Bovine colostrum and immune function after exercise

Strenuous and/or prolonged exercise causes transient perturbations in immune function. It is well accepted that this is one mechanism contributing to the higher occurrence of infection (e.g. upper respiratory tract infection (URTI)) in athletes, especially endurance athletes. URTI or upper respiratory tract (URT) symptoms can negatively affect training and competition performance but athletes must train intensively to be successful. Therefore, interventions that can legitimately enhance immune function and reduce URTI risk can be of benefit to athletes. Bovine colostrum supplementation has been investigated as a possible nutritional countermeasure to enhance (or maintain) immune function, and reduce URTI risk, following strenuous or prolonged exercise and during intensive training periods. There is convincing evidence that daily supplementation with bovine colostrum, for a number of weeks (and preliminary evidence for acute effects after a single dose), can maintain intestinal barrier integrity, immune function and reduce the chances of suffering URTI or URT symptoms in athletes or those undertaking heavy training. The mechanisms are not fully understood at present but there is preliminary evidence suggesting that the effects on immune function are attributable, at least in part, to small bioactive components that survive digestion and are biologically available after consumption, but further work is required. In summary, the balance of existing evidence does support the notion that bovine colostrum is beneficial for certain groups of athletes, such as those involved in strenuous training (e.g. endurance athletes), in terms of immunity and resistance to infection

Concomitant infections, parasites and immune responses.

Concomitant infections are common in nature and often involve parasites. A number of examples of the interactions between protozoa and viruses, protozoa and bacteria, protozoa and other protozoa, protozoa and helminths, helminths and viruses, helminths and bacteria, and helminths and other helminths are described. In mixed infections the burden of one or both the infectious agents may be increased, one or both may be suppressed or one may be increased and the other suppressed. It is now possible to explain many of these interactions in terms of the effects parasites have on the immune system, particularly parasite-induced immunodepression, and the effects of cytokines controlling polarization to the Th1 or Th2 arms of the immune response. In addition, parasites may be affected, directly or indirectly, by cytokines and other immune effector molecules and parasites may themselves produce factors that affect the cells of the immune system. Parasites are, therefore, affected when they themselves, or other organisms, interact with the immune response and, in particular, the cytokine network. The importance of such interactions is discussed in relation to clinical disease and the development and use of vaccines

Immunodepression as A Risk Factor of Infection in Patients with Acute Ischemic Stroke

Background: Immunodepression is an absence or deficient supply of the components of either humoral or cellular immunity, or both. Previous studies show that the central nervous system and the immune system interact in complex ways. Better insight into these interactions may be relevant to the treatment of patients with stroke and other forms of central nervous system injury. This study aimed to determine immunodepression as a risk factor of infection in patients with acute ischemic stroke. Subjects and Method: This was a cohort study conducted in Sultan Agung Islamic Hospital, Semarang, Central Java. A sample of 89 patients with post-acute ischemic stroke who had been hospitalized for ≥5 days was selected for this study as the exposed group and nonstroke patients as non-exposed group. The dependent variable was immunodepression infection as indicated by high leucocytes, high neutrophils, low lymphocytes, low monocytes. The independent variable was post-acute ischemic stroke. The data were obtained from the medical record. The data were analyzed by a chi-square test with Risk Ratio (RR) as the measure of association. Results: Post-acute ischemic stroke was associated with an increased risk of leucocytosis (RR= 3.95%; 95% CI= 1.59 to 3.27), neutrophilia (RR= 1.98; 95% CI= 1.69 to 12.63), lymphocytopenia (RR= 1.77; 95% CI= 1.51 to 1.98), monocytopenia (RR= 1.85%; 95% CI= 1.33 to 1.92). Conclusion: Acute ischemic stroke increases the risk of infection due to immunodepression. Keywords: acute ischemic stroke, immunodepression, infectio

The potential role of T-cells and their interaction with antigen-presenting cells in mediating immunosuppression following trauma-hemorrhage

