Pets (mostly domestic dogs and cats) play an important role in the daily lives of humans and their health has attracted growing attention from pet owners. The intestinal microbiota, a complex microbial community with barrier-protective, nutritional, metabolic, and immunological functions, is integral to host health. Dysbiosis has been related to a variety of diseases in humans and animals. Probiotics have been used in functional foods and dietary supplements to modulate intestinal microbiota and promote host health, which has been introduced in pet dogs and cats in recent years. Various canine- and feline-derived probiotic strains have been isolated and characterized. The administration of probiotics has shown positive effects on the gut health and can alleviate some intestinal diseases and disorders in dogs and cats, although the underlying mechanisms are largely unresolved. In this review, we summarize the current knowledge on the benefits of probiotics and discuss their possible mechanisms in dogs and cats in order to provide new insights for the further development and application of probiotics in pets.

Antimicrobial growth promoters (AGPs) are commonly used in the livestock industry at subtherapeutic levels to improve production efficiency, which is achieved mainly through modulation of the intestinal microbiota. However, how different classes of AGPs, particularly ionophores, regulate the gut microbiota remains unclear. In this study, male Cobb broiler chickens were supplemented for 14 days with or without one of five commonly used AGPs including three classical antibiotics (bacitracin methylene disalicylate, tylosin, and virginiamycin) and two ionophores (monensin and salinomycin) that differ in antimicrobial spectrum and mechanisms. Deep sequencing of the V3-V4 region of the bacterial 16S rRNA gene revealed that two ionophores drastically reduced a number of rare bacteria resulting in a significant decrease in richness and a concomitant increase in evenness of the cecal microbiota, whereas three antibiotics had no obvious impact. Although each AGP modulated the gut microbiota differently, the closer the antibacterial spectrum of AGPs, the more similarly the microbiota was regulated. Importantly, all AGPs had a strong tendency to enrich butyrate- and lactic acid-producing bacteria, while reducing bile salt hydrolase-producing bacteria, suggestive of enhanced metabolism and utilization of dietary carbohydrates and lipids and improved energy harvest, which may collectively be responsible for the growth-promoting effect of AGPs.

Vitamin D, a crucial fat-soluble vitamin, is primarily synthesized in the skin upon exposure to ultraviolet radiation and is widely recognized as a bone-associated hormone. However, recent scientific advancements have unveiled its intricate association with gut health. The intestinal barrier serves as a vital component, safeguarding the intestinal milieu and maintaining overall homeostasis. Deficiencies in vitamin D have been implicated in altering the gut microbiome composition, compromising the integrity of the intestinal mucosal barrier, and predisposing individuals to various intestinal pathologies. Vitamin D exerts its regulatory function by binding to vitamin D receptors (VDR) present in immune cells, thereby modulating the production of pro-inflammatory cytokines and influencing the intestinal barrier function. Notably, numerous studies have reported lower serum vitamin D levels among patients suffering from intestinal diseases, including inflammatory bowel disease, irritable bowel syndrome, and celiac disease, highlighting the growing significance of vitamin D in gut health maintenance. This comprehensive review delves into the latest advancements in understanding the mechanistic role of vitamin D in modulating the gut microbiome and intestinal barrier function, emphasizing its pivotal role in immune regulation. Furthermore, we consolidate and present relevant findings pertaining to the therapeutic potential of vitamin D in the management of intestinal diseases.

