In vivo demonstration of neuroinflammatory molecule expression in brain abscess with diffusion tensor imaging

Abstract

Background and purpose: Neuroinflammatory molecules, including tumor necrosis factor-alpha, interleukin1-beta, lymphocyte function associated molecule-1, and intercellular cell adhesion molecule-1 contribute to the development of brain abscess. We hypothesized that the high fractional anisotropy (FA) in the brain abscess cavity reflects the upregulation of these neuroinflammatory molecules.

Materials and methods: Diffusion tensor imaging (DTI) was performed in 24 patients with brain abscess and Staphylococcus aureus-treated as well as nontreated Jurket cell lines (at 4 time points: 1, 24, 48, and 72 hours). Neuroinflammatory molecules were quantified from the brain abscess cavity aspirate of the patients as well as from the heat-killed S aureus-treated and nontreated cell lines and correlated with DTI measures.

Results: The DTI-derived FA strongly correlated with the presence of neuroinflammatory molecules in the pus as well as in S aureus-treated cell lines; no such correlation was observed in nontreated cell lines.

Conclusions: These data indicate that neuroinflammatory molecules confer high diffusion anisotropy inside the brain abscess cavity. We propose that increased FA reflects upregulated inflammatory response in brain abscess.

Fig 1.

A 31-year-old female patient presenting with pyogenic brain abscess in the left temporal lobe. A, Axial T2-weighted image shows a well-defined hyperintense lesion with a hypointense wall. B, The lesion appears hypointense on the axial T1-weighted image with an isointense wall. C, On the postcontrast T1-weighted image, the lesion shows ring enhancement. D, DWI shows homogeneous hyperintensity in the cavity that appears hypointense on the MD map (E). The FA (F) and red-green-blue color-modulated FA map fused with the MD map (G) show that high FA in the abscess cavity is similar to what is observed in the contralateral inferior longitudinal fasciculus and midbrain (arrow).

Fig 2.

A 25-year-old male patient presenting with pyogenic brain abscess with a heterogeneously hyperintense lesion in the left temporal lobe. A, Axial T2-weighted image shows a hyperintense lesion with a hypointense wall. B, The lesion appears hypointense on the axial T1-weighted image with an isointense wall. C, On the postcontrast T1-weighted image, the lesion shows ring enhancement. D, The lesion appears heterogeneously hyperintense on the DWI in the cavity that appears heterogeneously hypointense on the MD map (E). The FA (F) and red-green-blue color-modulated FA map fused with MD map (G) show that high FA in the abscess cavity is similar to what is observed in the contralateral inferior longitudinal fasciculus and midbrain.

Fig 3.

A, Plots showing the relationship (A) between FA and IL1-β, TNF-α, and LFA-1. B, FA and sICAM-1 in pus from the abscess cavity. C–F, The relationship between FA and NMs in heat-killed S aureus–treated as well as nontreated cell lines at different time points (1, 24, 48, and 72 hours [hrs]) is depicted in the form of bar plots.

Fig 4.

A, Coronal images of MD, FA, and color-coded FA maps fused with MD of Jurket cell lines treated with heat-killed S aureus at 1, 24, and 48 hours (hr), respectively, show an increase in FA and MD. B, The corresponding maps for nontreated Jurket cells show very few changes in FA and MD. C, Expression of LFA-1, IL1-β, TNF-α, and GAPDH (housekeeping) genes in nontreated and heat-killed S aureus–treated Jurket cell lines at 1, 24, 48, and 72 hours.

Fig 5.

Cell aggregation at different time points in nontreated (A–C) and heat-killed S aureus–treated (D–F) cell lines. Photomicrographs of heat-killed S aureus–treated cell line with a time course show an increased degree of cell aggregation compared with that in nontreated cell line. hrs indicates hours.