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首页> 外文期刊>Infection and immunity >Cytokine Kinetics and Other Host Factors in Response to Pneumococcal Pulmonary Infection in Mice
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Cytokine Kinetics and Other Host Factors in Response to Pneumococcal Pulmonary Infection in Mice

机译：细胞因子动力学和其他宿主因素对小鼠肺炎球菌肺部感染的反应。

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There is a need for more insight into the pathogenesis ofStreptococcus pneumoniae pneumonia, as the fatality rate associated with this disease remains high despite appropriate antibiotherapy. The host response to pneumococci was investigated after intranasal inoculation of CD1 mice with 107 log-phase CFU of bacteria. We identified five major pathogenesis steps from initial infection to death. In step 1 (0 to 4 h), there was ineffective phagocytosis by alveolar macrophages, with concurrent release of tumor necrosis factor alpha (TNF), interleukin-6 (IL-6), and nitric oxide (NO) in bronchoalveolar lavage (BAL) fluid, TNF, IL-6, and interleukin-1 alpha (IL-1) in lung tissues, and IL-6 in serum, which were associated with tachypnea and hemoconcentration. In step 2 (4 to 24 h), bacterial growth in alveoli and polymorphonuclear cell recruitment from bloodstream to lung tissue (high myeloperoxidase levels) to alveoli were associated with high release of all three cytokines and leukotriene B4(LTB4) in tissue and BAL fluid, as well as transient spillover of IL-1 in serum. In step 3 (24 to 48 h), despite downregulation of TNF and IL-1 in BAL fluid and lungs, there was appearance of injury to alveolar ultrastructure, edema to interstitium, and increase in lung weight as well as regeneration of type II pneumocytes and increased secretion of surfactant; bacteria progressed from alveoli to tissue to blood, and body weight loss occurred. In step 4 (48 to 72 h), strong monocyte recruitment from blood to alveoli was associated with high NO release in tissue and BAL fluid, but there was also noticeable lymphocyte recruitment and leukopenia; bacteremia was associated with TNF and IL-6 release in blood and thrombocytopenia. In step 5 (72 to 96 h), severe airspace disorganization, lipid peroxidation (high malondialdehyde release in BAL fluid), and diffuse tissue damage coincided with high NO levels; there was further increase in lung weight and bacterial growth, loss in body weight, and high mortality rate. Delineation of the sequential steps that contribute to the pathogenesis of pneumococcal pneumonia may generate markers of evolution of disease and lead to better targeted intervention.
机译：需要进一步了解肺炎链球菌肺炎的发病机理，因为尽管进行了适当的生物治疗，与此疾病相关的死亡率仍然很高。在鼻内接种10 7 对数期细菌的CD1小鼠后，研究了宿主对肺炎球菌的反应。我们确定了从初始感染到死亡的五个主要发病机理步骤。在步骤1（0到4小时）中，肺泡巨噬细胞吞噬无效，同时在支气管肺泡灌洗液（BAL）中释放肿瘤坏死因子α（TNF），白介素6（IL-6）和一氧化氮（NO）。 ）肺组织中的液体，TNF，IL-6和白介素-1α（IL-1）以及血清中的IL-6，这与呼吸急促和血液浓缩有关。在第2步（4至24小时）中，肺泡中的细菌生长和从血液到肺组织（高髓过氧化物酶水平）到肺泡的多形核细胞募集与所有三种细胞因子和白三烯B 4 的高释放相关组织和BAL液中的（LTB 4 ）以及血清中IL-1的瞬时溢出。在第3步（24到48小时）中，尽管BAL液和肺中TNF和IL-1的表达下调，但肺泡超微结构受到损害，间质水肿，肺部重量增加，II型肺细胞再生和增加表面活性剂的分泌;细菌从肺泡发展到组织再到血液，并发生了体重减轻。在第4步（48至72小时）中，从血液到肺泡的强单核细胞募集与组织和BAL液中NO的高释放有关，但也有明显的淋巴细胞募集和白细胞减少。菌血症与血液和血小板减少症中的TNF和IL-6释放有关。在第5步（72至96小时）中，严重的空域紊乱，脂质过氧化（BAL液中丙二醛释放量高）和弥散性组织损伤与高NO值相吻合。肺重量和细菌生长进一步增加，体重减轻，死亡率高。描绘导致肺炎球菌性肺炎发病机理的顺序步骤可能会产生疾病演变的标志，并导致更好的针对性干预。

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