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首页> 外文期刊>Respiratory Research >Allergic lung inflammation alters neither susceptibility to Streptococcus pneumoniae infection nor inducibility of innate resistance in mice
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Allergic lung inflammation alters neither susceptibility to Streptococcus pneumoniae infection nor inducibility of innate resistance in mice

机译：肺部过敏性炎症既不会改变对肺炎链球菌感染的敏感性，也不会改变小鼠固有抗性的诱导性

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BackgroundProtective host responses to respiratory pathogens are typically characterized by inflammation. However, lung inflammation is not always protective and it may even become deleterious to the host. We have recently reported substantial protection against Streptococcus pneumoniae (pneumococcal) pneumonia by induction of a robust inflammatory innate immune response to an inhaled bacterial lysate. Conversely, the allergic inflammation associated with asthma has been proposed to promote susceptibility to pneumococcal disease. This study sought to determine whether preexisting allergic lung inflammation influences the progression of pneumococcal pneumonia or reduces the inducibilty of protective innate immunity against bacteria.MethodsTo compare the effect of different inflammatory and secretory stimuli on defense against pneumonia, intraperitoneally ovalbumin-sensitized mice were challenged with inhaled pneumococci following exposure to various inhaled combinations of ovalbumin, ATP, and/or a bacterial lysate. Thus, allergic inflammation, mucin degranulation and/or stimulated innate resistance were induced prior to the infectious challenge. Pathogen killing was evaluated by assessing bacterial CFUs of lung homogenates immediately after infection, the inflammatory response to the different conditions was evaluated by measurement of cell counts of bronchoalveolar lavage fluid 18 hours after challenge, and mouse survival was assessed after seven days.ResultsWe found no differences in survival of mice with and without allergic inflammation, nor did the induction of mucin degranulation alter survival. As we have found previously, mice treated with the bacterial lysate demonstrated substantially increased survival at seven days, and this was not altered by the presence of allergic inflammation or mucin degranulation. Allergic inflammation was associated with predominantly eosinophilic infiltration, whereas the lysate-induced response was primarily neutrophilic. The presence of allergic inflammation did not significantly alter the neutrophilic response to the lysate, and did not affect the induced bacterial killing within the lungs.ConclusionThese results suggest that allergic airway inflammation neither promotes nor inhibits progression of pneumococcal lung infection in mice, nor does it influence the successful induction of stimulated innate resistance to bacteria.
机译：背景技术保护宿主对呼吸道病原体的反应通常以炎症为特征。然而，肺部炎症并不总是保护性的，甚至可能对宿主有害。我们最近报道了通过诱导对吸入的细菌裂解物的强烈的炎性先天免疫应答，对肺炎链球菌（肺炎球菌）肺炎具有实质性保护作用。相反，已经提出了与哮喘有关的过敏性炎症，以增强对肺炎球菌疾病的易感性。这项研究试图确定预先存在的过敏性肺部炎症是否会影响肺炎球菌性肺炎的进展或降低针对细菌的先天性免疫的诱导能力。暴露于卵白蛋白，ATP和/或细菌裂解物的各种吸入组合后，吸入肺炎球菌。因此，在感染挑战之前诱发了过敏性炎症，粘蛋白脱粒和/或刺激的先天性抵抗力。感染后立即评估肺匀浆的细菌CFU来评估病原体的杀伤力，攻击后18小时通过测量支气管肺泡灌洗液的细胞计数来评估对不同条件的炎症反应，并在7天后评估小鼠的存活率。有和没有变应性炎症的小鼠的生存率差异，粘蛋白脱粒的诱导也没有改变生存率。正如我们之前所发现的，用细菌裂解液治疗的小鼠在7天时显示出明显提高的存活率，并且不会因存在过敏性炎症或粘蛋白脱颗粒而改变。过敏性炎症主要与嗜酸性粒细胞浸润有关，而裂解物诱导的反应主要是嗜中性粒细胞。过敏性炎症的存在并没有显着改变对溶胞产物的嗜中性反应，也没有影响肺内诱导的细菌杀灭。影响受激先天性细菌抗性的成功诱导。

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