Background: Since the onset of the Somali civil war in 1991, more than 1 million Somalis have been displaced from Somalia. Minnesota has the largest Somali population in the U.S. Informal tobacco prevalence estimates among Somali populations in the U.S. and the United Kingdom range from 13% to 37%, respectively. Little research has been conducted to determine the extent of Somali tobacco use.Purpose: This paper reports the results from a knowledge, attitudes, and practices (KAP) survey conducted and analyzed in 2009 that explores tobacco use and estimates prevalence among Somali adults aged >= 18 years in Minnesota.Methods: Modeled after validated state and national tobacco use surveys, the survey was adapted for Somalis and administered to ethnically Somali adults (N=392) from 25 neighborhood clusters, in Minnesota. Participants were chosen through probability proportional to size and multistage random sampling methods.Results: Estimated prevalence for cigarette use among Somalis was 24% (44% among men, 4% among women). Ever users were significantly more likely to be men, have attended college, and have friends who used cigarettes (p<0.0001). Belief in Islamic prohibition of tobacco was protective and affected current use and future intention to use tobacco (p<0.0001). The majority of Somali smokers were unwilling to use current cessation programs.Conclusions: Estimated cigarette use prevalence was lower than perceived prevalence (37%). Contrary to typical results, greater smoking prevalence was found among Somalis with higher education levels. Positive peer pressure and religion are protective factors from tobacco use and should be integrated into prevention and cessation programs. (Am J Prev Med 2012;43(5S3):S205-S213) (C) 2012 American Journal of Preventive Medicine

BACKGROUND:Somalis compose the largest African refugee group in the U.S., with more than 55,000 primary arrivals since 2000. Minnesota has the largest Somali population in the U.S. Despite its size, little research has been conducted to determine the extent of tobacco use among Somali youth. PURPOSE:This paper reports the results from a knowledge, attitudes, and practices (KAP) survey designed to explore factors related to tobacco-use prevention, initiation, and cessation, and to reliably estimate tobacco-use prevalence among Somali youth in grades 9 through 12 in Minnesota. METHODS:A KAP survey, modeled after validated state and national youth tobacco-use surveys, was adapted for Somali youth and administered to ethnically Somali youth (N = 302) from seven high schools in Minnesota in 2008. Participants were chosen through probability-proportional-to-size and multi-stage random sampling methods, and the results were analyzed in 2009. RESULTS:Somali high school students' estimated prevalence for "ever-users" of cigarettes was 12.8%, and current use was 4.7%. This is one quarter of the reported statewide smoking prevalence for Minnesota high school students (19.1%) and half of the nationwide prevalence for blacks/African Americans (11.6%). Ever-users were more likely to have close friends or live with someone who smoked cigarettes (p < 0.01). Belief in the Islamic prohibition of tobacco affected future intention to use tobacco (p < 0.01), as did the belief that using hookah/sheisha is less risky than smoking cigarettes (p < 0.01). CONCLUSIONS:Estimated cigarette use prevalence (4.7%) for Somali youth was substantially lower than among Minnesota high school students and also lower than perceived prevalence among Somalis. Positive peer pressure and religion appear to be protective factors in tobacco use and should be integrated into future Somali tobacco prevention and cessation programs, along with education on the risks of hookah/sheisha use.

BACKGROUND:Somalis compose the largest African refugee group living in the U.S., with more than 10,330 primary arrivals in fiscal year 2006 alone. Half of all Somalis in the U.S. live in Minnesota. Although tobacco use is a considerable problem among Somalis, especially among men, little research has examined factors affecting tobacco use and cessation.METHODS:A sequential exploratory design informed the overall study methodology. Key informant interviews (n=20) and focus group discussions (13 groups; n=91) were conducted with Somali adults and youth in the fall of 2006 and the summer of 2007, respectively. Participants were asked about tobacco-use prevalence, prevention, and cessation, and the marketing of tobacco.RESULTS:Perceived prevalence of tobacco use by Somalis is high at 50%. The main reason for initiating tobacco use was the influence of friends or peer pressure and included other social factors. Prevention and cessation messages suggested by participants include medical advice, education on the negative health effects of tobacco use, religion, and the support of family and friends. Barriers to cessation include lack of insurance coverage, lack of knowledge on where to find assistance, and lack of cessation support groups. Severe social stigma for Somali female smokers poses specific challenges to prevention and intervention efforts. Water-pipe smoking is perceived to be prevalent, particularly among female youth.CONCLUSIONS:Somalis view tobacco use as an important issue in their community. Religious and social support and demographically targeted approaches should be key factors in creating effective prevention and cessation programs and must address water-pipe smoking.

