumulation of plasma cells. Specifically, we sought to evaluate the effects of specific antigen and nonspecific activators from an infectious agent associated with chronic inflammation (Fusobacterium nucleatum, an organism prominent in chronic periodontal lesions) and the effect of the chronic inflammation itself. Chronic inflammation (14 to 17 days) was induced in horseradish peroxidase (HRP)-immune rabbits by subcutaneous injection of 50-mu-l of sterile alum in several sites in their backs. Controls included sites injected with saline or more acute sites examined after 3 days of alum inflammation. Sites were challenged with HRP (the antigen), sonicated F. nucleatum (the nonspecific activator), or both together to see whether F. nucleatum has an adjuvant effect. Three days after challenge, HRP-specific antibody-forming cells (AFC) were enumerated after peroxidase histochemistry. In noninflamed sites or sites with acute inflammation, virtually no HRP-specific AFC were evident. In contrast, chronic inflammation alone was sufficient to elicit a specific AFC response (congruent-to 10 cells per mm2). Addition of either F. nucleatum or HRP to the chronic lesion about doubled the number of HRP-specific AFC. However, a dramatic 8- to 15-fold (80 to 150/mm2) increase was seen in chronically inflamed sites challenged with antigen and activator together. Interestingly, the activator did not have this adjuvant effect in the acute sites or in normal skin. In short, accumulation of plasma cells in inflamed sites is promoted by chronic inflammation, activators of microbial origin, and specific antigen. This milieu can be expected to develop in some periodontal lesions and could help explain why gingival crevicular fluid from some sites may contain extraordinary levels of locally produced specific antibodies for certain antigens.