Objective: Trauma-hemorrhage results in depressed immune responses of antigen-presenting cells (APCs) and T-cells. Recent studies suggest a key role of depressed T-cell derived interferon (IFN)-g in this complex immune cell interaction. The aim of this study was to elucidate further the underlying mechanisms responsible for dysfunctional T-cells and their interaction with APCs following trauma-hemorrhage. Design: Adult C3H/HeN male mice were subjected to trauma-hemorrhage (3-cm midline laparotomy) followed by hemorrhage (blood pressure of 35�5mmHg for 90 min and resuscitation) or sham operation. At 24 h thereafter, spleens were harvested and T-cells (by Microbeads) and APCs (via adherence) were Isolated. Co-cultures of T-cells and APCs were established for 48 h and stimulated with concanavalin A and lipopolysaccharide. T-Cell specific cytokines known to affect APC function (i.e. interleukin(IL)-2, IL-4 and granulocyte-macrophage colony-stimulating factor (GM-CSF)) were measured in culture supernatants by Multiplex assay. The expression of MHC class II as well as co-stimulatory surface molecules on T-cells and APCs was determined by flow cytometry. Results: The release of IL-4 and GM-CSF by T-cells was suppressed following trauma-hemorrhage, irrespective of whether sham or trauma-hemorrhage APCs were present. Antigen-presenting cells from animals subjected to trauma-hemorrhage did not affect T-cell derived cytokine release by sham T-cells. In contrast, T-cells from traumahemorrhage animals depressed MHC class II expression of CD11c(þ) cells, irrespective of whether APCs underwent sham or trauma-hemorrhage procedure. Surprisingly, co-stimulatory molecules on APCs (CD80, CD86) were not affected by trauma-hemorrhage. Conclusions: These results suggest that beside IFN-g other T-cell derived cytokines contribute to immunosuppression following trauma-hemorrhage causing diminished MHC II expression on APCs. Thus, T-cells appear to play an important role in this interaction at the time-point examined. Therapeutic approaches should aim at maintenance of T-cell function and their interaction with APCs to prevent extended immunosuppression following trauma-hemorrhage

Systemic infections after acute stroke

After an acute stroke, systemic infection can complicate the recovery process and lead to a worse clinical outcome, including a higher risk of mortality. Post-stroke infection (PSI) is responsible for the majority of the mortality occurring between 1 week and 1 month after stroke, peaking towards the end of the second week. The effects of PSI on longer-term outcome and other aspects of recovery, such as cognition, mood and quality of life, are largely unknown. The cerebrovascular event itself may result in a systemic immunosuppressed state, hence lowering the threshold for subsequent systemic bacterial infections. Although there have been advances in the basic understanding of the pathophysiological mechanisms of PSI, clinical studies have not provided any clear guidelines on the best methods of managing or preventing PSI. This article provides a review of the current knowledge of the phenomenon of PSI and the possible future developments in the understanding and treatment of PSI

Sports foods and dietary supplements for optimal function and performance enhancement in track and field athletes

Numerous nutritional products are marketed with claims of optimizing athlete health and function and/or enhancing performance. Products that fall under the banner of “Sports Foods” or “Dietary Supplements,” may be used to support performance during training and competition or for enhancing aspects of training adaptation, recovery, immune function, and/or overall athlete health. Effective marketing campaigns and athlete endorsements may convince us that certain sports foods and supplements are fundamental in allowing athletes to reach their sporting goals. However, this approach is naive in understanding the true foundations of athlete success, such as the inherent genetic predisposition for athletic characteristics, the many hours of well-structured/periodized training, appropriate underlying nutrition, adequate sleep and recovery, and of course, good overall physical and mental health. Nevertheless, if these variables are all accounted for, there may be a role for sports foods and dietary supplements in an athlete’s training and competition routine, particularly within elite sport where marginal performance gains are pursued. The following review presents general considerations for track-and-field athletes using sports foods and dietary supplements to enhance performance, in addition to exploring the potential therapeutic/prophylactic use of these nutritional aids