Glutamate uptake by astrocytes has been postulated to play a neuroprotective role during brain inflammation. Using primary human fetal astrocyte cultures, we investigated the influence of selected cytokines on glutamate uptake activity. Interleukin (IL)-1β and tumor necrosis factor-α dose-dependently inhibited astrocyte glutamate uptake, whereas interferon (IFN)-γ alone stimulated this activity. The nitric oxide synthase inhibitor, NG-monomethyl-L-arginine, blocked IL-1β-mediated inhibition of glutamate uptake, suggesting involvement of nitric oxide in the effect of IL-1β. IL-1 receptor antagonist protein totally reversed the inhibitory effect of cytokines, suggesting a critical role of IL-1β. The anti-inflammatory cytokine IFN-β blocked cytokine (IL-1β plus IFN-γ)-induced inhibition of glutamate uptake with a corresponding reduction in nitric oxide generation. Taken together, these findings suggest that proinflammatory cytokines inhibit astrocyte glutamate uptake by a mechanism involving nitric oxide, and that IFN-β may exert a therapeutically beneficial effect by blocking cytokine-induced nitric oxide production in inflammatory diseases of the brain.

Mechanisms underlying human immunodeficiency virus-1 encephalopathy are not completely known; however, recent studies suggest that the viral protein gp41 may be neurotoxic via activation of inducible nitric oxide synthase (iNOS) in glial cells. In the present study, we investigated the NO-generating activity of primary human fetal astrocytes in response to gp41 and the relationship to microglial cell production of interleukin-1 (IL-1). Gp41 failed to trigger iNOS mRNA expression in highly enriched (>99%) astrocyte or microglial cell cultures. However, gp41-treated microglia released a factor(s) that triggered iNOS mRNA expression and NO production in astrocytes. Because IL-1 receptor antagonist protein blocked gp41-induced NO production, a pivotal role was suggested for microglial cell IL-1 production in astrocyte iNOS expression. Also, gp41 induced IL-1beta mRNA expression and IL-1 production in microglial cell but not astrocyte cultures. Using specific inhibitors, we found that gp41-induced IL-1beta production in microglia was mediated via a signaling pathway involving protein-tyrosine kinase. These data support the hypothesis that gp41 induces astrocyte NO production indirectly by triggering upregulation of microglial cell IL-1 expression.

Apoptosis of brain cells is observed in many inflammatory disorders of the central nervous system. Nitric oxide (NO) has been shown to induce apoptosis in several brain cell types, but not previously in astrocytes. In the present study, the hypothesis was examined that interleukin (IL)-1beta would induce production of NO by astrocytes which, in turn, would signal apoptotic death in these glial cells. TUNEL staining demonstrated apoptosis in astrocytes treated with IL-1beta. Using an ELISA method, IL-1 receptor antagonist protein completely abrogated this astrocyte apoptosis, while N(G)monomethyl-L-arginine partially prevented apoptosis but almost entirely blocked NO production. Thus, IL-1beta appears to signal apoptosis of astrocytes by a mechanism involving, in part, the induction of NO.

