Abstract
BackgroundOur previous research on the diversity of microbiota in the endotracheal tubes (ETTs) of neonates in the neonatal intensive care unit found that Pseudomonas aeruginosa (P. aeruginosa) and Streptococcus mitis (S. mitis) were the dominant bacteria on the ETT surface and the existence of S. mitis could promote biofilm formation and pathogenicity of P. aeruginosa. Toll-like receptor 4 (TLR4), which has been widely detected on the surface of airway epithelial cells, is the important component of the innate immune system. Therefore, we hypothesized that the co-existence of these two bacteria might impact the host immune system through TLR4 signaling.ResultsS. mitis rarely caused inflammation, whereas P. aeruginosa caused the most severe inflammation accompanied by increases in the number of inflammatory cells, interleukin (IL)-6 and tumor necrosis factor (TNF)-α expression, and total cell counts in BALF (p < 0.05). In the PAO1 + S. mitis group, moderate inflammation, reduced IL-6 and TNF-α protein levels, and decreased total cell counts were observed. Additionally, levels of these indicators were decreased lower in TLR4-deficient mice than in wild-type mice (p < 0.05).ConclusionsOur results demonstrated that infection with S. mitis together with P. aeruginosa could alleviate lung inflammation in acute lung infection mouse models possibly via the TLR4 signaling pathway.
Highlights
Our previous research on the diversity of microbiota in the endotracheal tubes (ETTs) of neonates in the neonatal intensive care unit found that Pseudomonas aeruginosa (P. aeruginosa) and Streptococcus mitis (S. mitis) were the dominant bacteria on the ETT surface and the existence of S. mitis could promote biofilm formation and pathogenicity of P. aeruginosa
Some studies have reported that Toll-like receptor 4 (TLR4)-deficient mice show increased lung inflammation and higher bacterial load, and TLR4 signaling may have a critical function in the fine tuning of inflammation during chronic mycobacterial infection [15]
We found that wild-type mice as well as TLR4-deficient mice infected with an S. mitis strain for 48 h showed little change in pulmonary lesions, supporting the common notion that S. mitis is a normal commensal bacteria in the human oropharynx [19,20,21]
Summary
Our previous research on the diversity of microbiota in the endotracheal tubes (ETTs) of neonates in the neonatal intensive care unit found that Pseudomonas aeruginosa (P. aeruginosa) and Streptococcus mitis (S. mitis) were the dominant bacteria on the ETT surface and the existence of S. mitis could promote biofilm formation and pathogenicity of P. aeruginosa. Toll-like receptor 4 (TLR4), which has been widely detected on the surface of airway epithelial cells, is the important component of the innate immune system. We hypothesized that the co-existence of these two bacteria might impact the host immune system through TLR4 signaling. Recent studies have confirmed that TLR2, 4, 5, and 9 play pivotal roles in the response to bacterial infections [10]. We hypothesized that TLR4 signaling might participate in the response to acute lung infection
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