Evaluating effects of rumen originated lipopolysaccharide on the pathogenesis of subacute rumen acidosis

Descripción del proyecto

Descifrar la patogénesis de la acidosis ruminal subclínica

La acidosis ruminal subclínica (SARA, por sus siglas en inglés) es un trastorno digestivo de las vacas lecheras que afecta a la salud del animal y a la rentabilidad de la industria en general. Está asociada a una mayor concentración de lipopolisacáridos ruminales, y los datos preliminares mostraron que los lipopolisacáridos participan en la patogénesis de la SARA a través de un aumento de las bacterias ruminales, que digieren almidón y producen lactato, así como la regulación al alza de los genes involucrados en la biosíntesis de lipopolisacáridos. Los objetivos del proyecto financiado con fondos europeos LIS son investigar en detalle el papel de los lipopolisacáridos en la patogénesis de la SARA y proporcionar la dirección para el desarrollo de productos posibles para su inactivación en el rumen.

Objetivo

Subacute ruminal acidosis (SARA) is a well-recognized digestive disorder of high yielding dairy cows that has a negative impact on both animal health and herd profitability. It is associated with increased ruminal lipopolysaccharide (LPS), and LPS has been reported to participate in the pathogenesis of SARA. LPS from E. coli (LPS-E) has been used to study its effects on the SARA pathogenesis. Our preliminary data showed that LPS-E participates in the pathogenesis of SARA by directly increasing the starch-digesting and lactate-producing ruminal bacteria and the genes involved in the LPS biosynthesis process. However, we do not know if LPS-E would be representative of LPS from ruminal bacteria (LPS-R), and thus we do not know how LPS released from SARA cows participate in the pathogenesis of SARA. Therefore, the objectives of this proposal are to 1) isolate LPS from the rumen bacteria by inducing SARA nutritional model in batch culture (WP1, 2, 5, 6 & 7); 2) and compare the effects of LPS-R with the LPS-E on ruminal fermentation, bacterial community composition (BCC), and function by using 16S rRNA sequencing and RNA sequencing in batch culture to elucidate the roles of LPS on the pathogenesis of SARA (WP1, 3, 4, 5, 6 & 7). We hypothesis that 1) LPS from ruminal bacteria could be collected from culture media through inducing SARA nutritional model in batch culture; 2) LPS-R and LPS-E will have different effects on ruminal fermentation, BCC, and functions, but both of the two LPS sources would stimulate the bacteria and genes involved in starch digestion, lactic acid production, and LPS biosynthesis. We expect that our proposal could 1) fulfill the gap of knowledge of the role of LPS on the SARA pathogenesis; 2) provide the direction for industries to develop the products (e.g. clay) could inactive LPS in the rumen; 3) help European dairy industries save at least 994.4 million euros per year due to lower SARA prevalence.