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These 219 genes differentiated between the host responses to Gram-negative bacteria, Gram-negative bacterial toxin (LPS) and Gram-positive bacteria.
However, it has been shown that the magnitude and regulation of IFNγ, CCL2 and CXCL9 may differ between the host responses of patient with PTB or extrapulmonary TB (ETB) [23] [25].
The diagnostic potential of riboleukograms is supported by two very recent independent reports that corroborate our mouse data (Figure 1D), indicating that circulating leukocyte RNA signatures in patients differentiate between the host responses to sterile versus infectious causes of systemic inflammation and between the host response to Gram-negative versus Gram-positive pathogens [38], [39].
We did not expect to see such significant differences between the host responses induced by FeP2 and PEPV which share 94.4 % nucleotide identity with each other and 85.3 and 84.0 % nucleotide identity with FWPV respectively [ 27].
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Further studies are needed to better understand the relationship between the host response and emergence of new variant strains and the dynamics of strain circulation within populations both locally and globally.
Based upon our ability to diagnose abdominal sepsis in pilot mouse studies [15], we hypothesized that the host response to infection could not only differentiate between infected and non-infected states, but could also be used clinically to differentiate between the host response to infectious agents and to model the host response to and recovery from infectious perturbations.
Sepsis, a leading cause of death in critically ill patients, is the result of complex interactions between the infecting microorganisms and the host responses that influence clinical outcomes.
Sepsis, a leading cause of death in critical care patients, is the result of complex interactions between the infecting microorganisms and the host responses that influence clinical outcomes [ 1].
These findings suggest a temporal relationship between RSV infection and the host response to RSV replication.
Inflammation within the oral cavity occurs due to dysregulation between microbial biofilms and the host response.
The disease is caused by the dimorphic fungus Paracoccidioides brasiliensis (Pb) and clinical forms of the disease range from asymptomatic pulmonary lesions to a systemic generalized infection, depending on the balance between fungal virulence and the host response [ 11, 12].
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