Cell Biology International ISSN 1065-6995 doi: 10.1002/cbin.10618 RESEARCH ARTICLE Basal neutrophil function in human aging: Implications in endothelial cell adhesion Joes Nogueira-Neto 1 , Andr e S. C. Cardoso 1 , Hugo P. Monteiro 2 , Fernando L. A. Fonseca 1,3 , Luiz Roberto Ramos 4 , Virginia B. C. Junqueira 1 and Karin A. Simon 1,5 * 1 Department of Biological Sciences, Federal University of S~ ao Paulo, Diadema, SP, Brazil 2 Department of Biochemistry/Molecular Biology, Federal University of S~ ao Paulo, S~ ao Paulo, SP, Brazil 3 Department of Hematology and Oncology, ABC School of Medicine, Santo Andr e, SP, Brazil 4 Department of Preventive Medicine, Federal University of S~ ao Paulo, S~ ao Paulo, SP, Brazil 5 Laborat orio de An alises Cl  ınicas e Toxicol  ogicas, Instituto de Ci^ encias Ambientais, Qu  ımicas e Farmac^ euticas, Universidade Federal de S~ ao Paulo, Rua S~ ao Nicolau, 210–1  Andar, Diadema 09913-030 SP, Brazil Abstract Much attention has been drawn to the pro-inflammatory condition that accompanies aging. This study compared parameters from non-stimulated neutrophils, obtained from young (18–30 years old [y.o.]) and elderly (65–80 y.o.) human volunteers. Measured as an inflammatory marker, plasmatic concentration of hs-CRP was found higher in elderly individuals. Non- stimulated neutrophil production of ROS and NO was, respectively, 38 and 29% higher for the aged group. From the adhesion molecules evaluated, only CD11b expression was elevated in neutrophils from the aged group, whereas no differences were found for CD11a, CD18, or CD62. A 69% higher non-stimulated in vitro neutrophil/endothelial cell adhesion was observed for neutrophils isolated from elderly donors. Our results suggest that with aging, neutrophils may be constitutively producing more reactive species in closer proximity to endothelial cells of vessel walls, which may both contribute to vascular damage and reflect a neutrophil intracellular disrupted redox balance, altering neutrophil function in aging. Keywords: aging; cell function; endothelial implications Introduction Although much has yet to be elucidated on the subject, aging has been intrinsically related to increased oxidative damage along an organism’s life course, contributing, when not directly causing, the general physiological and functional decline that characterizes the aging process. This relation- ship is frequently more pronounced in age-related degene- rative diseases (Junqueira et al., 2004, 2008). Oxidative damage results from an imbalanced pro and antioxidant condition in the organism, favoring oxidant species, namely reactive oxygen- and nitrogen-derived species (ROS and RNS, respectively). However, classical oxidative damage to biomolecules may not be the sole contribution of ROS and RNS to aging. The association of these reactive species to inflammatory developments has led to the hypothesis of “molecular inflammation,” stated as the molecular activation of pro-inflammatory genes by altered redox-sensitive cellular signal pathways that would eventually lead to fully expressed inflammatory tissues and organs, which is exacerbated by aging (Chung et al., 2006). Indeed, the term “inflamm-aging” was coined in order to describe the progressive pro-inflammatory condition found in elderly humans, even in the absence of an immune challenge, rendering the older subject more susceptible to age-related diseases, especially those with an inflammatory pathogenesis (Franceschi et al., 2000). Both adaptive and innate immunity components are affected by aging, and although the concept of immunose- nescence has originally focused on the adaptive immune system, there is growing evidence on its impact on innate immunity as well (Solana et al., 2012). Nevertheless, a pivotal step to acute inflammatory response is the recruitment of effector immune cells from blood and their migration  Corresponding author: e-mail: karsimon.unifesp@gmail.com Abbreviations: hs-CRP, high sensitivity c reaction protein; RNS, nitrogen-derived species; ROS, reactive oxygen-derived species; TLR, toll-like receptor; y.o., years old 796 Cell Biol Int 40 (2016) 796–802 © 2016 International Federation for Cell Biology