Firearm Ownership Among Military Veterans With PTSD: A Profile of Demographic and Psychosocial Correlates.

Post-traumatic stress disorder (PTSD), a condition that disproportionately affects military veterans, is associated with heightened rates of aggression and suicide. Although experience with firearms is common among this population, virtually nothing is known regarding who is more likely to own a firearm and whether firearm ownership is differentially associated with psychological and behavioral risk factors among veterans with PTSD. Of 465 veterans (79% male) entering PTSD treatment, 28% owned a firearm (median number of firearms among owners = 3, range = 1-40). Firearm owners reported higher income were less likely to be unemployed, and were more likely to be male, Caucasian, married, and living in permanent housing. Ownership was associated with higher combat exposure and driving aggression, yet lower rates of childhood and military sexual trauma, suicidal ideation, and incarceration. Ownership was not associated with previous suicide attempt, arrest history, number of traumas experienced, PTSD symptoms, or depression. Together, among a sample of treatment-seeking military veterans with PTSD, those who owned a firearm appeared to demonstrate greater stability across a number of domains of functioning. Importantly though, routine firearm safety discussions (e.g., accessibility restrictions; violence risk assessments) and bolstering of anger management skills remain critical when working with this high-risk population.

Diverse activation of microglia by chemokine (C-C motif) ligand 2 overexpression in brain.

BACKGROUND: The chemokine (C-C motif) ligand 2 (CCL2) is a monocyte chemoattractant protein that mediates macrophage recruitment and migration during peripheral and central nervous system (CNS) inflammation. METHODS: To determine the impact of CCL2 in inflammation in vivo and to elucidate the CCL2-induced polarization of activated brain microglia, we delivered CCL2 into the brains of wild-type mice via recombinant adeno-associated virus serotype 9 (rAAV-9) driven by the chicken ß-actin promoter. We measured microglial activation using histological and chemical measurement and recruitment of monocytes using histology and flow cytometry. RESULTS: The overexpression of CCL2 in the CNS induced significant activation of brain resident microglia. CD45 and major histocompatibility complex class II immunoreactivity significantly increased at the sites of CCL2 administration. Histological characterization of the microglial phenotype revealed the elevation of "classically activated" microglial markers, such as calgranulin B and IL-1ß, as well as markers associated with "alternative activation" of microglia, including YM1 and arginase 1. The protein expression profile in the hippocampus demonstrated markedly increased levels of IL-6, GM-CSF and eotaxin (CCL-11) in response to CCL2, but no changes in the levels of other cytokines, including TNF-α and IFN-γ. Moreover, real-time PCR analysis confirmed increases in mRNA levels of gene transcripts associated with neuroinflammation following CCL2 overexpression. Finally, we investigated the chemotactic properties of CCL2 in vivo by performing adoptive transfer of bone marrow-derived cells (BMDCs) isolated from donor mice that ubiquitously expressed green fluorescent protein. Flow cytometry and histological analyses indicated that BMDCs extravasated into brain parenchyma and colabeled with microglial markers. CONCLUSION: Taken together, our results suggest that CCL2 strongly activates resident microglia in the brain. Both pro- and anti-inflammatory activation of microglia were prominent, with no bias toward the M1 or M2 phenotype in the activated cells. As expected, CCL2 overexpression actively recruited circulating monocytes into the CNS. Thus, CCL2 expression in mouse brain induces microglial activation and represents an efficient method for recruitment of peripheral macrophages.