Anti-TREM1 monoclonal antibody, clone TREM-26 [R-PE]

Objective To investigate the role of sTREM-1 and PTX3 as markers of injection in febrile patients with SLE Methods In febrile (body temperature >= 38 degrees C) patients with SLE, blood samples of day 0, 1, 2, and 14 after presentation were drawn and relevant clinical data were, collected. The patients were allocated to an infection group (n=19) or disease flare group (n=14). Serum levels of sTREM-1 and PTX3 were measured by ELISA using the serum samples of SLE patients and age-and sex-matched healthy controls (n=31). Results A total of 33 febrile episodes occurred in 32 SLE patients (19 infections, 14 flares) were studied. sTREM-1 levels oil day 0 were, significantly higher in the infection group than in the flare group (109.9 pg/ml (median) vs. 48.0 pg/ml, p=0.002), but PTX3 levels were similar in these two groups. The difference of sTREM-1 levels between infection group and flare group was persistent on day 1 and 2 (day 1, p=0.007; day 2, p=0.034). The highest diagnostic value (sensitivity=1.0, specificity=0.664) of sTREM-1 was obtained at the threshold value of 53.2 pg/mL. Conclusion Sertan sTREM-1 levels were significantly higher in the infection group than in the flare group of febrile SLE patients. Our findings suggest that serum sTREM-1 levels could be used to determine whether SLE patients have contracted an infection.

Melioidosis, a severe human disease caused by the bacterium Burkholderia pseudomallei, has a wide spectrum of clinical manifestations ranging from acute septicemia to chronic localized illness or latent infection. Murine models have been widely used to study the pathogenesis of infection and to evaluate novel therapies or vaccines, but how faithfully they recapitulate the biology of human melioidosis at a molecular level is not known. In this study, mice were intranasally infected with either high or low doses of B. pseudomallei to generate either acute, chronic, or latent infection and host blood and tissue transcriptional profiles were generated. Acute infection was accompanied by a homogeneous signature associated with induction of multiple innate immune response pathways, such as IL-10, TREM1, and IFN signaling, largely found in both blood and tissue. The transcriptional profile in blood reflected the heterogeneity of chronic infection and quantitatively reflected the severity of disease. Genes associated with fibrosis and tissue remodeling, including matrix metalloproteases and collagen, were upregulated in chronically infected mice with severe disease. Transcriptional signatures of both acute and chronic melioidosis revealed upregulation of iNOS in tissue, consistent with the expression of IFN-gamma, but also Arginase-1, a functional antagonist of the iNOS pathway, and was confirmed by immunohistochemistry. Comparison of these mouse blood datasets by pathway and modular analysis with the blood transcriptional signature of patients with melioidosis showed that many genes were similarly perturbed, including Arginase-1, IL-10, TREM1, and IFN signaling, revealing the common immune response occurring in both mice and humans.