p. bakeri infections

under repeated infection protocols [124]. Screening of H. p. bakeri-induced IgG responses in such lines, identifying relevant QTL for antibody responses, Hydroxychloroquine in vivo as was done for inbred mouse strains [125], accompanied by single nucleotide polymorphisms, would thus offer an attractive means of determining host genes contributing to antibody-dependent protective immunity against helminths. H. p. bakeri has played an important role in the exploration of the host–parasite relationship of chronic nematode infections now for over six decades, providing a tractable experimental system that is easy to maintain in the laboratory and far more cost-effective than other laboratory nematode–rodent model systems. It is certainly going to continue to play a crucial role in the years ahead, as we apply the new technologies and

probe in even further detail the fine workings of the processes that NVP-BKM120 underlie the control, expression and evasion of immune responses to nematodes in mammals. NLH would like to thank the Swiss Vaccine Research Institute and acknowledge funding support from the Swiss National Foundation, Grant Number 310030.133104, for research on antibody-mediated immunity against H. p. bakeri. RP would like to acknowledge funding support for his research from Baxter Healthcare Grant Number BT11-000280. JMB would like to thank the Wellcome Trust and the MRC for funding genetic and immunological studies on H. p. bakeri, and especially the many Ph.D. students, postdocs, colleagues and visitors who have worked in his laboratories over the last 39 years, and whose contributions, inspiration, debate, advice and friendship have made research in this field such a pleasure. Jill Brown and Ann Lowe provided

technical assistance for which JMB is most grateful. All MTMR9 authors contributed equally to this manuscript. “
“Acinetobacter baumannii is a major cause of both community-associated and nosocomial infections worldwide. These infections are difficult to treat because the bacterium rapidly develops resistance to multiple antibiotics. However, little is known about the nature of the innate cellular response to A. baumannii infection. In the present study, we identified the cells infiltrating the lungs of mice with Acinetobacter pneumonia and analyzed their response to infection. Normal mice eradicated the A. baumannii infection within 3 days of inoculation. Neutrophils were rapidly recruited to the lungs, followed by macrophages and NK1.1+ cells. Neutrophil-depleted mice showed acute and severe symptoms, and all of the mice died within 3 days of inoculation. The majority of macrophage-depleted mice responded in a similar manner to the control mice. These results indicate that neutrophils are essential for the elimination of A. baumannii. Half of NK1.