Limits...
Immunolocalization of influenza A virus and markers of inflammation in the human Parkinson's disease brain.

Rohn TT, Catlin LW - PLoS ONE (2011)

Bottom Line: Although much is known regarding the molecular mechanisms leading to neuronal cell loss in Parkinson's disease (PD), the initiating event has not been identified.Prevailing theories including a chemical insult or infectious agent have been postulated as possible triggers, leading to neuroinflammation.Further supporting a role for neuroinflammation in PD was the identification of T-lymphocytes that colocalized with an antibody to caspase-cleaved Beclin-1 within the SNpc.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Boise State University, Boise, Idaho, United States of America. trohn@boisestate.edu

ABSTRACT
Although much is known regarding the molecular mechanisms leading to neuronal cell loss in Parkinson's disease (PD), the initiating event has not been identified. Prevailing theories including a chemical insult or infectious agent have been postulated as possible triggers, leading to neuroinflammation. We present immunohistochemical data indicating the presence of influenza A virus within the substantia nigra pars compacta (SNpc) from postmortem PD brain sections. Influenza A virus labeling was identified within neuromelanin granules as well as on tissue macrophages in the SNpc. Further supporting a role for neuroinflammation in PD was the identification of T-lymphocytes that colocalized with an antibody to caspase-cleaved Beclin-1 within the SNpc. The presence of influenza A virus together with macrophages and T-lymphocytes may contribute to the neuroinflammation associated with this disease.

Show MeSH

Related in: MedlinePlus

Degenerating oligodendrocytes co-localize with caspase-cleaved Beclin-1 in PD.(A and B): Representative labeling in control or PD cases utilizing mAB anti-Olig1 indicated staining of well-defined, healthy oligodendrocytes in age-matched control cases (A), as compared to PD cases where labeling was identified on oligodendrocytes exhibiting shrunken cell bodies (B). (C–E): Immunofluorescence double labeling in a representative PD case indicated the co-localization of the BeclinCCP antibody (red, C) with anti-Olig1 (green, D). Panel E displays the overlap image for both antibodies indicating the labeling of the BeclinCCP antibody within degenerating oligodendrocytes (yellow, E). F): Panel F depicts quantitative analysis indicating that approximately 87% of anti-Olig1-positive cells co-localized with the BeclinCCP antibody (p = 1.46×10−6). All scale bars are 10 µm.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3105060&req=5

pone-0020495-g003: Degenerating oligodendrocytes co-localize with caspase-cleaved Beclin-1 in PD.(A and B): Representative labeling in control or PD cases utilizing mAB anti-Olig1 indicated staining of well-defined, healthy oligodendrocytes in age-matched control cases (A), as compared to PD cases where labeling was identified on oligodendrocytes exhibiting shrunken cell bodies (B). (C–E): Immunofluorescence double labeling in a representative PD case indicated the co-localization of the BeclinCCP antibody (red, C) with anti-Olig1 (green, D). Panel E displays the overlap image for both antibodies indicating the labeling of the BeclinCCP antibody within degenerating oligodendrocytes (yellow, E). F): Panel F depicts quantitative analysis indicating that approximately 87% of anti-Olig1-positive cells co-localized with the BeclinCCP antibody (p = 1.46×10−6). All scale bars are 10 µm.

Mentions: Due to the pattern of labeling of the BeclinCCP antibody in SN white matter (Fig. 1E), it was predicted that labeled cells were oligodendrocytes. We observed staining of cells of similar size and morphology as compared to BeclinCCP staining following application of an oligodendrocyte antibody, anti-Olig1 in PD cases. Thus, single-labeling experiments with anti-Oligo1 indicated labeling of oligodendrocytes exhibiting shrunken cells bodies in PD cases, indicative of cells undergoing apoptosis (Fig. 3B), whereas in age-matched control cases, labeling of well-defined oligodendrocytes was observed (Fig. 3A). That the BeclinCCP antibody was labeling oligodendrocytes was confirmed following co-localization immunofluorescence experiments utilizing anti-Olig1 and BeclinCCP (Fig. 3C–E). Under these experimental conditions, quantitative analysis demonstrated that 87% of anti-Oligo1-positive cells co-localized with the BeclinCCP antibody (p = 1.46×10−6, ±S.E.M.) (Fig. 3F).


