Canalis R F, Zamboni L
Division of Head and Neck Surgery, Department of Surgery, Harbor-UCLA Medical Center and the UCLA School of Medicine, Los Angeles, California 90509, USA.
Laryngoscope. 2001 Jun;111(6):1020-6. doi: 10.1097/00005537-200106000-00016.
To identify the structural changes of the proliferative phase of rhinoscleroma which could be responsible for the chronicity of the disease.
Observational research.
Samples of friable tissue taken from the nasal mucosa of nine untreated patients were processed for light and ultrastructural microscopy.
The majority of changes contributing to the chronicity of the disease occurred in the subepithelium and followed three closely related but distinct events. In the first (infiltrative), subepithelial invasion by the Klebsiella was followed by its active multiplication and proliferation of capillaries. In the second (neutrophilic), large numbers of neutrophils were delivered into this space. Neutrophils actively phagocytized the Klebsiella but appeared to die at an accelerated rate without completing digestion of the microorganisms. In the third event (histiocytic), histiocytes entered the subepithelium and engaged in unrestrained phagocytosis of decaying neutrophils, Klebsiella, and debris. During this process, the histiocytes' phagosomes underwent massive dilation, thus becoming Mikulicz cells. Mikulicz cells were unable to consistently destroy the Klebsiella and eventually ruptured, releasing them into the interstitium. Evidence was found that an autophagic process might contribute to phagosome distention and to the rupture of the vacuolar membranes and cell wall.
Several critical changes responsible for the chronicity of rhinoscleroma occur during the proliferative phase of the disease. The majority of these take place in the subepithelium and include: 1) factors leading to the transformation of histiocytes into Mikulicz cells, 2) the inability of these cells to consistently destroy the Klebsiella, 3) their rupture releasing viable Klebsiella, and 4) the intrinsic resistance of the pathogen.
确定鼻硬结病增殖期的结构变化,这些变化可能是导致该疾病慢性化的原因。
观察性研究。
从9名未经治疗的患者的鼻粘膜采集易碎组织样本,进行光镜和超微结构显微镜检查。
导致疾病慢性化的大多数变化发生在基底膜下,并遵循三个密切相关但又不同的过程。第一个过程(浸润期),肺炎克雷伯菌侵入基底膜下,随后其活跃增殖并伴有毛细血管增生。第二个过程(嗜中性粒细胞期),大量嗜中性粒细胞进入该区域。嗜中性粒细胞积极吞噬肺炎克雷伯菌,但似乎加速死亡,未能完成对微生物的消化。在第三个过程(组织细胞期),组织细胞进入基底膜下,对腐烂的嗜中性粒细胞、肺炎克雷伯菌和碎片进行无节制的吞噬。在此过程中,组织细胞的吞噬体大量扩张,从而变成米库利奇细胞。米库利奇细胞无法持续消灭肺炎克雷伯菌,最终破裂,将它们释放到间质中。有证据表明自噬过程可能导致吞噬体扩张以及液泡膜和细胞壁破裂。
在鼻硬结病增殖期发生了一些导致疾病慢性化的关键变化。其中大多数发生在基底膜下,包括:1)导致组织细胞转化为米库利奇细胞的因素;2)这些细胞无法持续消灭肺炎克雷伯菌;3)它们破裂释放出存活的肺炎克雷伯菌;4)病原体的内在抗性。