On the basis of the clinical observation that the cerebrospinal fluid (CSF) of patients with cryptococcal meningitis contains high levels of the chemokine interleukin (IL)-8 but few polymorphonuclear leukocytes (PMNL), the production of IL-8 by cultured brain glial cells after stimulation with two serotypes of cryptococcal capsular polysaccharide glucuronoxylomannan (GXM) was studied, followed by an assessment of the effect of GXM on PMNL migration toward IL-8. GXM serotype A but not D was capable of inducing IL-8 production in human fetal microglial cell but not in astrocyte cultures. When added directly to the PMNL, GXM (both serotypes) potently blocked PMNL migration toward IL-8. The mechanism of GXM's inhibitory effect appeared to involve cross-desensitization. These findings suggest that GXM can induce IL-8 production in the brain but that GXM in the systemic circulation inhibits migration of PMNL toward IL-8.

IL-8 involvement in neutrophil activation and chemotaxis may be important in inflammatory responses within the central nervous system, secondary to meningitis, encephalitis, and traumatic injury. The source of IL-8 within the brain during these inflammatory processes, however, is unknown. To explore the role of microglia in the production of IL-8, human fetal microglia, which are the resident macrophages of the brain, were treated with LPS and pro- and anti-inflammatory cytokines to determine their effects on IL-8 production. We found that IL-8 protein levels increased in response to LPS or IL-1 beta, or to TNF-alpha, which also corresponded to elevated IL-8 mRNA levels by RT-PCR. Pretreatment with IL-4, IL-10, or TGF-beta 1 potently inhibited the stimulatory effects of these proinflammatory agents. These findings indicate that human microglia synthesize IL-8 in response to proinflammatory stimuli, and that anti-inflammatory cytokines down-regulate the production of this chemokine. These results may have important therapeutic implications for certain central nervous system insults involving inflammation.

In the present study, we tested the hypothesis that interleukin (IL)-10 down-regulates human microglial cell IL-8 release by inhibiting activation of nuclear factor kappa B (NF-kappaB). Immunohistochemical staining demonstrated that IL-10 markedly suppressed lipopolysaccharide (LPS)- and IL-1beta-stimulated IL-8 expression. NF-kappaB involvement was suggested by the finding that pyrrolidinedithiocarbamate, a known inhibitor of NF-kappaB activation, blocked LPS- and IL-1beta-induced IL-8 production. Consistent with our hypothesis, IL-10 treatment of LPS- and IL-1beta-stimulated microglia was associated with a marked decrease in NF-kappaB translocation from the cytoplasm to the nucleus.

An understanding of how viral replication in glial cells responds to proinflammatory cytokines is important in delineating HIV-1 neuropathogenesis. Because no information is available in the literature regarding the regulatory effects of exogenous cytokines on acute HIV-1 replication in human brain cells, we studied the impact of cytokine treatment on viral p24 Ag expression. Based upon reports using mononuclear phagocytes derived from somatic sources, we hypothesized that TNF-alpha, IL-1 beta, and IL-6 would up-regulate the expression of HIV-1(SF162) (a monocytotropic strain) in purified microglial cells and in mixed brain cell cultures. This hypothesis was not supported. In fact, a contrary, unexpected result was obtained; whereas in purified microglial cultures TNF-alpha displayed a mild stimulatory effect on HIV-1 expression (15% increase in p24 Ag production compared with control cultures), surprisingly, IL-1 beta and IL-6 were highly suppressive (91 and 83% inhibition of HIV expression, respectively). In contrast to the findings in microglial cell cultures, TNF-alpha profoundly suppressed (84%) HIV-1 expression in mixed brain cell cultures, as did IL-1 beta (82%), and IL-6 was moderately suppressive (55% inhibition). In an attempt to identify factors responsible for the differential effects of TNF-alpha in the two brain cell infection models, it was found that compared with microglial cell cultures, TNF-alpha treatment of mixed brain cell cultures released significantly greater amounts of RANTES (regulated upon activation, normal T cell expressed and secreted) and macrophage inflammatory protein-1 alpha, beta-chemokines that have been suggested to have anti-HIV-1 effects. Thus, these data suggest that proinflammatory cytokines possess anti-HIV-1 activity in the central nervous system.