The concordance between upper and lower respiratory microbiota in children with Mycoplasma pneumoniae pneumonia

Abstract

In recent years, the morbidity of Mycoplasma pneumoniae pneumonia (MPP) has dramatically increased in China. An increasing number of studies indicate that an imbalance in the respiratory microbiota is associated with respiratory infection. We selected 28 hospitalized patients infected with M. pneumoniae and 32 healthy children. Nasopharyngeal (NP) and oropharyngeal (OP) swabs were collected from healthy children, whereas NP, OP and bronchoalveolar lavage (BAL) specimens were collected from patients. Microbiota analysis was performed on all microbial samples using 16 S ribosomal RNA (16 S rRNA) sequencing. The NP microbial samples in healthy children were divided into two groups, which were dominated by either Staphylococcus or mixed microbial components. The respiratory microbiota in pneumonia patients harbored a lower microbial diversity compared to healthy children, and both the NP and OP microbiota of patients differed significantly from that of healthy children. Hospitalized MPP children with a higher abundance of Mycoplasma in the BAL fluid (BALF) microbiota tended to suffer longer hospitalization lengths and higher peak fevers and serum C-reactive protein levels. Concordance analysis explained the succession of imbalanced NP microbiota to the OP and lung in diseased children. However, the association of the abundance of Mycoplasma in BALF microbiota with that in NP or OP microbiota varied among individuals, which suggested the sensitivity of BALF in MPP diagnostics, mirroring MPP severity.

Shen-ling-bai-zhu-san ameliorates inflammation and lung injury by increasing the gut microbiota in the murine model of Streptococcus pneumonia-induced pneumonia

“…Microbial balance in the specific tissue was associated with the development of disease [27]. Increasing studies have demonstrated that microbial diversity in the BLAF was significantly decreased and relationship with the disease severity in patients with pneumonia such as bacterial pneumonia, Mycoplasma pneumoniae pneumonia [28,29]. In the BLAF of patients with Spn-induced pneumonia, Spn were accumulated and had low microbial diversity because Spn secreted the abundant various virulence factors to inhibit the other bacterial survival [30].…”

An integrated respiratory microbial gene catalogue to better understand the microbial aetiology of Mycoplasma pneumoniae pneumonia

“…Increasingly, reports demonstrate that specific dominant bacteria are associated with severe acute respiratory infections [6, 15, 46], but there have been no meaningful correlations identified between disease severity and M. pneumonia —or indeed between the other species of reassembled bacteria found in the OP microbiota of children with MPP. In our previous studies, we confirmed the succession of M. pneumoniae infection in NP to OP and lung, and determined an association between M. pneumoniae load in the lung microbiota with disease severity [14].…”

“…Morbidity and mortality related to MPP is increasing in Chinese children. The development of RM studies has improved our understanding of the microbial aetiology of MPP by revealing infection-associated RM imbalances [13, 14]. However, microbial functions and host–microbiota interactions in the RM of patients with MPP remain to be explored, particularly for novel microbial species.…”

“…Previous studies by our group have revealed altered RM in children with MPP [13, 14]. However, current RM research has mainly focused on analysis of 16S rRNA [6, 7, 15, 16], which only provides cues about known bacterial components at the genus level.…”

Association between inflammation factors and Mycoplasma pneumoniae in children

“…Mycoplasma pneumoniae is a common respiratory pathogen that is responsible for the community-acquired pneumonia (CAP), especially in children. [1–3] Furthermore, it also triggers the exacerbation of asthmatic symptoms and wheezes in children. [4–9] It has been reported that M pneumoniae accounts for 7% to 40% of all CAP in children 3 to 15 years of age.…”