Acute lung injury (ALI) and the more severe acute respiratory distress syndrome 
are common responses to a variety of infectious and noninfectious insults. We 
used a mouse model of ALI induced by intratracheal administration of sterile 
bacterial wall lipopolysaccharide (LPS) to investigate the changes in innate 
lung microbiota and study microbial community reaction to lung inflammation and 
barrier dysfunction induced by endotoxin insult. One group of C57BL/6J mice 
received LPS via intratracheal injection (n = 6), and another received sterile 
water (n = 7). Bronchoalveolar lavage (BAL) was performed at 72 h after 
treatment. Bacterial DNA was extracted and used for qPCR and 16S rRNA gene-tag 
(V3-V4) sequencing (Illumina). The bacterial load in BAL from ALI mice was 
increased fivefold (P = 0.03). The community complexity remained unchanged 
(Simpson index, P = 0.7); the Shannon diversity index indicated the increase of 
community evenness in response to ALI (P = 0.07). Principal coordinate analysis 
and analysis of similarity (ANOSIM) test (P = 0.005) revealed a significant 
difference between microbiota of control and ALI groups. Bacteria from families 
Xanthomonadaceae and Brucellaceae increased their abundance in the ALI group as 
determined by Metastats test (P < 0.02). In concordance with the 16s-tag data, 
Stenotrohomonas maltophilia (Xanthomonadaceae) and Ochrobactrum anthropi 
(Brucellaceae) were isolated from lungs of mice from both groups. Metabolic 
profiling of BAL detected the presence of bacterial substrates suitable for both 
isolates. Additionally, microbiota from LPS-treated mice intensified 
IL-6-induced lung inflammation in naive mice. We conclude that the morbid 
transformation of ALI microbiota was attributed to the set of inborn 
opportunistic pathogens thriving in the environment of inflamed lung, rather 
than the external infectious agents.