Simple Summary Gastrointestinal diseases in poultry are more significant because of high economic loss due to production loss, reduced feed efficiency, mortality, compromising bird welfare, and sometimes zoonotic importance. With the removal of antibiotic growth promoters in the diet, gastrointestinal disease incidences have grown in recent years. Gastrointestinal diseases have been shown to affect bone growth negatively; however, possible mechanisms have yet to be confirmed in chickens. Abstract Bone serves as a multifunctional organ in avian species, giving structural integrity to the body, aiding locomotion and flight, regulating mineral homeostasis, and supplementing calcium for eggshell formation. Furthermore, immune cells originate and reside in the bone marrow, sharing a milieu with bone cells, indicating a potential interaction in functions. In avian species, the prevalence of gastrointestinal diseases can alter the growth and the immune response, which costs a great fortune to the poultry industry. Previous studies have shown that coccidiosis and necrotic enteritis can dramatically reduce bone quality as well. However, possible mechanisms on how bone quality is influenced by these disease conditions have not yet been completely understood, other than the reduced feed intake. On the other hand, several mediators of the immune response, such as chemokines and cytokines, play a vital role in the differentiation and activation of osteoclasts responsible for bone resorption and osteoblasts for bone formation. In the case of Eimeria spp./Clostridium perfringens coinfection, these mediators are upregulated. One possible mechanism for accelerated bone loss after gastrointestinal illnesses might be immune-mediated osteoclastogenesis via cytokines-RANKL-mediated pathways. This review article thus focuses on osteoimmunological pathways and the interaction between host immune responses and bone biology in gastrointestinal diseases like coccidiosis and necrotic enteritis affecting skeletal health.

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Osteoimmunology: A Link between Gastrointestinal Diseases and Skeletal Health in Chickens

Campylobacter jejuni is an important foodborne pathogen. Despite the lack of clinical signs associated with its colonization in poultry, it has been reported to interact with the intestinal immune system. However, little is known about the interaction between C. jejuni and the chicken immune system, especially in the context of hepatic dissemination. Therefore, to follow up on our previous study showing intestinal colonization and hepatic spread of C. jejuni, cecal tonsils and liver samples were collected from these birds to determine the mRNA levels of chemokines and cytokines. Serum samples were also collected to determine serum amyloid A (SAA) concentrations and specific IgY titers. Lack of Th17 induction was observed in the cecal tonsils of only the liver-contaminated groups. This hepatic dissemination was accompanied by innate, Th1 and Th2 immune responses in livers, as well as an increase in SAA concentrations and specific IgY levels in sera. Campylobacter appears to be able to restrain the induction of the chicken gut immunity in particular conditions, possibly enhancing its hepatic dissemination and thus eliciting systemic immune responses. Although Campylobacter is often recognized as a commensal-like bacterium in chickens, it seems to modulate the gut immune system and induce systemic immunity.

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Intestinal Colonization of Campylobacter jejuni and Its Hepatic Dissemination Are Associated with Local and Systemic Immune Responses in Broiler Chickens

Efficacy of Bacillus subtilis to replace in-feed antibiotics of broiler chickens under necrotic enteritis-challenged experiments: A systematic review and meta-analysis

A meta-analysis of the effect of Eimeria spp. and/or Clostridium perfringens infection on the microbiota of broiler chickens.

Effects of dietary yeast cell wall supplementation on growth performance, intestinal Campylobacter jejuni colonization, innate immune response, villus height, crypt depth, and slaughter characteristics of broiler chickens inoculated with Campylobacter jejuni at d 21.

SUMMARY. Because of the trend of cage-free egg production, infections with the nematode Ascaridia galli are receiving increased attention. The aim of this study was to establish a timeline for the influence of A. galli on the expression of key cytokines related to a parasitic immune response, and on the composition of the jejunal microbiota. Twenty-eight male layer-type birds were challenged at 24, 25, and 26 days of age. An additional 28 birds were kept as uninfected controls. Starting on Day 31, three birds of each group were euthanized every week until 8 wk postinfection (PI). The number of larvae isolated from the intestinal wall decreased over time, until no larvae were seen at 7 and 8 wk PI. At 5 wk PI, there was a numerical upregulation of all cytokines (TGF-β, IFN-γ, IL-4, IL-8, IL-10, IL-13) in the infected group, but this change was only statistically significant for IL-13. At this time point, larvae were expected to have developed into adults that would have shed eggs in the feces. However, no adult worms were seen and there was no egg shedding. For the microbiota analysis, there were significant differences in the alpha diversity (Faith's phylogenetic diversity) between challenge and control groups, and the beta diversity analysis showed slight differences between samples, suggesting that the age of the birds was the main reason for the separation of groups. These findings suggest that the upregulation of all cytokines evaluated in Week 5 might be the reason for resolution of the infection. Possible explanations are that a high infection dose and the fact that birds were fed with a more nutritionally dense feed might have contributed to the birds' immune system clearing the infection before the worms were able to reach maturity. RESUMEN. La infección por Ascaridia galli no altera significativamente la microbiota intestinal y se elimina tras cambios en la expresión de citocinas. Debido a la tendencia de la producción de huevos libres de jaulas, las infecciones con el nematodo Ascaridia galli están recibiendo una mayor atención. El objetivo de este estudio fue establecer una línea de tiempo para la influencia de A. galli en la expresión de citoquinas clave relacionadas con una respuesta inmune parasitaria y en la composición de la microbiota yeyunal. Veintiocho aves macho de tipo postura fueron desafiadas a los 24, 25 y 26 días de edad. Se mantuvieron 28 aves adicionales como controles no infectados. A partir del día 31, se practicó la eutanasia a tres aves de cada grupo cada semana hasta las 8 semanas posteriores a la infección (PI). El número de larvas aisladas de la pared intestinal disminuyó con el tiempo, hasta que no se observaron larvas a las 7 y 8 semanas después de la infección. A las cinco semanas post-infección, hubo una regulación ascendente numérica de todas las citoquinas (TGF-β, IFN-γ, IL-4, IL-8, IL-10, IL-13) en el grupo infectado, pero este cambio solo fue estadísticamente significativo para IL-13. En ese momento, se esperaba que las larvas se hubieran convertido en adultos que eliminarían huevos en las heces. Sin embargo, no se observaron nemátodos adultos y no hubo eliminación de huevos. Para el análisis de microbiota, hubo diferencias significativas en la diversidad alfa (diversidad filogenética de Faith) entre los grupos de desafío y control y el análisis de diversidad beta mostró ligeras diferencias entre las muestras, lo que sugiere que la edad de las aves fue la razón principal de la separación de los grupos. Estos hallazgos sugieren que la regulación al alza de todas las citocinas evaluadas en la semana 5 podría ser el motivo de la resolución de la infección. Las posibles explicaciones son que una dosis alta de infección y el hecho de que las aves fueran alimentadas con un alimento más denso desde el punto de vista nutricional podrían haber contribuido a que el sistema inmunitario de las aves eliminara la infección antes de que los nemátodos pudieran alcanzar la madurez.

Andrea Pietruska

Papers

A meta-analysis of the effect of Eimeria spp. and/or Clostridium perfringens infection on the microbiota of broiler chickens.

Effects of dietary yeast cell wall supplementation on growth performance, intestinal Campylobacter jejuni colonization, innate immune response, villus height, crypt depth, and slaughter characteristics of broiler chickens inoculated with Campylobacter jejuni at d 21.

Infection with Ascaridia galli Does Not Significantly Alter Intestinal Microbiota and Is Cleared After Changes in the Expression of Cytokines