Macrophage-microglia were isolated from primary mixed brain cell cultures of normal newborn mice. They were successfully maintained in vitro for at least 8 weeks. Purity of the cultures was 97-100%, as determined by endocytosis of latex beads, non-specific staining through Fc receptors, EA and EAC rosette formation. These cells were non-specific esterase-positive, but peroxidase-negative. Electron-microscope observations revealed morphological similarities to mature macrophages. Isolated macrophage-microglia seldom incorporated [3H]thymidine in vitro. By means of 51Cr release assay, using monoclonal antibodies against mouse major histocompatibility complex (MHC) antigens and complement, we detected class I MHC (H-2) antigen on unstimulated macrophage-microglia, and both class I and class II (Ia) antigens on gamma-interferon-treated cells. These observations suggest possible immunoregulatory functions of macrophage-microglia in the central nervous system, as is characteristic of other cells of monocyte lineage.

We used a monoclonal antibody (10A8), derived from mice immunized with fractions enriched in Golgi apparatus of rat brain neurons, to isolate an intrinsic membrane sialoglycoprotein of 160 KD from rat brain. By immunoelectron microscopy the sialoglycoprotein, named MG-160, was localized in medical cisternae of the Golgi apparatus of neurons, glia, adenohypophysis, and cultured rat pheochromocytoma (PC 12). The monoclonal antibody (MAb) reacted only with rat tissues. Because the epitope(s) recognized by a monoclonal antibody may be restricted, localization of an antigen by a single MAb may not reflect the extent of the distribution of antigen in various species and tissues. Therefore, to further investigate the presence and localization of MG-160 or of an antigenically related protein in several species and tissues, we used a polyclonal antiserum raised against MG-160 purified by antibody (10A8) affinity chromatography. Immunoblots of crude microsomal fractions from rat brain probed with the antiserum against MG-160 showed two to three prominent bands of approximately 160, 150, and 68 KD. Immunoblots of crude microsomal fractions from human, chicken, and frog brains showed prominent bands of 130-140 and 68 KD. Immunoblots of crude membrane fractions from Saccharomyces cerevisiae showed prominent bands of approximately 110-120 and 80 KD. Light microscopic immunocytochemical studies with frog, chicken, mouse, rat, rabbit, bovine, and human brains and with several other rat and human tissues showed a staining pattern consistent with the Golgi apparatus. Immunoelectron microscopy with rat and human brain and with rat myocardium and pituitary showed prominent and exclusive staining of cis, medial, and occasionally trans cisternae of the Golgi apparatus. The cisternae of the trans Golgi network were not stained. These findings are consistent with the hypothesis that a polypeptide related to MG-160 is present in the Golgi apparatus of several tissues in human, rodents, chicken, and frog and possibly in Saccharomyces cerevisiae. The antiserum to MG-160 represents a reliable reagent for immunohistochemical visualization of the Golgi apparatus in brain and several other human tissues obtained at autopsy, fixed with Bouin's, and embedded in paraffin.

Acute suppurative thyroiditis is a very uncommon disorder, most often arising in children with congenital conditions connecting the thyroid directly to the oropharynx, such as a piriform fistula or thyroglossal duct. Accordingly, the most common causative agents are those which can colonize the oral mucosa and spread to the thyroid contiguously, such as Streptococcus species, Staphylococcus species and anerobes. In adults, a hematogenous spread to a pre-existing altered thyroid gland is often the postulated pathogenetic mechanism, and it is exceedingly rare in the United States. We report the case of an 81-yr-old woman with acute suppurative thyroiditis secondary to Escherichia coli (E. coli) infection. The patient presented with fevers, chills, dysuria and recent painful neck swelling. Thyroid ultrasound and neck computed tomography revealed a multinodular goiter and an intra-thyroid abscess. An otolaryngology evaluation and barium swallow failed to show a piriform fistula. Thyroid hormone levels were consistent with hyperthyroidism. Urine cultures were positive for E. coli. The patient subsequently developed a clinical picture consistent with severe thyrotoxicosis, which rapidly resolved after medical treatment, appropriate antibiotics and surgical drainage of the thyroid. Abscess material also grew E. coli. Thus, acute suppurative thyroiditis secondary to sepsis can complicate an otherwise asymptomatic multinodular goiter and should be promptly treated with broad-spectrum antibiotics and/or surgical drainage to avoid serious consequences, including severe thyrotoxicosis.