Expression of Macrophage Inflammatory Protein 1-α is Elevated in Alzheimer's Vessels and is Regulated by Oxidative Stress

Tripathy, Debjani; Thirumangalakudi, Lakshmi; Grammas, Paula

doi:10.3233/jad-2007-11405

Cited by 41 publications

(32 citation statements)

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“…Interestingly, increased expression of these chemokines has been reported in AD (Tripathy et al, 2007(Tripathy et al, , 2010Xia et al, 2000), whereas increased T cell expression of CCR5 and CXCR2 has also been reported (Liu et al, 2010;Man et al, 2007;Reale et al, 2008). Infiltration of immune cells may also be a consequence of increased bloodebrain barrier permeability, which we have observed in aged animals (Blau et al, 2012) and APP/PS1 mice (Minogue et al, unpublished), and which is known to occur after B. pertussis infection (Linthicum et al, 1982).…”

Section: Discussionmentioning

confidence: 57%

Respiratory infection promotes T cell infiltration and amyloid-β deposition in APP/PS1 mice

McManus

Higgins

Mills

et al. 2014

Neurobiology of Aging

113

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Section: Discussionmentioning

confidence: 57%

Respiratory infection promotes T cell infiltration and amyloid-β deposition in APP/PS1 mice

McManus

Higgins

Mills

et al. 2014

Neurobiology of Aging

113

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“…CCL3 is produced by macrophages as well as lymphocytes and is a chemoattractant for a number of different cell subsets including lymphocytes, macrophages and neutrophils (Maurer and von Stebut, 2004). High levels of this chemokine are associated with neuroinflammatory diseases including multiple sclerosis and Alzheimer’s disease (Tripathy et al, 2007; Zhang et al, 2000). Potentially relevant to the observation of increased CCL3 in this study, elevated levels of CCL3 have been reported in both prenatal and postnatal brain homogenates of offspring of MIA dams (Garay et al, 2012; Meyer et al, 2006); however, it was not determined whether or not macrophages were the major source of this chemokine.…”

Section: Discussionmentioning

confidence: 99%

Maternal immune activation leads to activated inflammatory macrophages in offspring

Onore

Schwartzer

Careaga

et al. 2014

Brain, Behavior, and Immunity

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Several epidemiological studies have shown an association between infection or inflammation during pregnancy and increased risk of autism in the child. In addition, animal models have illustrated that maternal inflammation during gestation can cause autism-relevant behaviors in the offspring; so called maternal immune activation (MIA) models. More recently, permanent changes in T cell cytokine responses were reported in children with autism and in offspring of MIA mice; however, the cytokine responses of other immune cell populations have not been thoroughly investigated in these MIA models. Similar to changes in T cell function, we hypothesized that following MIA, offspring will have long-term changes in macrophage function. To test this theory, we utilized the poly (I:C) MIA mouse model in C57BL/6J mice and examined macrophage cytokine production in adult offspring. Pregnant dams were given either a single injection of 20 mg/kg polyinosinic–polycytidylic acid, poly (I:C), or saline delivered intraperitoneally on gestational day 12.5. When offspring of poly (I:C) treated dams reached 10 weeks of age, femurs were collected and bone marrow-derived macrophages were generated. Cytokine production was measured in bone marrow-derived macrophages incubated for 24 h in either growth media alone, LPS, IL-4/LPS, or IFN-γ/LPS. Following stimulation with LPS alone, or the combination of IFN-γ/LPS, macrophages from offspring of poly (I:C) treated dams produced higher levels of IL-12(p40) (p < 0.04) suggesting an increased M1 polarization. In addition, even without the presence of a polarizing cytokine or LPS stimulus, macrophages from offspring of poly (I:C) treated dams exhibited a higher production of CCL3 (p = 0.05). Moreover, CCL3 levels were further increased when stimulated with LPS, or polarized with either IL-4/LPS or IFN-γ/LPS (p < 0.05) suggesting a general increase in production of this chemokine. Collectively, these data suggest that MIA can produce lasting changes in macrophage function that are sustained into adulthood.

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“…Although there are many theories about AD occurrence and development, more and more data showed that the immune inflammatory reaction involving pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-a, contribute to the progression of AD (Bossu et al 2007;Bradt et al 1998;Combs et al 2000;Griffin 2006). In AD, in addition to the increase in IL-1, IL-6, and TNF-a, anti-inflammatory cytokines (IL-4, IL-10, IL-13) are usually decreased (Szczepanik et al 2001a) and other inflammatory mediators (prostaglandin E2, nitric oxide (NO), macrophage colony stimulating factor, macrophage chemoattractant protein) are increased (Tripathy et al 2007).…”

Section: Neuro-inflammationmentioning

confidence: 99%

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

2011

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Oxidative stress has been proposed to be an important factor in the pathogenesis of Alzheimer's disease (AD) and contributed to β-amyloid (Aβ) generation. Interaction between oxidative stress and neuro-inflammation leads to Aβ generation. AD is associated with an increase in blood-brain barrier (BBB) permeability due to tight junction involvement. Oxidative stress decreases the expression of low-density lipoprotein receptor-related protein 1 and up-regulates receptor for advanced glycation end products in BBB and increases the BBB permeability, which could potentially lead to increased deposition of Aβ within AD brain. Apoptosis takes place in the pathogenesis of AD, and oxidative stress contributes to apoptosis through both extrinsic pathway and intrinsic pathway. Oxidative stress-induced apoptosis may be a potential factor to Aβ generation. Aβ generation requires two sequential cleavages of APP, with the two proteolytic enzymes: β-secretase and γ-secretase. Oxidative damage up-regulates Aβ via inducing activity of β- and γ-secretases. In this review, we will focus on the mechanism and pathway that oxidative stress contributes to Aβ generation.

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Expression of Macrophage Inflammatory Protein 1-α is Elevated in Alzheimer's Vessels and is Regulated by Oxidative Stress

Cited by 41 publications

References 0 publications

Respiratory infection promotes T cell infiltration and amyloid-β deposition in APP/PS1 mice

Respiratory infection promotes T cell infiltration and amyloid-β deposition in APP/PS1 mice

Maternal immune activation leads to activated inflammatory macrophages in offspring

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

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