http://precedings.nature.com/tags/infection Recently posted documents tagged with 'infection' Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://precedings.nature.com/documents/2985/version/1 Streptococcus equi subspecies equi (S. equi) is a clonal, equine host-adapted pathogen of global importance that causes a highly contagious suppurative lymphodendopathy of the head and neck, more commonly known as Strangles. The disease is highly prevalent, can be severe and spread easily by visibly infected animals or by carrier animals that show no clinical signs of disease. Antibiotic treatment is usually ineffective. However, the majority of horses develop immunity to re-infection, suggesting that vaccination should be a feasible way to prevent the infection. Live attenuated vaccine strains of S. equi are available but adverse reactions have been reported and they suffer from a short duration of immunity. Thus, a safe and effective vaccine against S. equi is highly desirable. In this report, Welsh mountain ponies vaccinated with a combination of seven recombinant S. equi proteins, were significantly protected from experimental infection by S. equi, resembling the spontaneous disease. The protective antigens consisted of five surface localized proteins and two IgG endopeptidases. The results from a second vaccination trial indicate that the endopeptidases were important for good protection. The similarity of S. equi to other pyogenic streptococci suggests that our findings have broader implications for the prevention of streptococcal infections. http://precedings.nature.com/documents/2985/version/1 Thu, 26 Mar 2009 17:23:17 UTC Protective vaccination in the horse against Streptococcus equi with recombinant antigens hdl:10101/npre.2009.2985.1 2009-03-26 Jan-Ingmar Flock Nature Precedings 2009-03-26T17:23:17Z Manuscript Immunology Microbiology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2005/version/1 Current thinking emphasizes the primacy of CD14 in facilitating TLR recognition of microbes to initiate proinflammatory signaling events and the importance of p38-MAPK in augmenting such responses. Herein, this paradigm is challenged by demonstrating that recognition of Borrelia burgdorferi not only triggers an inflammatory response in the absence of CD14, but one that is uncontrolled as a consequence of impaired PI3K/AKT/p38-MAPK signaling and negative regulation of TLR2. CD14 deficiency results in hyperphosphorylation of AKT and reduced activation of p38. Such aberrant signaling leads to decreased negative regulation by SOCS1, SOCS3, and CIS thereby engendering a more severe and persistent inflammatory response to B. burgdorferi. Perturbation of this CD14/p38-MAPK-dependent mechanism of immune regulation may underlie development of infectious chronic inflammatory syndromes. http://precedings.nature.com/documents/2005/version/1 Wed, 25 Jun 2008 10:07:23 UTC CD14 Modulates PI3K/AKT/p38-MAPK Licensing of Negative Regulators of TLR Signaling to Restrain Chronic Inflammation hdl:10101/npre.2008.2005.1 2008-07-01 Timothy J. Sellati Nature Precedings 2008-06-25T10:07:23Z Manuscript Immunology Microbiology http://creativecommons.org/licenses/by/3.0/