Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1997 Apr;150(4):1267-74.

Interleukin-8 receptor B immunoreactivity in brain and neuritic plaques of Alzheimer's disease

Affiliations

Interleukin-8 receptor B immunoreactivity in brain and neuritic plaques of Alzheimer's disease

M Xia et al. Am J Pathol. 1997 Apr.

Abstract

Cytokines mediate inflammatory responses through their receptors in the hematopoietic system. In a search for potential mediators of inflammatory responses in Alzheimer's disease, we examined brain for cytokine receptors. Herein we describe interleukin-8 receptor B (IL-8RB, also termed CXCR2) immunoreactivity in the central nervous system. Strong IL-8RB immunoreactivity is present in both Alzheimer's disease and control brains. Neurons, dendrites, and axons are clearly immunoreactive. In Alzheimer's disease, IL-8RB immunoreactivity is also present in some swollen dystrophic neurites of neuritic plaques. Double staining and confocal microscopic analysis reveals that these IL-8RB-positive neurites in plaques are neurofilament positive and are distinct from astrocytic or microglial processes. In general, these IL-8RB-positive neurities do not co-localize with PHF-1 or AT8 (hyperphosphorylated tau) immunoreactive neurites but instead co-localize with beta PP-positive neurites. These results demonstrate for the first time IL-8RB immunoreactivity in the central nervous system and imply a new role for this receptor outside the hematopoietic system. The strong presence of IL-8RB on neurons and the potential of glial cells to produce IL-8 suggest that this system might mediate neuronal-glial interactions.

PubMed Disclaimer

References

    1. J Neuropathol Exp Neurol. 1995 Mar;54(2):276-81 - PubMed
    1. Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3270-4 - PubMed
    1. Hum Pathol. 1995 Aug;26(8):816-23 - PubMed
    1. Am J Pathol. 1995 Nov;147(5):1248-60 - PubMed
    1. Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10738-41 - PubMed

Publication types

MeSH terms