Desirable and undesirable immunotropic effects of antibiotics: immunomodulating properties of cefaclor

The effect exerted on complex immunoregulatory functions of the immune system is an important criterion when selecting an antibiotic. When assessing the effect of an antibiotic on the immune system, one should also take into consideration the existence of functional relationships between the immune system and the nervous and hormonal systems. Among these three systems, there are common factors that modify biological processes. This makes it possible for the antibiotic not only to interact directly with the elements of the immune system, but also to exert indirect influences on potential neurotropic and endocrinotropic effects of the drug. Besides highly effective bactericidal activity, cefaclor demonstrates the ability to exert a favorable effect on some of the specific and non-specific immune responses and immunoregulation mechanisms, which may be important from a clinical point of view. Cefaclor enhances phagocytosis and bactericidal activity of granulocytes and macrophages, and favorably modifies the cooperation of monocytes and T lymphocytes. In this way, it corrects, both in vivo and in vitro, the immunoregulatory disturbances induced and aggravated by an infection. This effect is reflected by an improvement in the impaired immunoregulating activity of T lymphocytes, and is manifest both as an increase in suppressive activity and a correction of the monokine level ratio in relation to the decrease of proinflammatory monokine IL-1 and a relative increase of antiinflammatory IL-1ra. By normalizing the disturbed immunoregulation mechanism, cefaclor enhances the protective potential of the immune reaction while it also reduces the risk of immunogenic clinical complications such as persistent inflammatory conditions and allergic and/or autoaggressive responses. Such immunomodulating properties of cefaclor may be useful in the clinical treatment of patients with immune disorders leading to chronic inflammation and secondary allergic or autoaggressive reactions.