High serum sICAM-1 is correlated with cerebral microbleeds and hemorrhagic transformation in ischemic stroke patients.
Wu Bo-Na,Wu Jing,Hao Dong-Lin,Mao Lun-Lin,Zhang Jin,Huang Ting-Ting
British journal of neurosurgery
Intercellular adhesion molecule 1 (ICAM-1) is an adhesive protein involved in inflammatory responses and endothelial dysfunction. ICAM-1 expression is upregulated in cerebrovascular tissue affected by stroke. We investigated whether serum soluble ICAM-1 (sICAM-1) levels are associated with cerebral microbleeds (CMBs) and risk of hemorrhagic transformation (HT). 148 patients with acute ischemic stroke were enrolled. Serum sICAM-1 levels were measured and compared between patients and healthy controls. Multivariate logistic regression analysis was performed to estimate the relationship between serum sICAM-1 levels and the HT risk. Serum sICAM-1 levels were significantly higher in ischemic stroke patients compared with healthy controls ( < .001), and higher in patients with CMBs ( = 81) compared with patients without CMBs ( = 67) ( < .001). Patients with high sICAM-1 levels (≥250.5 ng/mL) were more likely to have hypertension, diabetes mellitus, previous stroke, and CMBs compared with patients with low sICAM-1 levels. In stroke patients with CMBs, higher serum sICAM-1 levels were independently associated with increased HT risk. Serum sICAM-1 levels are associated with presence of CMBs and increased risk of HT in ischemic stroke patients.
Interaction among smoking status, single nucleotide polymorphisms and markers of systemic inflammation in healthy individuals.
Luetragoon Thitiya,Rutqvist Lars E,Tangvarasittichai Orathai,Andersson Bengt-Åke,Löfgren Sture,Usuwanthim Kanchana,Lewin Nongnit L
Cigarette smoke contains toxic and carcinogenic substances that contribute to the development of cancer and various diseases. Genetic variation might be important, because not all smokers develop smoking-related disease. The current study addressed the possible interactions among selected single nucleotide polymorphisms (SNPs) in genes related to systemic inflammation, smoking status, the levels of circulating immune response cells and plasma biomarkers of systemic inflammation. Sixty-four healthy blood donors were recruited, 31 of whom were current smokers and 33 were never-users of tobacco products, references. Compared to references, the smokers showed significantly increased levels of circulating total white blood cells, lymphocytes, monocytes, neutrophils, basophils and C-reactive protein (CRP). Smokers also more frequently exhibited circulating cell phenotypes that are associated with an immunocompromised state: CD8 cells in the lymphocyte group, CD13 CD11 , CD13 CD14 , CD13 CD56 cells in the monocyte group and CD13 CD11 , CD13 CD56 cells in the neutrophil group. We observed an interaction among SNPs, smoking status and some of the studied biomarkers. The average plasma CRP level was significantly higher among the smokers, with the highest level found among those with the CRP rs1800947 CC genotype. Additionally, an increased CD8 GZB cells in the CD8 group were found among smokers with the GZB rs8192917 AA genotype. Thus, smoking appears to be associated with systemic inflammation and increased levels of circulating immunosuppressive cells. The extent of these effects was associated with SNPs among the smokers. This observation may contribute to a better understanding of the genetic susceptibility of smoking-related disease and the variations observed in clinical outcomes.