Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Host-seeking adult Dermacentor reticulatus ticks were examined for the prevalence of Francisella tularensis in an active natural focus of tularemia along the lower reaches of the Dyje (Thaya) river in South Moravia (Czech Republic) and adjacent Lower Austria, in four localities of the flood plain forest-meadow ecosystem during the spring of 1996. The ticks were pooled (10 male or female ticks per group) and inoculated subcutaneously in 4-week-old SPF mice. Dead mice were sectioned, the spleens were homogenized in PBS and passaged in mice, and impression smears from the spleens, liver and heart blood were stained by Giemsa. Twenty-five isolates of F. tularenis were recovered from 1098 pooled D. reticulatus: the minimum infection rate (MIR) is 2.3%. MIRs for 629 female and 469 male D. reticulatus were 2.4% and 2.1%, respectively. The prevalence varied according to locality, but did not significantly differ between the Moravian (2.2%) and Austrian (2.8%) sites. The monitoring of D. reticulatus for F. tularensis might be a valuable contribution to the surveillance of tularemia in Europe.
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PMID:Francisella tularensis in Dermacentor reticulatus ticks from the Czech Republic and Austria. 1004 75

Francisella tularensis is a Gram-negative intracellular pathogen that causes the zoonosis tularemia. Because F. tularensis LPS causes weak TLR4 activation, we hypothesized that administration of a synthetic TLR4 agonist, aminoalkyl glucosaminide phosphate (AGP), would boost the innate immune system and compensate for reduced TLR4 stimulation. Intranasal administration of AGPs induced intrapulmonary production of proinflammatory cytokines and chemokines. Mice treated with AGPs before and after inhalation of Francisella novicida exhibited augmented cytokine and inflammatory responses to infection; reduced bacterial replication in lung, liver, and spleen; and increased survival, whereas all PBS-treated control mice died within 4 days of infection, all AGP-treated mice showed prolonged time-to-death, and 30-60% of AGP-treated mice survived. The protective effect of AGP was lost in mice lacking IFN-gamma. Long-term survivors developed specific Th1 splenocyte responses and specific Abs dominated by IgG2 isotypes. Survivors were fully protected from rechallenge with aerosolized F. novicida. Thus, preventive administration of AGP successfully modulated innate immune responses to aerosolized F. novicida, leading to protective immunity to pneumonic tularemia. This is the first report of the protective effect of a TLR ligand on resistance to F. novicida-induced pneumonic tularemia.
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PMID:Administration of a synthetic TLR4 agonist protects mice from pneumonic tularemia. 1849 Jul 59