Immunolocalization of influenza A virus and markers of inflammation in the human Parkinson's disease brain.

Rohn TT, Catlin LW - PLoS ONE (2011)

Degenerating oligodendrocytes co-localize with caspase-cleaved Beclin-1 in PD.(A and B): Representative labeling in control or PD cases utilizing mAB anti-Olig1 indicated staining of well-defined, healthy oligodendrocytes in age-matched control cases (A), as compared to PD cases where labeling was identified on oligodendrocytes exhibiting shrunken cell bodies (B). (C–E): Immunofluorescence double labeling in a representative PD case indicated the co-localization of the BeclinCCP antibody (red, C) with anti-Olig1 (green, D). Panel E displays the overlap image for both antibodies indicating the labeling of the BeclinCCP antibody within degenerating oligodendrocytes (yellow, E). F): Panel F depicts quantitative analysis indicating that approximately 87% of anti-Olig1-positive cells co-localized with the BeclinCCP antibody (p = 1.46×10−6). All scale bars are 10 µm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3105060&req=5

pone-0020495-g003: Degenerating oligodendrocytes co-localize with caspase-cleaved Beclin-1 in PD.(A and B): Representative labeling in control or PD cases utilizing mAB anti-Olig1 indicated staining of well-defined, healthy oligodendrocytes in age-matched control cases (A), as compared to PD cases where labeling was identified on oligodendrocytes exhibiting shrunken cell bodies (B). (C–E): Immunofluorescence double labeling in a representative PD case indicated the co-localization of the BeclinCCP antibody (red, C) with anti-Olig1 (green, D). Panel E displays the overlap image for both antibodies indicating the labeling of the BeclinCCP antibody within degenerating oligodendrocytes (yellow, E). F): Panel F depicts quantitative analysis indicating that approximately 87% of anti-Olig1-positive cells co-localized with the BeclinCCP antibody (p = 1.46×10−6). All scale bars are 10 µm.
Mentions: Due to the pattern of labeling of the BeclinCCP antibody in SN white matter (Fig. 1E), it was predicted that labeled cells were oligodendrocytes. We observed staining of cells of similar size and morphology as compared to BeclinCCP staining following application of an oligodendrocyte antibody, anti-Olig1 in PD cases. Thus, single-labeling experiments with anti-Oligo1 indicated labeling of oligodendrocytes exhibiting shrunken cells bodies in PD cases, indicative of cells undergoing apoptosis (Fig. 3B), whereas in age-matched control cases, labeling of well-defined oligodendrocytes was observed (Fig. 3A). That the BeclinCCP antibody was labeling oligodendrocytes was confirmed following co-localization immunofluorescence experiments utilizing anti-Olig1 and BeclinCCP (Fig. 3C–E). Under these experimental conditions, quantitative analysis demonstrated that 87% of anti-Oligo1-positive cells co-localized with the BeclinCCP antibody (p = 1.46×10−6, ±S.E.M.) (Fig. 3F).

Bottom Line: Although much is known regarding the molecular mechanisms leading to neuronal cell loss in Parkinson's disease (PD), the initiating event has not been identified.Prevailing theories including a chemical insult or infectious agent have been postulated as possible triggers, leading to neuroinflammation.Further supporting a role for neuroinflammation in PD was the identification of T-lymphocytes that colocalized with an antibody to caspase-cleaved Beclin-1 within the SNpc.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Boise State University, Boise, Idaho, United States of America. trohn@boisestate.edu

ABSTRACT
Although much is known regarding the molecular mechanisms leading to neuronal cell loss in Parkinson's disease (PD), the initiating event has not been identified. Prevailing theories including a chemical insult or infectious agent have been postulated as possible triggers, leading to neuroinflammation. We present immunohistochemical data indicating the presence of influenza A virus within the substantia nigra pars compacta (SNpc) from postmortem PD brain sections. Influenza A virus labeling was identified within neuromelanin granules as well as on tissue macrophages in the SNpc. Further supporting a role for neuroinflammation in PD was the identification of T-lymphocytes that colocalized with an antibody to caspase-cleaved Beclin-1 within the SNpc. The presence of influenza A virus together with macrophages and T-lymphocytes may contribute to the neuroinflammation associated with this disease.

Show MeSH
Related in: MedlinePlus