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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: NFκB signaling drives pro-granulocytic astroglial responses to neuromyelitis optica patient IgG

Fig. 1

Granulocytic infiltrate occurs in the absence of demyelination, terminal complement complex formation, and overt tissue destruction in NMO white matter. a H&E staining reveals robust perivascular inflammation in the white matter of autopsy tissue collected from an NMO patient (scale bar = 100 μM). b An enlarged view of (a) and the magnified inset confirm the presence of eosinophils as a component of this perivascular infiltration (scale bar = 50 μM). c Staining for the astrocyte marker GFAP demonstrates the presence of reactive astrocytes with abnormal morphology in close association with granulocytic perivascular infiltration in a section consecutive to a. The inset highlights the increased size of a GFAP+ astrocyte (scale bar = 100 μM). d The perivascular granulocytic infiltration and astrocyte reactivity are present in a non-demyelinating NMO lesion as shown by the presence of intact proteolipid protein (PLP) staining in a section consecutive to a and c (scale bar = 100 μM). e A second example of perivascular granulocytic infiltration involving neutrophils and eosinophils (inset) in the white matter of an NMO patient is shown by H&E staining. The inset highlights the presence of eosinophils (scale bar = 50 μM). f Staining for the astrocyte marker GFAP in a section consecutive to e confirms the presence of numerous reactive astrocytes proximal to the perivascular inflammation (scale bar = 50 μM). g PLP staining reveals that in a section consecutive to (e) and (f) the myelin is intact, indicating that granulocytic infiltrate is found in the absence of demyelination (scale bar = 50 μM). h The complete absence of staining for the terminal complement protein C9neo in a section consecutive to e, f, and g shows that granulocytic recruitment to this site is not dependent on formation of the terminal complement complex (scale bar = 100 μM)

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