Background: Extensive work has been accomplished to characterize the intestinal bacterial community, known as the microbiota, and its association with host health and disease. However, very little is known about the spatiotemporal development and the origin of a minor intestinal fungal community, known as the mycobiota, in humans and animals, particularly in avian species. Results: In this study, we comprehensively characterized the biogeography and succession of the gastrointestinal (GI) mycobiota of broiler chickens and further revealed the fungal sources that are responsible for initial and long-term establishment of the mycobiota in the GI tract. Using Illumina sequencing of the internal transcribed spacer 2 (ITS2) region of fungal rRNA genes, we detected significant spatial and temporal differences in the mycobiota along the GI tract. In contrary to the microbiota, the mycobiota was more diverse in the upper than the lower GI tract with no apparent trend of succession up to 42 days of age. The intestinal mycobiota was dominated by the phyla Ascomycota and Basidiomycota with Gibberella, Aspergillus, and Candida being the most abundant genera. Although the chicken mycobiota was highly dynamic, Fusarium pseudonygamai was dominant throughout the GI tract regardless of age in this study. The core chicken mycobiome consisted of 26 fungal taxa accounting for greater than 85% of the fungal population in each GI location. However, we observed high variations of the intestinal mycobiota among different studies. We also showed that the total fungal population varied greatly from 1.0 × 10⁴ to 1.1 × 10⁶ /g digesta along the GI tract and only accounted for less than 0.06% of the bacteria in day-42 broilers. Finally, we revealed that the mycobiota from the hatchery environment was responsible for initial colonization in the GI tract of newly hatched chickens, but was quickly replaced by the fungi in the diet within 3 days. Conclusions: Relative to the intestinal microbiota that consists of trillions of bacteria in hundreds of different species and becomes relatively stabilized as animals age, the chicken intestinal mycobiota is a minor microbial community that is temporally dynamic with limited diversity and no obvious pattern of successive changes. However, similar to the microbiota, the chicken mycobiota is spatially different along the GI tract, although it is more diverse in the upper than the lower GI tract. Dietary fungi are the major source of the intestinal mycobiota in growing chickens.

Background: The emergence of antimicrobial resistance has necessitated the development of effective alternatives to antibiotics for livestock and poultry production. This study investigated a possible synergy between butyrate and forskolin (a natural labdane diterpene) in enhancing innate host defense, barrier function, disease resistance, growth performance, and meat quality of broilers. Methods: The expressions of representative genes involved in host defense (AvBD9 and AvBD10), barrier function (MUC2, CLDN1, and TJP1), and inflammation (IL-1β) were measured in chicken HD11 macrophages in response to butyrate and forskolin in the presence or absence of bacterial lipopolysaccharides (LPS). Intestinal lesions and the Clostridium perfringens titers were also assessed in C. perfringens-challenged chickens fed butyrate and forskolin-containing Coleus forskohlii (CF) extract individually or in combination. Furthermore, growth performance and carcass characteristics were evaluated in broilers supplemented with butyrate and the CF extract for 42 d. Results: Butyrate and forskolin synergistically induced the expressions of AvBD9, AvBD10, and MUC2 in chicken HD11 cells (P < 0.05) and the synergy was maintained in the presence of LPS. Butyrate and forskolin also suppressed LPS-induced IL-1β gene expression in HD11 cells in a synergistic manner (P < 0.05). The two compounds significantly reduced the intestinal lesions of C. perfringens-challenged chickens when combined (P < 0.05), but not individually. Furthermore, butyrate in combination with forskolin-containing CF extract had no influence on weight gain, but significantly reduced feed intake (P < 0.05) with a strong tendency to improve feed efficiency (P = 0.07) in a 42-d feeding trial. Desirably, the butyrate/forskolin combination significantly decreased abdominal fat deposition (P = 0.01) with no impact on the carcass yield, breast meat color, drip loss, or pH of d-42 broilers. Conclusions: Butyrate and forskolin has potential to be developed as novel antibiotic alternatives to improve disease resistance, feed efficiency, and carcass composition of broilers.

The rising concern of antimicrobial resistance highlights a need for effective alternatives to antibiotics for livestock production. Butyrate, forskolin, and lactose are three natural products known to induce the synthesis of host defense peptides (HDP), which are a critical component of innate immunity. In this study, the synergy among butyrate, forskolin, and lactose in enhancing innate host defense, barrier function, and resistance to necrotic enteritis and coccidiosis was investigated. Our results indicated that the three compounds synergistically augmented the expressions of multiple HDP and barrier function genes in chicken HD11 macrophages. The compounds also showed an obvious synergy in promoting HDP gene expressions in chicken jejunal explants. Dietary supplementation of a combination of 1 g/kg sodium butyrate, 10 mg/kg forskolin-containing plant extract, and 10 g/kg lactose dramatically improved the survival of chickens from 39% to 94% (p < 0.001) in a co-infection model of necrotic enteritis. Furthermore, the three compounds largely reversed growth suppression, significantly alleviated intestinal lesions, and reduced colonization of Clostridium perfringens or Eimeria maxima in chickens with necrotic enteritis and coccidiosis (p < 0.01). Collectively, dietary supplementation of butyrate, forskolin, and lactose is a promising antibiotic alternative approach to disease control and prevention for poultry and possibly other livestock species.