Abstract

During the periparturient period there is a significant increase in the incidence of multiple metabolic and infectious diseases in dairy cows. Dairy cows are fed high-grain diets immediately after calving to support production of large amounts of milk. Mounting evidence indicates these types of diets are associated with the release of high amounts of endotoxins in the rumen fluid. If infected, the udder and uterus additionally become important sources of endotoxins during the postpartum period. There is increasing evidence that endotoxins translocate from rumen, uterus, or udder into the systemic circulation and trigger chronic low-grade inflammatory conditions associated with multiple diseases including fatty liver, mastitis, retained placenta, metritis, laminitis, displaced abomasum, milk fever, and downer cow syndrome. Interestingly, endotoxin-related diseases are triggered by a bacterial component and not by a specific bacterium. This makes prevention of these type of diseases different from classical infectious diseases. Prevention of translocation of endotoxins into the host systemic circulation needs to take priority and this could be achieved with a new approach: mucosal vaccination. In this review article, we discuss all the aforementioned issues in detail and also report some of our trials with regards to mucosal vaccination of periparturient dairy cows.

Highlights

  • Despite improvements to production and efficiency within the dairy industry, the high incidence of disease from 3 weeks prepartum to 3 weeks postpartum, termed the transition period, remains a major cause of high culling rates as well as significant economic losses for the producer [1]

  • While E. coli LPS stimulates cells through TLR4, LPS from Porphyromonas gingivalis, which is an is an intermediate shape between conical and cylindrical, stimulates TLR2 receptors. This differential intermediate shape between conical and cylindrical, stimulates TLR2 receptors. This differential receptor stimulation results in marked differences to gene transcription with E. coli LPS inducing the receptor stimulation results in marked differences to gene transcription with E. coli LPS inducing the transcription of tumor necrosis factor α (TNF), interleukin (IL)-1, interferon (IFN)-γ, and the IL-12 transcription of tumor necrosis factor α (TNF), interleukin (IL)‐1, interferon (IFN)‐γ, and the IL‐12 subunit p40, while P. gingivalis, which exclusively binds to TLR2, induces only the transcription of subunit p40, while P. gingivalis, which exclusively binds to TLR2, induces only the transcription of IL-1 and totoa alesser

  • While the proportions of Gram-negative bacteria (GNB) and Gram-positive bacteria (GPB) were found to be nearly caused an increase in bacteria of phyla Firmicutes and Actinobacteria and a decrease in Proteobacteria and equal in the control group, there was a distinct difference seen with the SARA‐inducing diet

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Summary

Introduction

Despite improvements to production and efficiency within the dairy industry, the high incidence of disease from 3 weeks prepartum to 3 weeks postpartum, termed the transition period, remains a major cause of high culling rates as well as significant economic losses for the producer [1]. Lipopolysaccharide and LTA are the main components of bacterial cell wall membranes of GNB and GPB species, respectively, and are vital to their stability and function [20]. These molecules are known as endotoxins and while they are not harmful when embedded in the cell membrane, once released they are highly immunostimulatory and largely responsible for the signs of bacterial 63. O‐chain,ofisautolysins the outermost region of LPSenvironment, and its important proteins in colonization of the host, delivery in a competitive structure is highly variable, consisting of one to eight glycosyl residues The variation within this area for bacterial survival to kill other competitors, or nutrient acquisition (for more details read [22]). Of LPS by exerting theGNB sameisolates biological effects as natural E. coli lipid A [23,24]

The general structureofofGram-negative
A Structure
Gastrointestinal
Mammary Gland
Uterus
Translocation of Endotoxin
Possible Mechanisms of Paracellular Transport
Paracellular pathwayofofLPS
Possible Mechanisms of Transcellular Transport
Possible
Acute and Subacute Ruminal Acidosis
Fatty Liver
Mastitis
Retained Placenta
Metritis and Endometritis
Laminitis
Displaced Abomasum
Milk Fever
Downer Cow Syndrome
Why Mucosal Vaccination Against LPS and LTA?
Induction of the Mucosal Immune Responses
Diagram
Connectivity and Compartmentalization of the Mucosal Immune System
Optimal of Immunization
Optimal
Endotoxin and Immunological Memory
Conclusions and parenteral
Findings
1.Funding

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