A pilot study of immune network remodeling under challenge in Gulf War Illness

Broderick, Gordon; Kreitz, Andrea; Fuite, J.; Fletcher, Mary A; Vernon, Suzanne D.; Klimas, Nancy G.

doi:10.1016/j.bbi.2010.10.011

Cited by 70 publications

(63 citation statements)

References 78 publications

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“…We used a maximal exercise challenge to improve detection as NF-jB (Kim et al, 2009) and many other components of immune function (Walsh et al, 2011) are responsive to exercise as are neuro-endocrine modulators thereof, such as cortisol and neuropeptide Y (NPY) (Jonsdottir, 2000). Consistent with this, our group found previously that IL-1, an NF-jB modulator, exerted a strong influence on exercise-induced immune cell signaling in GWI (Broderick et al, 2011). Based on this, we hypothesized that cholinergic modulation of endocrineimmune function during exercise would differ in GWI subjects.…”

Section: Introductionsupporting

confidence: 53%

“…In addition, measurement of intracellular cytotoxic protein concentrations was performed using quantitative fluorescence. Levels of intracellular perforin, granzyme A or granzyme B, conjugated to phycoerythrin within lymphocytes subsets, both NK cells and CD8+ T cells, were simultaneously assessed with a 5-color system using a maximum-yield protocol (Maher et al, 2002;Broderick et al, 2011). Summary statistics for these markers are listed at each phase of exercise for each subject group in Table S3.…”

Section: Cell Cytometry and Cytotoxicitymentioning

confidence: 99%

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Altered immune pathway activity under exercise challenge in Gulf War Illness: An exploratory analysis

Broderick

Ben‐Hamo

Vashishtha

et al. 2013

Brain, Behavior, and Immunity

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Section: Introductionsupporting

confidence: 53%

Section: Cell Cytometry and Cytotoxicitymentioning

confidence: 99%

Altered immune pathway activity under exercise challenge in Gulf War Illness: An exploratory analysis

Broderick

Ben‐Hamo

Vashishtha

et al. 2013

Brain, Behavior, and Immunity

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“…This is consistent with notions that GWI may be due to a systemic imbalance in immune signaling [51][52][53].…”

Section: Discussionsupporting

confidence: 78%

“…More recent work confirms this finding while also suggesting that this may occur in the more complex context of a mixed Th1:Th2 response [51]. Additionally, Whistler et al found evidence of innate immune involvement with GWI subjects exhibiting impaired immune function as characterized by decreased NK cytotoxicity, altered gene expression associated with NK cell function, altered pro-inflammatory cytokines, and T-cell ratios compared to control subjects [53].…”

Section: Discussionsupporting

confidence: 61%

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Theory-Driven Models for Correcting Fight or Flight" Imbalance in Gulf War Illness"

Broderick¹

2012

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Complementary proteomic approaches reveal mitochondrial dysfunction, immune and inflammatory dysregulation in a mouse model of Gulf War Illness

Zakirova

Reed

Crynen

et al. 2017

Proteomics Clinical Apps

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PurposeLong‐term consequences of combined pyridostigmine bromide (PB) and permethrin (PER) exposure in C57BL6/J mice using a well‐characterized mouse model of exposure to these Gulf War (GW) agents were explored at the protein level.Experimental designWe used orthogonal proteomic approaches to identify pathways that are chronically impacted in the mouse CNS due to semiacute GW agent exposure early in life. These analyses were performed on soluble and membrane‐bound protein fractions from brain samples using two orthogonal isotopic labeling LC‐MS/MS proteomic approaches—stable isotope dimethyl labeling and iTRAQ.ResultsThe use of these approaches allowed for greater coverage of proteins than was possible by either one alone and revealed both distinct and overlapping datasets. This combined analysis identified changes in several mitochondrial, as well as immune and inflammatory pathways after GW agent exposure.Conclusions and clinical relevanceThe work discussed here provides insight into GW agent exposure dependent mechanisms that adversely affect mitochondrial function and immune and inflammatory regulation. Collectively, our work identified key pathways which were chronically impacted in the mouse CNS following acute GW agent exposure, this may lead to the identification of potential targets for therapeutic intervention in the future.Long‐term consequences of combined PB and PER exposure in C57BL6/J mice using a well‐characterized mouse model of exposure to these GW agents were explored at the protein level. Expanding on earlier work, we used orthogonal proteomic approaches to identify pathways that are chronically impacted in the mouse CNS due to semiacute GW agent exposure early in life. These analyses were performed on soluble and membrane‐bound protein fractions from brain samples using two orthogonal isotopic labeling LC‐MS/MS proteomic approaches—stable isotope dimethyl labeling and iTRAQ. The use of these approaches allowed for greater coverage of proteins than was possible by either one alone and revealed both distinct and overlapping datasets. This combined analysis identified changes in several mitochondrial, as well as immune and inflammatory pathways after GW agent exposure. The work discussed here provides insight into GW agent exposure dependent mechanisms that adversely affect mitochondrial function and immune and inflammatory regulation at 5 months postexposure to PB + PER.

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A pilot study of immune network remodeling under challenge in Gulf War Illness

Cited by 70 publications

References 78 publications

Altered immune pathway activity under exercise challenge in Gulf War Illness: An exploratory analysis

Altered immune pathway activity under exercise challenge in Gulf War Illness: An exploratory analysis

Theory-Driven Models for Correcting Fight or Flight" Imbalance in Gulf War Illness"

Complementary proteomic approaches reveal mitochondrial dysfunction, immune and inflammatory dysregulation in a mouse model of Gulf War Illness

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