Crohn’s disease and ulcerative colitis are chronic inflammatory disorders of the gut that cause major life-long disability. Afflicting mostly young people at an age when they are most active both in their private and professional life, inflammatory bowel disease (IBD) represents an important public health problem affecting the patients education, working abilities, social life and quality of life. The cause of IBD is multiple and so far not completely understood. However, genetic factors, environmental factors and the gut bacteria play a role in disease development.
Conventional therapy of active IBD pre-dominantly target anti-inflammatory immune responses, largely due to cytokine release within the intestine. Thus, therapeutic treatment mainly includes anti-inflammatory drugs, immunosuppressants, biologic agents, and antibiotics . However, these agents may cause severe adverse effects and are therefore not suitable for long-term treatment of IBD. Moreover, conventional drugs block manifestation or consequences of inflammation in acute disease. Thus, there is a necessity for therapeutic strategies that target improvement of impaired barrier function in remission. Suitable candidates are dietary supplements and food components such as colostrum. Although natural therapies are commonly associated with lower toxicity and fewer side effects than conventional drugs, the scientific proof of their effectiveness and safety is demanded .
Colostrum, the secretion produced by the mammary glands during the first three days post-partum, contains many functional nutrients. These include immunoglobulins, growth factors, and antimicrobial peptides. The potential of colostrum to affect gastrointestinal infections and to reduce the incidence of immune-mediated diseases is well established [3, 4]. In accordance with this, we recently demonstrated the protective effect of orally applied colostrum in a murine colitis model . Beneficial effects were characterized by improvement of clinical colorectal inflammation symptoms and by the induction of immunoregulatory mechanisms, predominantly of the innate immune system arm. Thus, identification of factors responsible for preventing experimental colitis might provide the basis for developing a long-term treatment regimen.
In IBD patients, local production of polymeric IgA (pIgA) is altered and this affects both immunological homeostasis and humoral immune responses [6, 7]. IgA does not activate the classical complement pathway and inhibits the production of pro-inflammatory cytokines in response to lipopolysaccharide (LPS), thereby maintaining mucosal integrity . SIgA preparations from colostrum are active against various microbial antigens and inhibit adhesion and invasion by enteropathogenic Escherichia coli in vitro[9, 10]. Colostral sIgA influences the development of the gastrointestinal immune system in milk-fed infants; however, little is known about the effectiveness of oral sIgA in maintaining gut barrier functions in adults.
Another colostral peptide with a broad range of immunomodulatory properties is lactoferrin (Lf), a member of the iron-binding glycoprotein family. Lf is predominately found in mucosal secretions and neutrophilic granules . Lf concentration and iron saturation differ among species; bovine (bLf) and human (hLf) Lfs show strong sequence homology . BLf has been reported to stimulate mucosal and systemic immune responses when given orally [13, 14]. Moreover, there is experimental evidence that Lf reduces the severity of colitis in rodents [15, 16].
In the present study, we explored the potential of orally applied colostral bLf and sIgA for modulating immune responses and recovery from dextran sodium sulfate (DSS)-induced murine colitis. Whole bovine colostrum (BC) improved the clinical severity of colitis, whereas bLf had no effect. SIgA influenced DSS-mediated immune cell redistribution and specifically altered colonic cell infiltration. Therefore, it might be an interesting candidate for promoting regeneration from acute colitis.