PubMedCrossRef 33 Abraham E: Neutrophils and acute lung injury

PubMedCrossRef 33. Abraham E: Neutrophils and acute lung injury. Crit Care Med 2003,31(4 Suppl):S195–199.PubMedCrossRef 34. Marks M, Burns T, Abadi M, Seyoum B, Thornton J, Tuomanen E, Pirofski LA: Influence of neutropenia on the course of serotype 8 pneumococcal pneumonia in mice. Infect Immun 2007,75(4):1586–1597.PubMedCrossRef 35. Lynch JP: Hospital-acquired pneumonia: risk factors, microbiology, and treatment. Chest 2001,119(2 Suppl):373S-384S.PubMedCrossRef Author contributions ARB, CH, and PJR performed the experiments

and generated the data. ARB and CJO contributed to the conception and design of the experiments performed as well as the writing of the manuscript. All authors read and approved the final manuscript.”
“Background A diphtheria-like infectious disease caused by Corynebacterium ulcerans is increasing in clinical

importance in developed countries and is now regarded as “diphtheria” in Europe [1, 2]. Infection with C. ulcerans occurs find more in a wide range of hosts, including cats, dogs, pigs, cows, and whales [3–9]. The first clearly documented case of zoonotic transmission involved a dog, as reported by Lartigue et al. [5]. This is in contrast to the causative agent of classical diphtheria, C. diphtheriae, whose host species is thought to be limited to humans [10]. Nevertheless, the selleck compound two species share a common feature: upon lysogenization of tox-encoding bacteriophages, they become toxigenic and are able to produce the potent PND-1186 molecular weight diphtheria toxin [1, 10]. This toxin is known to contribute to disease progression, occasionally leading to death. It is encoded by a single gene designated tox, mafosfamide situated inside prophages lysogenized in the bacterial genome of C. diphtheriae[11]. The prophages are capable of induction, by ultraviolet light or DNA-damaging agents such as mitomycin C, and yield β-, δ-, ω- and other functional bacteriophage particles [12]. Some types of bacteriophages can infect both C. diphtheriae and C. ulcerans[13–16]. Furthermore, the C. ulcerans tox gene is also encoded in a genome

region surrounded by phage attachment (att) sites conserved between the two species [7, 16]. The nucleotide sequences of C. ulcerans tox genes were published by Sing et al. They showed some diversity in the genetic sequence among C. ulcerans strains, in contrast to the highly conserved C. diphtheriae tox gene [17, 18]. In 2003, the nucleotide sequence of the whole genome of C. diphtheriae strain NCTC13129 was reported [19]. The sequence information revealed some striking features of the bacterial genome, such as the presence of as many as 13 pathogenicity islands (PAIs) [19], uncommon among C. diphtheriae strains [20]. The presence of a tox-positive prophage flanked by the att regions was confirmed and supported the findings of previous reports [21]. Despite comparable clinical importance, the genomic sequence of toxigenic C. ulcerans has not yet been reported. In the present study, we determined the nucleotide sequence of the toxigenic C.

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