Lipopolysaccharide stimulates the growth of bacteria that contribute to ruminal acidosis

Lipopolysaccharide (LPS) has been reported to contribute to a ruminal acidosis of cattle by affecting ruminal bacteria. The goal of this study was to determine how LPS affects the growth of ruminal bacteria pure cultures, including those that contribute to ruminal acidosis. We found that dosing LPS (200,000 EU) increased maximum specific growth rate of four ruminal bacterial species (Streptococcus bovis JB1, Succinivibrio dextrinosolvens 24, Lactobacillus ruminis RF1, Selenomonas ruminantium HD4). Interestingly, all the species ferment sugars and produce lactate, contributing to acidosis. Species that consume lactate or ferment fiber were not affected by LPS. We found that S. bovis JB1 failed to grow in LPS as the carbon source in the media; growth of S. bovis JB1 was increased by LPS when glucose was present. Growth of Megasphaera. elsdenii T81 that consumes lactate was not different between the detoxified (lipid A delipidated) and regular LPS. However, maximum specific growth rate of S. bovis JB1 was greater in regular LPS than detoxified LPS. Mixed bacteria from dual-flow continuous culture system were collected to determine changes of metabolic capabilities of bacteria by LPS and genes associated to LPS biosynthesis were increased by LPS. In summary, LPS was not toxic to bacteria and lipid A of LPS stimulated the growth of lactate-producing bacteria. Our results indicate that LPS is not only increased during acidosis, but it may also contribute to ruminal acidosis development by increasing the growth of lactic acid producing bacteria. Importance Gram-negative bacteria contain LPS coating their thin peptidoglycan cell wall. Presence of LPS has been suggested to be associated with a metabolic disorder of cattle - ruminal acidosis - through affecting ruminal bacteria. Ruminal acidosis could reduce feed intake and milk production, and increase the incidence of diarrhea, milk fat depression, liver abscesses, and laminitis. However, how LPS affects bacteria associated with ruminal acidosis has not been studied. Here, we investigated how LPS affects the growth of ruminal bacteria by pure cultures, including those that contribute to acidosis, and the functional genes of ruminal bacteria. Thus, this work serves to further our understanding of the roles of LPS in the pathogenesis of ruminal acidosis, as well as providing information that may be useful for the prevention of ruminal acidosis and then reduce economic losses for farmers.