RESUMO
The most characteristic pathological change in mycobacterial infection is caseous necrosis followed by tuberculous cavity formation due to the cellular immunity induced by antigenic proteins and adjuvant active cell wall components. Mycobacterial cell well contains unique hydrophobic compounds possessing mycolic acids (a long branched-chain high molecular weight fatty acid) and shows distinctive properties such as acid-fastness and wax-like hydrophobicity. Mycobacteria do not produce exotoxin and the virulence cannot be determined by a single toxic substance, but the cell wall components to contact with the host cells are the most important surface molecule at the early stage of infection. Cord factor (trehalose 6,6'-dimycolate) is the most classical virulence factor which is lethally toxic for mice. However, cord factor exists among various species of mycobacteria and even in Nocardia and Rhodococcus. Furthermore, cord factor can produce granulomas without protein antigen in mice and it shows antitumor or non-specific prevention promotion of infection and induction promotion of various cytokines. Sulfolipid (tetracyl trehalose sulfate) also plays a role as a virulence factor by phagocytic process inhibition. Glycopeptidolipid (GPL) from M. avium and phenolglycolipid (PGL) from M. leprae also appeared to be immunomodulatory molecules which inhibit the developing of cellular immunity. Lipoarabinomannan (LAM) is also unique amphipatic molecule, like gram-negative endotoxin. Here, we discuss the involvement of various surface molecutes to contribute to pathogenesis in mycobacterial infection and immunity.