The Secretome of Mycoplasma capricolum subsp. capricolum in Neutral and Acidic Media

Members of the mycoplasmas are known to have some the smallest free-living prokaryotes. They are characterized by their small genomes (0.58 – 2.20 Mb) and lack of a cell wall [1]. The availability of complete genome sequences of several mycoplasmas provides a great opportunity to understand the minimal genome biology of these small bacteria [2]. Considerable advances have been made towards understanding the pathogenesis of mycoplasmas; of particular interest is the interaction of these pathogens with the immune system, macrophage activation, cytokine induction, superantigens, autoimmune manifestations, and the evasion of host immune responses. However, despite the wealth of new genetic information emerging from bacterial genome sequencing, many newly discovered genes remain functionally unclassified [3]. It is suggested that these mollicutes are phylogenetically related to Gram-positive bacteria whereby their genomes were reduced through multiple events of mutations. This implies that these simple bacteria are not found at the root of the phylogenetic tree but are more likely late evolutionary products [4]. Owing to their reduced genomes mycoplasmas have limited biosynthetic capabilities and therefore tend to take on a parasitic lifestyle in which they obtain nutrients and other metabolic building blocks such as amino acids, nucleotides, fatty acids, and sterols from their hosts [1]. Generally Mycoplasmas enter their host and multiply over long periods of time, slowly wearing down the host [1]. This is one reason perhaps why mycoplasmas have been linked to AIDS pathogenesis and to malignant transformation, chromosomal aberrations, the Gulf War Syndrome, and other unexplained and complex illnesses, including chronic fatigue syndrome, Crohn’s disease, and various arthritis’ [5]. These microorganisms have developed a variety of mechanisms in order to deal with host immune responses including; mimicry of host antigens, survival within phagocytic and non-phagocytic host cells and the generation of phenotypic plasticity [1]. One of the most important questions about the pathogenesis of mycoplasmas is how they cause damage to the host cells and to what extent is the damage clinically apparent in the host.