Allergic lung inflammation alters neither susceptibility to Streptococcus pneumoniae infection nor inducibility of innate resistance in mice.
Allergic lung inflammation alters neither susceptibility to Streptococcus pneumoniae infection nor inducibility of innate resistance in mice.
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DOI：
10.1186/1465-9921-10-70
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发表时间：
2009-07-27
影响因子：
5.8
通讯作者：
Evans SE
中科院分区：
文献类型：
--
作者：
Clement CG;Tuvim MJ;Evans CM;Tuvin DM;Dickey BF;Evans SE
对呼吸道病原体的保护性宿主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有力的炎性先天免疫应答来对肺炎链球菌（肺炎球菌）肺炎的实质性保护。相反，与哮喘相关的过敏性炎症被认为会促进对肺炎球菌疾病的易感性。本研究试图确定是否预先存在的过敏性肺部炎症影响肺炎球菌性肺炎的进展或减少对细菌的保护性先天免疫的诱导性。为了比较不同的炎症和分泌刺激对肺炎防御的影响，在暴露于各种吸入的卵白蛋白、ATP和/或细菌裂解物的组合后，用吸入性肺炎球菌对经腹腔注射卵白蛋白致敏的小鼠进行攻击。因此，过敏性炎症、粘蛋白脱粒和/或刺激的先天性抗性在感染性攻击之前被诱导。通过在感染后立即评估肺匀浆的细菌CFU来评估病原体杀灭，通过在攻击后18小时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天后评估小鼠存活率。我们发现有和没有过敏性炎症的小鼠的存活率没有差异，诱导粘蛋白脱粒也没有改变存活率。正如我们之前发现的那样，用细菌裂解物处理的小鼠在第七天的存活率显着增加，并且这并没有因过敏性炎症或粘蛋白脱颗粒的存在而改变。过敏性炎症主要与嗜酸性粒细胞浸润相关，而裂解物诱导的反应主要是嗜酸性粒细胞。过敏性炎症的存在没有显著改变对裂解物的嗜酸性反应，也没有影响肺内诱导的细菌杀灭。这些结果表明，过敏性气道炎症既不促进也不抑制小鼠肺炎球菌肺部感染的进展，也不影响对细菌刺激的先天性抗性的成功诱导。
Protective 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. To 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. We 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. These 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.
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DOI：
10.1016/s0140-6736(03)15021-0
发表时间：
2003-12-13
期刊：
Lancet (London, England)
影响因子：
--
作者：
File TM
通讯作者：
File TM
影响因子：
14.2
作者：
Juhn, Young J.;Kita, Hirohito;Jacobson, Robert M.
通讯作者：
Jacobson, Robert M.
影响因子：
7.3
作者：
RICE, WR;SINGLETON, FM
通讯作者：
SINGLETON, FM
DOI：
10.1165/rcmb.2007-0336rc
发表时间：
2008-03-01
影响因子：
6.4
作者：
Ueno, Keiko;Koga, Takeshi;Kim, K. Chul
通讯作者：
Kim, K. Chul
影响因子：
158.5
作者：
Bisgaard, Hans;Hermansen, Mette Northman;Pipper, Christian Bressen
通讯作者：
Pipper, Christian Bressen