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      Influence of meat and bone meal, phytase, and antibiotics on broiler chickens challenged with subclinical necrotic enteritis: 2. intestinal permeability, organ weights, hematology, intestinal morphology, and jejunal gene expression

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          Abstract

          Undigested proteins entering the hindgut may favor the proliferation of Clostridium perfringens. Using phytase to eliminate the need for meat and bone meal ( MBM) as a P source may reduce potential infection with C. perfringens. A study was conducted to determine the impact of MBM, phytase, and antibiotics ( AB) on intestinal permeability and morphology, organ weights, and jejunal gene expression in Ross 308 chickens challenged with subclinical necrotic enteritis ( NE). Male Ross 308-day-old chicks (672 each) were randomly allocated to 8 treatments with 6 replicate pens each housing 14 birds. A 2 × 2 × 2 factorial arrangement of treatments was used: MBM (no or yes); AB (no or yes—Zn bacitracin 100 in S and 50 ppm in G/F and salinomycin Na 60 ppm in all phases); phytase (500 or 1,500 FTU/kg, both using 500 FTU matrix values) using wheat-SBM-canola meal diets. Birds were challenged with Eimeria spp on day 9, and C. perfringens strain EHE-NE18 on day 14 and 15. An AB × MBM interaction ( P < 0.05) was detected for relative gizzard weight (with contents) being lower in birds fed MBM and AB compared to those fed MBM and no AB. A MBM × AB interaction ( P > 0.01) was detected for lymphocyte counts being lower with MBM and AB compared to MBM without AB. A phytase × AB interaction ( P < 0.05) was observed for villi length being increased with high phytase and no AB compared to with AB. Inclusion of MBM increased ( P < 0.05) blood FICT-d concentration, whereas AB decreased it ( P < 0.05). Antibiotics increased RBC ( P < 0.05), Hgb ( P < 0.05), and PCV ( P < 0.05) and expression of Ca-binding protein, CALB1 ( P > 0.05). Inclusion of MBM decreased expression of MUC2 ( P < 0.05). Results indicate that dietary MBM has a detrimental effect on gut health of broilers but this may be counteracted using AB.

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          Enteric Pathogens and Their Toxin-Induced Disruption of the Intestinal Barrier through Alteration of Tight Junctions in Chickens

          Maintaining a healthy gut environment is a prerequisite for sustainable animal production. The gut plays a key role in the digestion and absorption of nutrients and constitutes an initial organ exposed to external factors influencing bird’s health. The intestinal epithelial barrier serves as the first line of defense between the host and the luminal environment. It consists of a continuous monolayer of intestinal epithelial cells connected by intercellular junctional complexes which shrink the space between adjacent cells. Consequently, free passing of solutes and water via the paracellular pathway is prevented. Tight junctions (TJs) are multi-protein complexes which are crucial for the integrity and function of the epithelial barrier as they not only link cells but also form channels allowing permeation between cells, resulting in epithelial surfaces of different tightness. Tight junction’s molecular composition, ultrastructure, and function are regulated differently with regard to physiological and pathological stimuli. Both in vivo and in vitro studies suggest that reduced tight junction integrity greatly results in a condition commonly known as “leaky gut”. A loss of barrier integrity allows the translocation of luminal antigens (microbes, toxins) via the mucosa to access the whole body which are normally excluded and subsequently destroys the gut mucosal homeostasis, coinciding with an increased susceptibility to systemic infection, chronic inflammation and malabsorption. There is considerable evidence that the intestinal barrier dysfunction is an important factor contributing to the pathogenicity of some enteric bacteria. It has been shown that some enteric pathogens can induce permeability defects in gut epithelia by altering tight junction proteins, mediated by their toxins. Resolving the strategies that microorganisms use to hijack the functions of tight junctions is important for our understanding of microbial pathogenesis, because some pathogens can utilize tight junction proteins as receptors for attachment and subsequent internalization, while others modify or destroy the tight junction proteins by different pathways and thereby provide a gateway to the underlying tissue. This review aims to deliver an overview of the tight junction structures and function, and its role in enteric bacterial pathogenesis with a special focus on chickens. A main conclusion will be that the molecular mechanisms used by enteric pathogens to disrupt epithelial barrier function in chickens needs a much better understanding, explicitly highlighted for Campylobacter jejuni, Salmonella enterica and Clostridium perfringens. This is a requirement in order to assist in discovering new strategies to avoid damages of the intestinal barrier or to minimize consequences from infections.
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            Intestinal microbiota and metabolites--Implications for broiler chicken health and performance1

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              Coccidia-induced mucogenesis promotes the onset of necrotic enteritis by supporting Clostridium perfringens growth.

              This study tested the hypothesis that a host mucogenic response to an intestinal coccidial infection promotes the onset of necrotic enteritis (NE). A chick NE model was used in which birds were inoculated with Eimeria acervulina and E. maxima and subsequently with Clostridium perfringens (EAM/CP). A second group of EAM/CP-infected birds was treated with the ionophore narasin (NAR/EAM/CP). These groups were compared to birds that were either non-infected (NIF), or infected only with E. acervulina and E. maxima (EAM), or C. perfringens (CP). The impact of intestinal coccidial infection and anti-coccidial treatment on host immune responses and microbial community structure were evaluated with histochemical-, cultivation- and molecular-based techniques. Barrier function was compromised in EAM/CP-infected birds as indicated by elevated CFUs for anaerobic bacteria and C. perfringens in the spleen when compared to NIF controls at day 20, with a subsequent increase in intestinal NE lesions and mortality at day 22. These results correlate positively with a host inflammatory response as evidenced by increased ileal interleukin (IL)-4, IL-10 and IFN-gamma RNA expression. Concurrent increases in chicken intestinal mucin RNA expression, and goblet cell number and theca size indicate that EAM/CP induced an intestinal mucogenic response. Correspondingly, the growth of mucolytic bacteria and C. perfringens as well as alpha toxin production was greatest in EAM/CP-infected birds. The ionophore narasin, which directly eliminates coccidia, reduced goblet cell theca size, IL-10 and IFN-gamma expression, the growth of mucolytic bacteria including C. perfringens, coccidial and NE lesions and mortality in birds that were co-infected with coccidia and C. perfringens. Collectively the data support the hypothesis that coccidial infection induces a host mucogenic response providing a growth advantage to C. perfringens, the causative agent of NE.
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                Author and article information

                Contributors
                Journal
                Poult Sci
                Poult Sci
                Poultry Science
                Elsevier
                0032-5791
                1525-3171
                11 March 2020
                May 2020
                11 March 2020
                : 99
                : 5
                : 2581-2594
                Affiliations
                []School of Environmental and Rural Science, University of New England, Armidale, NSW 2351, Australia
                []AB Vista, Marlborough, Wiltshire, SN8 4AN, United Kingdom
                Author notes
                [1 ]Corresponding author: rswick@ 123456une.edu.au
                Article
                S0032-5791(20)30065-1
                10.1016/j.psj.2019.12.049
                7597457
                32359594
                a6b5710e-2f17-49e3-8df1-5abfd738ae94
                © 2020 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 27 September 2019
                : 29 December 2019
                Categories
                Metabolism and Nutrition

                meat and bone meal,phytase,intestinal health,gene expression and necrotic enteritis

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