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Mycoplasma pneumoniae carriage evades induction of protective mucosal antibodies
European Respiratory Journal ( IF 16.6 ) Pub Date : 2022-04-07 , DOI: 10.1183/13993003.00129-2021
Ruben Cornelis Anthonie de Groot 1 , Silvia Cristina Estevão 1 , Patrick Michael Meyer Sauteur 2 , Aditya Perkasa 1 , Theo Hoogenboezem 3 , Emiel Benny Margriet Spuesens 1 , Lilly Maria Verhagen 4 , Anna Maria Christiane van Rossum 5 , Wendy Wilhelmina Josephina Unger 6
Affiliation  

Background

Mycoplasma pneumoniae is the most common bacterial cause of pneumonia in children hospitalised for community-acquired pneumonia (CAP). Prevention of infection by vaccines may be an important strategy in the presence of emerging macrolide-resistant M. pneumoniae. However, knowledge of immune responses to M. pneumoniae is limited, complicating vaccine design.

Methods

We studied the antibody response during M. pneumoniae respiratory tract infection and asymptomatic carriage in two different cohorts.

Results

In a nested case–control study (n=80) of M. pneumoniae carriers and matched controls we observed that carriage by M. pneumoniae does not lead to a rise in either mucosal or systemic M. pneumoniae-specific antibodies, even after months of persistent carriage. We replicated this finding in a second cohort (n=69) and also found that during M. pneumoniae CAP, mucosal levels of M. pneumoniae-specific IgA and IgG did increase significantly. In vitro adhesion assays revealed that high levels of M. pneumoniae-specific antibodies in nasal secretions of paediatric patients prevented the adhesion of M. pneumoniae to respiratory epithelial cells.

Conclusions

Our study demonstrates that M. pneumoniae-specific mucosal antibodies protect against bacterial adhesion to respiratory epithelial cells, and are induced only during M. pneumoniae infection and not during asymptomatic carriage. This is strikingly different from carriage with bacteria such as Streptococcus pneumoniae where mucosal antibodies are induced by bacterial carriage.



中文翻译:

携带肺炎支原体逃避保护性黏膜抗体的诱导

背景

肺炎支原体是因社区获得性肺炎 (CAP) 住院的儿童最常见的肺炎细菌原因。在新出现的耐大环内酯类肺炎支原体存在的情况下,通过疫苗预防感染可能是一项重要策略。然而,对肺炎支原体的免疫反应知识有限,使疫苗设计复杂化。

方法

我们研究了两个不同队列中肺炎支原体呼吸道感染和无症状携带期间的抗体反应。

结果

在一项针对肺炎支原体携带者和匹配对照的巢式病例对照研究 (n=80) 中,我们观察到肺炎支原体的携带不会导致黏膜或全身肺炎支原体特异性抗体升高,即使经过数月持久的运输。我们在第二个队列(n=69)中重复了这一发现,并且还发现在肺炎支原体CAP 期间,肺炎支原体特异性 IgA 和 IgG的粘膜水平确实显着增加。体外粘附试验表明,儿科患者鼻腔分泌物中高水平的肺炎支原体特异性抗体可防止肺炎支原体的粘附到呼吸道上皮细胞。

结论

我们的研究表明,肺炎支原体特异性黏膜抗体可防止细菌粘附到呼吸道上皮细胞,并且仅在肺炎支原体感染期间而不是在无症状携带期间被诱导。这与携带细菌如肺炎链球菌的情况截然不同,后者的粘膜抗体是由细菌携带引起的。

更新日期:2022-04-07
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