BackgroundPasteurella pneumotropica is a ubiquitous bacterium that is frequently isolated from laboratory rodents and causes various clinical symptoms in immunodeficient animals. Currently two RTX toxins, PnxIA and PnxIIA, which are similar to hemolysin-like high-molecular-weight exoproteins are known in this species. In this study, we identified and analyzed a further RTX toxin named PnxIIIA and the corresponding type I secretion system.ResultsThe RTX exoprotein, PnxIIIA, contains only a few copies of the RTX repeat-like sequence and 3 large repeat sequences that are partially similar to the outer membrane protein found in several prokaryotes. Recombinant PnxIIIA protein (rPnxIIIA) was cytotoxic toward J774A.1 mouse macrophage cells, whereas cytotoxicity was attenuated by the addition of anti-CD11a monoclonal antibody. rPnxIIIA could bind to extracellular matrices (ECMs) and cause hemagglutination of sheep erythrocytes. Binding was dependent on the 3 large repeat sequences in PnxIIIA. Protein interaction analyses indicated that PnxIIIA is mainly localized in the outer membrane of P. pneumotropica ATCC 35149 in a self-assembled oligomeric form. PnxIIIA is less cytotoxic to J774A.1 cells than PnxIA and PnxIIA.ConclusionsThe results implicate that PnxIIIA is located on the cell surface and participates in adhesion to ECMs and enhanced hemagglutination in the rodent pathogen P. pneumotropica.

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There are marked sex differences in the Harderian gland of the C3H/He strain of mice. Female (but not male) glands contain large amounts of porphyrin, which are readily visible as solid depositions within the lumina. The histology and porphyrin content of the Harderian gland were examined in intact and in pregnant mice and in mice subjected to combinations of adrenalectomy, gonadectomy and administration of sex steroid hormones. In male mice, castration approximately doubled the amount of porphyrin in the Harderian gland. Castration plus adrenalectomy increased the levels over 30-fold, to levels similar to those found in female mice, although adrenalectomy alone produced no significant effect. Administration of testosterone to the male mice which had been castrated and adrenalectomized prevented the increases while progesterone treatment produced further increases in porphyrins. In intact females, the amount of porphyrin varied with the phase of the oestrous cycle; being lowest during metoestrus and highest during dioestrus. In ovariectomized-adrenalectomized females, the effects of administered sex hormones on the amount of porphyrin in the gland were the same as in males. In pregnant mice, the level was no significantly different from that in intact oestrous animals.

To evaluate the role of various growth factors in naturally occurring cell death during development of the neural retina, we examined the effects ofsuch factors on the nuclear morphology and the size of DNA in cultured chick embryonic neural retina cells. Basic fibroblast growth factor (bFGF) increased internucleosomal cleavage of DNA and nuclear fragmentation in a timeand dose-dependent manner. The effect was inhibited by anti-bFGF antibody, suramin, and cycloheximide. Epidermal growth factor, platelet-derived growth factor, nerve growth factor, tumor necrosis factor-a, and dexamethasone had no effect. These results provide evidence that bFGF may eventually act as a lethal factor inducing apoptotic cell death during the development of the neural retina in chick embryo. Abbreviations used: bFGF, basic fibroblast growth factor; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; WST, water-soluble tetrazolium salt.

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