Dynamic progression of the calf's microbiome and its influence on host health

Abstract

The first year of a calf's life is a critical phase as its digestive system and immunity are underdeveloped. A high level of stress caused by separation from mothers, transportation, antibiotic treatments, dietary shifts, and weaning can have long-lasting health effects, which can reduce future production parameters, such as milk yield and reproduction, or even increase the mortality of calves. The early succession of microbes throughout the gastrointestinal tract of neonatal calves follows a sequential pattern of colonisation and is greatly influenced by their physiological state, age, diet, and environmental factors; this leads to the establishment of region- and site-specific microbial communities. This review summarises the current information on the various potential factors that may affect the early life microbial colonisation pattern in the gastrointestinal tract of calves. The possible role of host-microbe interactions in the development and maturation of host gut, immune system, and health are described. Additionally, the possibility of improving the health of calves through gut microbiome modulation and using antimicrobial alternatives is discussed. Finally, the trends, challenges, and limitations of the current research are summarised and prospective directions for future studies are highlighted.

Keywords: Calve; Feeding; Gastrointestinal tract; Host health; Immune system; Microbiome.

Fig. 1

Factors that influence the initial establishment and development of microbial communities throughout the GIT of neonatal calves. Figure created with BioRender.com.

Fig. 2

Mucosa-associated lymphoid tissues (MALTs) dependent activation of immune responses in mucosal surface of calves. A) Microfold (M) cell transport microbial antigens from the luminal surface to the underlying MALT cells, where they stimulate specific T- and B- lymphocytes, resulting in the production of dIgA by B-cells, which are translocated as sIgA to the apical epithelial surface. PAMPs can alter the expression of TLRs and activate host immunity. B) Upregulation of HTR4 and HTR2B genes expression by mucosa-associated bacteria. These gene codes for the serotonin receptors that regulate GLP-2 secretion by enteroendocrine L cells via interaction of 5-HT with serotonin receptors. C) Breakdown of tight junctions, transport of pathogens and activation of inflammatory responses. Abbreviations: PAMPs, pathogen-associated molecular patterns; dIgA, dimeric immunoglobulin A; sIgA, secretory immunoglobulin A; pIgR, polymeric Ig receptor; TLRs, toll-like receptors; EC cell, enterochromaffin cell; 5-HT, 5-hydroxytryptamine/serotonin; HTR4, 5-hydroxytryptamine receptor 4; HTR2B, 5-hydroxytryptamine receptor 2B; GLP-2, glucagon-like peptide-2. Figure created with BioRender.com.

Fig. 3

Combination of big data repositories with machine learning algorithms to create prediction tools for sustainable animal productions strategies.