As a multifunctional polypeptide, epidermal growth factor (EGF) increases growth performance or enhances resistance to diseases in commercial broilers under adverse conditions. In this study, a recombinant Lactococcus lactis was established to produce the secretory form of bioactive gEGF. The results of in vitro testing showed that gEGF promoted the proliferation of chicken embryo fibroblast cells. A total of 63 5-day-old broiler chickens were evenly divided into three groups and treated with either M17 medium (the control group), supernatant of LL-pNZ8149 fermentation product (the P-LL group), or supernatant of LL-pNZ8149-gEGF fermentation product (the gEGF group). In two weeks, many measurements of growth, immunity and the intestines were significantly higher in the gEGF group than those in the control and the P-LL groups. Our study showed that the bioactive gEGF could be expressed with Lactococcus lactis expression system with the potential to enhance growth performance, immune function, and intestinal development in broiler chickens.

• Lactococcus lactis
• broiler chickens
• gallus epidermal growth factor
• growth performance
• immune function
• intestinal development

Epidermal growth factor (EGF) is an important growth factor in regulation of cell proliferation, differentiation, survival and apoptosis. Studies showed that food-grade Lactococcus lactis (L. lactis) and NICE expression system have superior performance in exogenous protein expression. This study aimed to construct and express porcine EGF (pEGF), and use L. lactis as vehicle for producing and delivering pEGF. Furthermore, investigating biological activity of pEGF and exploring applications feasibility of combination effects of L. lactis and pEGF on early weaned piglets’ production.

A recombinant Lactococcus lactis which produced and secreted pEGF at 1000 ng/ml in culture supernatant was generated. Secreted pEGF was a fully biologically active protein, as demonstrated by its capacity to stimulate L929 mouse fibroblast cell line proliferation in vitro. For in vivo study, forty piglets were randomly allocated to control, antibiotic control, empty vector-expressing L. lactis (LL-EV) and pEGF-secreting L. lactis (LL-pEGF). After 14 d of rearing, final body weight and average daily gain in LL-pEGF were greater (P < 0.05, 8.95 vs. 8.37 kg, 206.1 vs. 157.7 g/day, respectively) than those in control, but no significant differences between LL-pEGF, LL-EV and antibiotic control. Overall period average daily feed intake was higher in LL-pEGF, LL-EV and antibiotic control than in control (P < 0.05, 252.9, 255.6, 250.0, 207.3 g/day, respectively). No significant difference was observed on ADFI/ADG. LL-pEGF increased villous height in the duodenum, jejunum and ileum than in control and LL-EV (P < 0.05). Sucrase in the 3 intestinal segments, aminopeptidase A in the duodenum and Jejunum, aminopeptidase N and dipeptidase IV in the duodenum in LL-pEGF were higher than those in control (P < 0.05). Furthermore, Escherichia coli and Enterococcus counts decreased in the ileum and Lactobacillus increased in the ileum and cecum digesta in LL-pEGF compare with the control (P < 0.05). Lactobacillus increased in the cecum in LL-EV compared with control and antibiotic control (P < 0.05).

We have generated a recombinant Lactococcus lactis which produced and secreted fully biologically active porcine EGF. Oral administration of pEGF-secreting L. lactis had beneficial effects on intestinal health and performance of early-weaned piglets.

The process of intestinal adaptation (“enteroplasticity”) is complex and multifaceted. Although a number of trophic nutrients and non-nutritive factors have been identified in animal studies, successful, reproducible clinical trials in humans are awaited. Understanding mechanisms underlying this adaptive process may direct research toward strategies that maximize intestinal function and impart a true clinical benefit to patients with short bowel syndrome, or to persons in whom nutrient absorption needs to be maximized. In this review, we consider the morphological, kinetic and membrane biochemical aspects of enteroplasticity, focus on the importance of nutritional factors, provide an overview of the many hormones that may alter the adaptive process, and consider some of the possible molecular profiles. While most of the data is derived from rodent studies, wherever possible, the results of human studies of intestinal enteroplasticity are provided.

• Diabetes
• Diet
• Hormonal regulation
• Intestinal resection
• Mechanisms
• Morphology
• Nutrient absorption
• Short bowel syndrome
• Signals

Intestinal failure is a condition characterized by malnutrition and/or dehydration as a result of the inadequate digestion and absorption of nutrients. The most common cause of intestinal failure is short bowel syndrome, which occurs when the functional gut mass is reduced below the level necessary for adequate nutrient and water absorption. This condition may be congenital, or may be acquired as a result of a massive resection of the small bowel. Following resection, the intestine is capable of adaptation in response to enteral nutrients as well as other trophic stimuli. Identifying factors that may enhance the process of intestinal adaptation is an exciting area of research with important potential clinical applications.

• Small intestine
• Transport
• Morphology
• Resection
• Short bowel syndrome
• Absorption
• Diet
• Gene expression
• Hyperplasia
• Enterocytes

• Adaptation, Physiological/physiology
• Animals
• Disease Models, Animal
• Feeding Behavior/physiology
• Gastrointestinal Hormones/physiology
• Humans
• Intestinal Mucosa/metabolism
• Intestinal Mucosa/physiopathology
• Rats
• Short Bowel Syndrome/metabolism
• Short Bowel Syndrome/physiopathology
• Short Bowel Syndrome/surgery
• Signal Transduction/physiology
• Swine