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Antibiotics are among the most successful drugs in medicine. Their power in therapy as well as in prophylaxis was so convincing that for most of the older antibiotics, controlled clinical trials were never performed. The advent of antibiotics dramatically altered the prognosis of bacterial infections, such as streptococcal endocarditis, purulent meningitis, and sepsis caused by staphylococci and Gram-negative bacteria. From a historical point of view the ability to prescribe antibiotics changed the therapeutic power of physicians in an unprecedented fashion. Although antibiotics have lost quite a bit of their glamour due to increasing antimicrobial resistance of microorganisms, this sense of power probably still underlies antibiotic prescribing.

The different manifestations of infection with Mycobacterium tuberculosis reflect the balance between the bacillus and host defense mechanisms. Traditionally, protective immunity to tuberculosis has been ascribed to T-cell-mediated immunity, with CD4 + T cells playing a crucial role. Recent immunological and genetic studies support the long-standing notion that innate immunity is also relevant in tuberculosis. In this review, emphasis is on these natural, innate host defense mechanisms, referring to experimental data (e.g., studies in gene knockout mice) and epidemiological, immunological, and genetic studies in human tuberculosis. The first step in the innate host defense is cellular uptake of M. tuberculosis, which involves different cellular receptors and humoral factors. Toll-like receptors seem to play a crucial role in immune recognition of M. tuberculosis, which is the next step. The subsequent inflammatory response is regulated by production of pro- and anti-inflammatory cytokines and chemokines. Different natural effector mechanisms for killing of M. tuberculosis have now been identified. Finally, the innate host response is necessary for induction of adaptive immunity to M. tuberculosis. These basic mechanisms augment our understanding of disease pathogenesis and clinical course and will be of help in designing adjunctive treatment strategies.

The invasion of human beings or other multi-cellular organisms by micro-organisms usually leads to inflammation. Depending on the virulence of the micro-organism, the size of the inoculum, and the quality of the host’s defence mechanisms, the inflammatory response will be confined to the local site or may extend and involve the entire body. The subsequent appearance of inflammatory cells and their programmed action are controlled by a plethora of humoral substances, many of which belong to the so-called cytokines.

Health of infants in developing countries is constantly challenged by pathogens. Unfortunately, the immune system of newborn infants is immature, developing during the first year of life to attain adequate immunocompetence at about one year of age. During the first few months of life, maternal antibodies (especially IgG) acquired in utero circulate and protect the newborn. In addition, via breast milk, the infant acquires considerable amounts of immunoglobulins (mostly sIgA) and possibly other humoral and cellular components of the mother’s immune defence. The protective effect of sIgA in breast milk is restricted to the gut. The precise role of the other immunomodulatory components of breast milk, remains unclear.

Under normal conditions, large areas of the human body surfaces are colonized with microorganisms. The skin and the mucous membranes of the oropharynx, nasopharynx, intestinal tract, and parts of the genital tract each have their own microflora.1 These patterns of colonization are determined by microbial factors, exogenous factors, and host factors.