Human epidermal Langerhans cells (LC) isolated from normal skin were infected in vitro with human immunodeficiency virus type 1 (HIV1). To control the permissivity of LC for HIV1, cells isolated from the epidermal sheet of normal skin by trypsinization were cocultured with HIV1-carrying promonocytic cells (U937) and observed by electron microscopy. An early sign of infection occurring in the coculture was the formation of retroviral type buds from LC membrane. Different steps in the process of viral budding up to virus release into the extracellular space were observed by electron microscopy. Treatment with either coupled phorbol esters/bacterial lipopolysaccharide or a recombinant cytokine (tumour necrosis factor alpha) did not significantly enhance viral production. The ability of in vitro infected LC to transmit virus to other haematopoietic cells and the consequences of such an infection on antigen-presenting function of LC remain to be elucidated.

Cells, Cultured↗

PubMedDate not supplied

Glycogen particles in methionine sulfoximine epileptogenic rodent brain and liver after the administration of methionine and actinomycin D.

Rats and mice were submitted either to the convulsant methionine sulfoximine (MSO) alone or to MSO combined with actinomycin D or methionine respectively. Twenty-four hours after the intraperitoneal administration of these compounds, the animals were killed and tissue samples were prepared for electron microscopy. Methionine sulfoximine induced 'grand mal' type seizures which were abolished by methionine. In saline controls, glycogen was as beta particles located in the cytoplasm of astrocytes, i.e. in perikarya and processes. Liver glycogen was as perinuclear masses of alpha and beta particles or as alpha particles scattered in all the cytoplasm. When the rodents were treated with MSO, glycogen was as alpha and beta particles which invaded all areas of the astrocyte cytoplasm, this increase being tremendous in perivascular end feet. Actinomycin D slowed down the accumulation of glycogen particles while methionine completely abolished it. In any case, glycogen particles were confined to the astrocytes and were never seen in other types of cells. In liver, MSO induced an important decrease or a complete disappearance of glycogen particles. When the convulsant was combined with actinomycin D or with methionine, the figures looked like those of controls. These results have been discussed in relation to the mechanism of glycogenesis in central nervous system of rodents submitted to MSO.

Animals↗

PubMedDate not supplied

Glycogen content and fructose-1, 6-biphosphatase activity in methionine sulfoximine epileptogenic mouse brain and liver after protein synthesis inhibition.

Mice given intraperitoneal injections of methionine sulfoximine (MSO) (100 mg/kg body weight) showed tonic-clonic seizures 7 to 8 h later. The protein synthesis inhibitors actinomycin D and cycloheximide, when combined with MSO delayed the onset of seizures. Methionine completely abolished the convulsions and metyrapone delayed them for some hours. Twenty-four h after the administration of the convulsant, the activity of the gluconeogenic enzyme, fructose-1, 6-biphosphatase (FBPase), and the glycogen content were determined in different areas of the brain. MSO induced an increase in both FBPase activity and glycogen content. These effects were antagonized by the inhibitors of protein synthesis. Metyrapone partly inhibited MSO-induced increases of FBPase activity and glycogen content whereas methionine completely abolished them. MSO decreased glycogen content in liver but had no effect on blood glucose level 24 h after its administration. These findings suggested that in MSO epileptogenic brain, glycogen accumulation may proceed from an enhanced gluconeogenesis.

Animals↗

PubMedDate not supplied

[Considerations on the bioenergetics of chicken brain development].

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Animals↗