ABSTRACT
The ruminal ecosystem is inhabited by complex communities of microbes that include
bacteria, protozoa, archaea, fungi, and viruses. The immune system of the animal has
evolved to maintain tolerance to innocuous gut commensals and allow the induction
of protective responses to pathogens. However, ruminal microbes can also promote local
and systemic inflammation. The ruminal epithelium–vascular interface allows absorption
of fermentation products and also serves as a selective barrier to prevent translocation
and systemic dissemination of bacteria, bacterial toxins, and immunogenic factors.
Ruminal dysbiosis that increases ruminal acidity and osmolarity may increase permeability
and even induce a breach in the integrity of the epithelial and vascular endothelial
barriers, thus facilitating entry of bacteria or bacterial antigens into the portal
vein. Upon reaching the liver, bacteria and their products can cause local inflammation
and alter function of the organ; if they manage to bypass the liver, they can cause
systemic inflammation and affect other organs. Shifts in microbial populations associated
with dysbiosis result in increases in concentrations of potentially toxic and inflammatory
substances that include lipopolysaccharides, lipoteichoic acids, and leukotoxins,
among others. Lipopolysaccharides are constituents of all gram-negative bacteria,
which are the dominant ruminal microbes. The entry of lipopolysaccharides into the
systemic circulation, either from the rumen or lower gut, could trigger the release
of proinflammatory cytokines, reactive oxygen and nitrogen intermediates, and bioactive
lipids. An activated immune system drastically increases its demand for nutrients;
however, the nutritional requirements of an activated immune system in the context
of systemic physiology are still unknown. In conclusion, ruminal microbes and their
products generate many complex interactions with the host immune system, and dysbiosis
has the potential to induce systemic inflammation. Although inflammation is generally
a protective reaction, the persistence of inflammatory mediators could have negative
consequences for the host.
Key words
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Article info
Publication history
Accepted:
October 2,
2017
Received:
July 6,
2017
Footnotes
The authors declare no conflict of interest.
Identification
Copyright
Copyright © 2017, American Registry of Professional Animal Scientists. All rights reserved.
