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Effects of Chronic Stress and Intestinal Inflammation on Commercial Poultry Health and Performance: Part I

Escrito por: Guillermo Tellez
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Stress

Conteúdo disponível em: English

Effects of Chronic Stress and Intestinal Inflammation on Commercial Poultry Health

Currently, animal production systems require a constant search to reduce the effects of stress and chronic inflammation to improve energy use by producing animals.

Although there is no a “silver bullet” to prevent multifactorial conditions associated with chronic stress, several studies show improvement in intestinal microbial balance, metabolism, and intestinal integrity through alternative products such as:

This being an international scientific trend, due to the anti-inflammatory, antioxidant and immunomodulatory effects, as well as improvement in intestinal integrity.

Substitution of antibiotics in production systems with alternative products, improved management practices, strict biosecurity, quality ingredients, absence of diseases (Mycoplasma/Salmonella), and effective immunization programs are efficient strategies for health objectives and productivity.

In this work, we focus on reviewing the significant repercussions of chronic stress and intestinal inflammation on the health and performance of commercial birds.

CHICKEN GASTROINTESTINAL TRACT ARCHITECTURE AND PLAYERS

 

In addition to absorbing and digesting water and food, the intestinal tract contains a diverse and complex microbial community (Celluzzi and Masotti, 2016), as well as an enteric nervous system (ENS) of metazoans considered the “second brain” of the organism (Schneider et al., 2019).

In addition to this complexity in the structure and microbial relationships, in chickens, the gut-associated lymphoid tissue (GALT) contains the highest concentration of immune cells in the organism, showing its relevance (Peralta et al., 2017; Casteleyn et al., 2010).

The intestinal microbiome can influence host biology, nutrition, immunity, and the neuroendocrine system (Dimitrov, 2011). GIT function appears to be mediated by short-chain fatty acids (SCFA) generated by bacterial fermentation (Wu et al., 2017), communication between the microbiota and neurons (Megur et al., 2020), the endocrine system (Fukui et al., 2018), the immune system (Maslowski and Mackay, 2011) and modulation of the intestinal epithelial barrier (Sharma et al., 2010).

Enteroendocrine cells (EECs) are found throughout the GIT epithelium and produce several hormones (Gribble and Reimann, 2019).

The first GIT hormones discovered were:

Over 50 hormones or bioactive peptides have been identified, making the GIT the primary organ displaying endocrine, neuroendocrine, autocrine, or paracrine activities (Rao and Wang, 2010; Gribble and Reimann, 2017).

In metazoans, intestinal enterochromaffin cells, a subpopulation of numerous EECs, produce 90% of the neurotransmitter serotonin (5-hydroxytryptamine) (Lund et al., 2018).

The intestinal microbiota partially controls the secretion of serotonin, dopamine, oxytocin, and endorphins produced by EECs (Forsythe et al., 2010; Liang et al., 2014; Mayer et al., 2014). There is great wisdom in the old saying “gut feelings”.

Prolonged stress and inflammation negatively impact the microbiota-braingut axis, causing dysbacteriosis and disrupting the tight junction proteins with systemic translocation of bacteria and other antigens (Figure 2).

During chronic stress and, as a result, chronic intestinal inflammation, energy for growth and reproduction is diverted away from these functions to sustain the inflammatory response. Poultry is no exception to this rule.

HPA AXIS

PATHOGENS AND DISEASES

Bacterial infections are considered one of the main GIT-associated infections, which due to their infection process and presence, are inducers of acute or even chronic inflammatory processes (Yamamoto et al., 2013).

In murine models, Salmonella growth is aided, ironically, by acute inflammatory responses to pathogenic bacteria in the intestine, as there is increased migration of neutrophils and production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) as a result of the Salmonella infection disrupting the balance of the microbiota (Winter et al., 2010a).

An increase in molecular oxygen in the lumen of the gut depletes important commensal anaerobes like Bacteroidetes and Clostridiales, which are essential butyric acid-producing bacteria (Rigottier-Gois, 2013).

The thiosulfate oxidation to tetrathionate is also a ROS by-product (Winter et al., 2010b). In murine models, it has been shown that Salmonella uses tetrathionate to strengthen its development (Winter et al., 2010b); tetrathionate broth is a component of enriched media for the culture of Salmonella in diagnostic laboratories.

Figure 1. Interactions between the host (poultry species) and intrinsic or extrinsic factors that influence gut health (created with BioRender.com).

However, a recent study has found that this differs for chickens (Saraiva et al., 2021).

Interestingly, the deletion of both genes does not attenuate the pathogen but slightly decreases the numbers of Salmonella Enteritidis and Salmonella Typhimurium in caecum in poultry, reducing inflammation and allowing the bacteria to more easily invade gut epithelial cells and disseminate systemically, leading to severe clinical signs and higher mortality rates (Saraiva et al., 2021).

Figure 2. Chronic stress (regardless of its source) has a direct impact on the hypothalamic–pituitary–adrenal axis (HPA axis), the brain-microbiota-gut axis (BMG axis), and the endocrine and immunological systems. Intestinal and chronic systemic inflammations originate from disruptions in the delicate balance and environment of the intestinal microbiota (dysbacteriosis) and alterations in tight junction proteins among enterocytes causing leaky gut. Prolonged oxidative stress induced by the inflammatory process causes phospholipid peroxidation in cell and mitochondrial membranes, leading to apoptosis, cellular necrosis, and multiple organ failure (created with BioRender.com).

DEFENSE NF-kB TNFA CYTOKINES CYTOKINE STORM

ROS AND RNS AND THEIR EFFECTS ON A MOLECULAR LEVEL

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