Campylobacter jejuni carbon starvation protein A (CstA) is involved in peptide utilization, motility and agglutination, and has a role in stimulation of dendritic cells.

Campylobacter jejuni is the most frequent cause of severe gastroenteritis in the developed world. The major symptom of campylobacteriosis is inflammatory diarrhoea. The molecular mechanisms of this infection are poorly understood compared to those of less frequent disease-causing pathogens. In a previous study, we identified C. jejuni proteins that antibodies in human campylobacteriosis patients reacted with. One of the immunogenic proteins identified (Cj0917) displays homology to carbon starvation protein A (CstA) from Escherichia coli, where this protein is involved in the starvation response and peptide uptake. In contrast to many bacteria, C. jejuni relies on amino acids and organic acids for energy, but in vivo it is highly likely that peptides are also utilized, although their mechanisms of uptake are unknown. In this study, Biolog phenotype microarrays have been used to show that a ΔcstA mutant has a reduced ability to utilize a number of di- and tri-peptides as nitrogen sources. This phenotype was restored through genetic complementation, suggesting CstA is a peptide uptake system in C. jejuni. Furthermore, the ΔcstA mutant also displayed reduced motility and reduced agglutination compared to WT bacteria; these phenotypes were also restored through complementation. Murine dendritic cells exposed to UV-killed bacteria showed a reduced IL-12 production, but the same IL-10 response when encountering C. jejuni ΔcstA compared to the WT strain. The greater Th1 stimulation elicited by the WT as compared to ΔcstA mutant cells indicates an altered antigenic presentation on the surface, and thus an altered recognition of the mutant. Thus, we conclude that C. jejuni CstA is important not only for peptide utilization, but also it may influence host-pathogen interactions.

Response to ionising radiation in Duchenne muscular dystrophy.

Using lymphoblastoid cell cultures the response to gamma (gamma)-radiation, was examined in 6 Duchenne muscular dystrophy (DMD) patients; 2 clinically normal males as negative controls, and 2 patients with ataxia telangiectasia (AT) showing sensitivity to ionising radiation as positive controls. In a series of experiments, cell recovery and growth at day 2 post radiation, was determined after 5 separate gamma-irradiation dose levels: 50, 100, 150, 200 and 300 rads. The DMD cell strains showed a radiation dose response that was significantly greater than in cells from 2 normal males, while both DMD and normal cells were significantly less responsive than were AT-sensitive cell strains.

Alteration in cell division, morphology and motility induced by the toxic principle of lupinosis.

A number of experiments are described in which the effect of the toxins causing lupinosis on cell morphology and motility is examined. The toxins arrested cells in metaphase leading to abnormal profiles, and inhibited leucocyte migration. Similar results were obtained with colchicine on cell division and, from the evidence obtained, it is suggested that the mechanism of action of the two agents is similar and that the same binding sites are probably involved.