Isolation of Raoultella ornithinolytica in a HIV positive patient with a lung abscess.

A 38 year old male HIV positive patient with a history of intravenous drug use presented with chest pains, cough, sputum and weight loss and radiology demonstrated the evolution of a right basal lung abscess. A lung biopsy sent for 16S rRNA analysis and sputum cultured about the same time demonstrated Raoultella ornithinolytica . No other causative pathogens were clearly identified. He gradually improved with a 4 week course of intravenous cefazolin. R. ornithinolytica is a rare, but recognised pathogen.

Inhibition of islet immunoreactivity by adiponectin is attenuated in human type 1 diabetes.

CONTEXT: Adiponectin is an adipocyte-derived cytokine with insulin-sensitizing and antiinflammatory properties. These dual actions have not previously been examined in the context of human disease. OBJECTIVES: Our objective was to examine the adiponectin axis in type 1 diabetes (T1D). T1D is an autoimmune inflammatory disease resulting from pancreatic ß-cell destruction, in which insulin resistance associates with progression to disease. DESIGN, PATIENTS, AND INTERVENTIONS: We measured circulating adiponectin and adiponectin receptor expression on blood-immune cells from 108 matched healthy, T1D, and type 2 diabetic subjects. We tested adiponectin effect on T cell proliferation to islet antigens and antigen-presenting function of monocyte-derived dendritic cells (mDCs). Lastly, we assessed the effect of a 3-week lifestyle intervention program on immune cell adiponectin receptor expression in 18 healthy subjects. RESULTS: Circulating concentrations of adiponectin were not affected by T1D. However, expression of adiponectin receptors on blood monocytes was markedly reduced and inversely associated with insulin resistance. Reduced adiponectin receptor expression resulted in increased T cell proliferation to islet-antigen presented by autologous mDCs. We demonstrated a critical role for adiponectin in down-regulating the costimulatory molecule CD86 on mDCs, and this function was impaired in T1D. We proceeded to show that lifestyle intervention increased adiponectin receptor but reduced CD86 expression on monocytes. CONCLUSIONS: These data indicate that T cells are released from the antiinflammatory effects of adiponectin in T1D and suggest a mechanism linking insulin resistance and islet immunity. Furthermore, we suggest that interventions that reduce insulin resistance could modulate the inflammatory process in T1D.