Publications by authors named "Daniel Moussa"

3 Publications

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Vaccination in pregnancy: A call to all providers for help.

Cleve Clin J Med 2021 03 1;88(3):157-162. Epub 2021 Mar 1.

Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH.

Vaccination in pregnancy is an important part of maternity care, but maternal immunization rates continue to be below national benchmarks. Influenza and tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccinations have been shown to be safe and provide important protections to pregnant women, the fetus, and neonates. Although obstetrician-gynecologists provide the bulk of pregnancy care, general internists and medical specialists have frequent clinical encounters with maternity patients and should assist in immunization education and administration.
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http://dx.doi.org/10.3949/ccjm.88a.20111DOI Listing
March 2021

Cognitive deficits develop 1month after diffuse brain injury and are exaggerated by microglia-associated reactivity to peripheral immune challenge.

Brain Behav Immun 2016 May 14;54:95-109. Epub 2016 Jan 14.

Department of Neuroscience, The Ohio State University, 333 W. 10th Ave, Columbus, OH, United States; Center for Brain and Spinal Cord Repair, The Ohio State University, 460 W. 12th Ave, Columbus, OH, United States; Institute for Behavioral Medicine Research, The Ohio State University, 460 Medical Center Dr., Columbus, OH, United States. Electronic address:

Unlabelled: Traumatic brain injury (TBI) elicits immediate neuroinflammatory events that contribute to acute cognitive, motor, and affective disturbance. Despite resolution of these acute complications, significant neuropsychiatric and cognitive issues can develop and progress after TBI. We and others have provided novel evidence that these complications are potentiated by repeated injuries, immune challenges and stressors. A key component to this may be increased sensitization or priming of glia after TBI. Therefore, our objectives were to determine the degree to which cognitive deterioration occurred after diffuse TBI (moderate midline fluid percussion injury) and ascertain if glial reactivity induced by an acute immune challenge potentiated cognitive decline 30 days post injury (dpi). In post-recovery assessments, hippocampal-dependent learning and memory recall were normal 7 dpi, but anterograde learning was impaired by 30 dpi. Examination of mRNA and morphological profiles of glia 30 dpi indicated a low but persistent level of inflammation with elevated expression of GFAP and IL-1β in astrocytes and MHCII and IL-1β in microglia. Moreover, an acute immune challenge 30 dpi robustly interrupted memory consolidation specifically in TBI mice. These deficits were associated with exaggerated microglia-mediated inflammation with amplified (IL-1β, CCL2, TNFα) and prolonged (TNFα) cytokine/chemokine expression, and a marked reactive morphological profile of microglia in the CA3 of the hippocampus. Collectively, these data indicate that microglia remain sensitized 30 dpi after moderate TBI and a secondary inflammatory challenge elicits robust microglial reactivity that augments cognitive decline.

Statement Of Significance: Traumatic brain injury (TBI) is a major risk factor in development of neuropsychiatric problems long after injury, negatively affecting quality of life. Mounting evidence indicates that inflammatory processes worsen with time after a brain injury and are likely mediated by glia. Here, we show that primed microglia and astrocytes developed in mice 1 month following moderate diffuse TBI, coinciding with cognitive deficits that were not initially evident after injury. Additionally, TBI-induced glial priming may adversely affect the ability of glia to appropriately respond to immune challenges, which occur regularly across the lifespan. Indeed, we show that an acute immune challenge augmented microglial reactivity and cognitive deficits. This idea may provide new avenues of clinical assessments and treatments following TBI.
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http://dx.doi.org/10.1016/j.bbi.2016.01.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4828283PMC
May 2016

Methylene blue attenuates traumatic brain injury-associated neuroinflammation and acute depressive-like behavior in mice.

J Neurotrauma 2015 Jan 13;32(2):127-38. Epub 2014 Nov 13.

1 Department of Neuroscience, Ohio State University , Columbus, Ohio.

Traumatic brain injury (TBI) is associated with cerebral edema, blood brain barrier breakdown, and neuroinflammation that contribute to the degree of injury severity and functional recovery. Unfortunately, there are no effective proactive treatments for limiting immediate or long-term consequences of TBI. Therefore, the objective of this study was to determine the efficacy of methylene blue (MB), an antioxidant agent, in reducing inflammation and behavioral complications associated with a diffuse brain injury. Here we show that immediate MB infusion (intravenous; 15-30 minutes after TBI) reduced cerebral edema, attenuated microglial activation and reduced neuroinflammation, and improved behavioral recovery after midline fluid percussion injury in mice. Specifically, TBI-associated edema and inflammatory gene expression in the hippocampus were significantly reduced by MB at 1 d post injury. Moreover, MB intervention attenuated TBI-induced inflammatory gene expression (interleukin [IL]-1β, tumor necrosis factor α) in enriched microglia/macrophages 1 d post injury. Cell culture experiments with lipopolysaccharide-activated BV2 microglia confirmed that MB treatment directly reduced IL-1β and increased IL-10 messenger ribonucleic acid in microglia. Last, functional recovery and depressive-like behavior were assessed up to one week after TBI. MB intervention did not prevent TBI-induced reductions in body weight or motor coordination 1-7 d post injury. Nonetheless, MB attenuated the development of acute depressive-like behavior at 7 d post injury. Taken together, immediate intervention with MB was effective in reducing neuroinflammation and improving behavioral recovery after diffuse brain injury. Thus, MB intervention may reduce life-threatening complications of TBI, including edema and neuroinflammation, and protect against the development of neuropsychiatric complications.
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http://dx.doi.org/10.1089/neu.2014.3514DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4291210PMC
January 2015