Phagocytosis of Mycoplasma pneumoniae and Acholeplasma laidlawii measured as inhibition of [3H]uridine uptake by macrophages.

Many studies of the interaction between phagocytes and mycoplasmas have given controversial results. This is probably due both to the small size of the microorganisms and their ability to attach to the cell membrane, making it difficult to distinguish between adsorption and ingestion. To overcome these difficulties we took advantage of a phenomenon we noted occurring concomitantly with phase-contrast microscope-monitored phagocytosis of heat-killed C. albicans, i.e., a reduction of [3H]uridine uptake by macrophages from culture medium. This approach allowed us to measure the ability of mouse peritoneal macrophages and the macrophage-like P 388 D 1 continuous cell line to phagocytose Mycoplasma pneumoniae and Acholeplasma laidlawii. Live, UV-killed and specific antiserum-opsonized mycoplasmas were tested. A. laidlawii was ingested under all the conditions mentioned above, while live M. pneumoniae was not phagocytosed unless UV-killed. Phagocytosis of UV-killed M. pneumoniae was directly verified by transmission electron microscopy studies. Data obtained with opsonized M. pneumoniae indicated no ingestion by mouse peritoneal macrophages and incomplete phagocytosis with P388 D 1 macrophages, suggesting that different responses by different types of phagocytes can be observed. In spite of a lack of information concerning the biological meaning of the inhibition of macrophage RNA metabolism during phagocytosis, our data suggest that this phenomenon may be used to study the phagocytosis of microorganisms which are difficult to visualize.

Complications of plasma-exchange.

Complications in apheresis affect on the average 40% of treated patients and 10-14% of the procedures. The mortality rate is 1/500 treated patients. The utilization of more complex techniques, central catheters, plasma infusion and even more the superimposition of different factors increase the incidence and gravity of side effects. Very influent are also the underlying pathologies and the clinical conditions; particularly at risk are patients with TTP/HUS and GBS. However, PE represents a relatively safe therapy in which prevention of complications requires a particularly diligent personnel and a careful evaluation of indications.

Apheresis and biocompatibility: complement activation.

When blood comes into contact with plastic surfaces of extracorporeal circuits activation of different biological systems occurs, among them the complement. This will be activated mainly through the alternative pathway but also through the classical one. The activation through the latter pathway occurs when antibodies directed against polymeric materials used for the production of extracorporeal circuits or substances utilized for their sterilization are produced by the patient's immunosystem. Even if complement activation occurs almost constantly during apheretic procedures the natural inhibitory mechanisms of this system attenuate and disguise this phenomenon. Important and clinical manifestations occur in particular patients or in case of technologically more complex techniques. In apheresis the complement activation may be implicated in the relatively frequent complications such as fever and chills, hypotension, as well as in the rare but severe cases of ARDS.

Megabladder in experimental Chagas disease: pathological features of the bladder wall.

Mega-organs, primarily in the digestive tract, are well known to occur in chronic Chagas disease. Acute experimental infection with Trypanosoma cruzi results in parasitism of a wide range of cells, tissues, and organs, including the urinary bladder. Infection of BALB/c mice with 100,000 bloodstream forms of the Y strain of T. cruzi induced acute infection with intense parasitism of all layers of the urinary bladder. Parasites were found in the mucosa, lamina propria, muscular, adventitial connective, and fat tissue. Desquamate epithelial cells with amastigotes in the bladder lumen were also found. After 60 days of infection, mice inoculated with 50 bloodstream forms developed dilated, thin-walled bladders that had inflammatory infiltrates and foci of fibrosis replacing areas of damaged muscular layer. These lesions result from direct damage to the muscle fibers by the T. cruzi, leading to myosites, muscle damage, and scarring. Direct damage of paraganglia cells secondary to parasitism, leading to dilatation, damage of muscle fibers, and scarring with replacement of muscular tissue with connective tissue, should also be considered as a cause of functional disturbance of the urinary bladder.