Exercise and Neutrophil Activity: A Possible Neuroendocrine Connection
Alan J. Husband in Psychoimmunology CNS-Immune Interactions, 2019
This chapter presents circumstantial evidence supporting the hypothesis that growth hormone is the connecting link between moderate exercise and the priming of neutrophil microbicidal activity. A more likely connection between the stress of physical exercise and the response of the neutrophil may lie in the exercise-induced neuroendocrine changes. It is possible that the suppressed neutrophil activity we observed, at rest, in the original group of highly-trained athletes is related to the release of immunosuppressive hormones like cortisol during training sessions that regularly exceed a critical threshold of exercise intensity. At the cellular level, exercise-induced priming of neutrophil microbicidal activity may involve the recruitment of previously unreactive cells into a pool that responds to both physiological and soluble stimuli. Regular physical activity is associated with good health and longevity while a sedentary lifestyle has been implicated as an important risk factor in morbidity and mortality from cardiovascular disease and cancer.
Case 3: Cyclic Neutropenia
Laurel J. Gershwin in Case Studies in Veterinary Immunology, 2017
Neutrophils are an important first line of defense against bacterial pathogens. Formed in the bone marrow from myeloid precursors, mature neutrophils are released into the blood on a regular basis. The neutrophil is responsive to several chemotactic factors that are released from epithelial and other cells after contact with damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs). This chapter examines neutrophils that are incapable of leaving the blood vascular space in response to chemotactic stimuli, and explores neutrophils that are unable to ingest and kill. Cyclic episodes of neutropenia occur in a regular pattern in dogs affected with this condition, leading to episodes of infection when peripheral neutrophil counts fall to less than 1000/μL. The history of recurrent infection and the breed and coat color of the dog strongly suggested cyclic neutropenia. The cycle occurs at approximately 10- to 12-day intervals, with periods of neutropenia often followed by a brief neutrophilia.
Subcorneal bullous dermatosis
Lionel Fry in Atlas of Bullous Diseases, 2020
Subcorneal bullous dermatosis is a relatively rare dermatosis characterized by a flaccid blister and the accumulation of neutrophils in the subcorneal region of the epidermis. The chemoattractant factors for the neutrophils have not been investigated, although interleukin-8 has been shown to be present in the stratum corneum and granular region of the epidermis. There are reports of There are reports being associated with an immunoglobulin A monoclonal gammopathy and pyoderma gangrenosum , which is also associated with neutrophil infiltration. Generalized pustular psoriasis presents with sheets of pustules which are usually smaller and more numerous. In addition, in pustular psoriasis the onset is sudden, and may be accompanied by constitutional upset. Subcorneal bullous dermatosis is commoner in females and usually presents in middle-aged adults. The main lesion is a flaccid blister with pus cells in the lower half of the lesion.
Lung Neutrophil Retention and Injury After Intestinal Ischemia/Reperfusion
Published in Microcirculation, 1997
Feng Xiao, Michael J. Eppihimer, Jay A. Young, Khoa Nguyen, Donna L. Carden
Objective: To define the mechanisms responsible for the lung leukosequestration and injury elicited by intestinal ischemia/reperfusion (I/R). Methods: The effect of 120 minutes of superior mesenteric artery occlusion and 90 minutes of reperfusion on neutrophil deformability, lung neutrophil retention, and pulmonary microvascular permeability was determined. Results: Compared with control surgery, intestinal I/R resulted in a significant increase in neutrophil stiffness (mean yield pressure [Pyieid], 1–533 ± 0.075 and 2.302 ± 0.288 cm H2O, respectively) and lung neutrophil content (6.3 ± 1.4 and 31.5 ± 6.4 U/g wet weight, respectively). These changes were not affected by inhibition of neutrophil adherence before gut reperfusion. However, the increased lung microvascular permeability elicited by gut I/R (0.111 ± 0.020 [control surgery] and 0.255 ± 0.041 [I/R] mL/min/cm H2O/100 g lung tissue) was significantly attenuated by administration of antibodies directed against neutrophil or endothelial determinants of leukocyte adhesion. Conclusions: The results of this study suggest that intestinal I/R is a potent inflammatory stimulus that elicits an increase in neutrophil stiffness and lung neutrophil retention independent of neutrophil-endothelial cell adhesion. In contrast, the increased lung microvascular permeability elicited by gut I/R is attenuated by strategies that interfere with neutrophil-endothelial cell adhesion.
Superoxide dismutase (SOD) as a potential inhibitory mediator of inflammation via neutrophil apoptosis
Published in Free Radical Research, 2005
Kozo Yasui, Norimoto Kobayashi, Takashi Yamazaki, Kazunaga Agematsu, Satoshi Matsuzaki, Susumu Ito, Setsuko Nakata, Atsushi Baba, Kenichi Koike
Superoxide dismutase (SOD) is supposed to be an effective agent for neutrophil-mediated inflammation in the area of critical medicine. We investigated the involvement of SOD in the regulation of neutrophil apoptosis. Exogenously added SOD effectively induced neutrophil apoptosis, and the fluorescence patterns determined using annexin-V and the 7-AAD were similar to those seen in Fas-mediated neutrophil apoptosis. Neutrophils are short-lived leukocytes that need to be removed safely by apoptosis. The clearance of apoptotic neutrophils from sites of inflammation is a crucial determinant of the resolution of inflammation. Catalase inhibited the neutrophil apoptosis and caspase-3 activation. Spontaneous apoptosis, hydrogen peroxide and anti-Fas antibody-induced apoptosis of neutrophils were accelerated in Down's syndrome patients, in whom the SOD gene is overexpressed. Hydrogen peroxide was thought to be a possible major mediator of ROS-induced neutrophil apoptosis in caspase-dependent manner. Neutrophil apoptosis represents a crucial step in the mechanism governing the resolution of inflammation and has been suggested as a possible target for the control of neutrophil-mediated tissue injury. SOD may be a potential inhibitory mediator of neutrophil-mediated inflammation.
Neutrophil Cathepsin G and Tumor Cell RAGE Facilitate Neutrophil Anti-Tumor Cytotoxicity
Published in OncoImmunology, 2019
Ronit Vogt Sionov, Tanya Fainsod-Levi, Tamir Zelter, Lola Polyansky, Christine T. Pham, Zvi Granot
ABSTRACT Neutrophils are a heterogeneous population of myeloid cells which may either promote or hinder tumor growth and progression. Anti-tumor neutrophils have the capacity to kill tumor cells in a contact-dependent manner. However, the molecular mechanisms underlying tumor cell recognition by neutrophils remained unexplored. Tumor cells were shown to express aberrant glycosylation patterns and neutrophils are equipped with receptors capable of recognizing such glycosylations. Accordingly, we hypothesized that the receptor for advanced glycation end products (RAGE) may facilitate neutrophil recognition of tumor cells. Indeed, RAGE decoy receptors and RAGE-specific blocking antibodies dramatically reduce tumor cell susceptibility to neutrophil cytotoxicity. Unexpectedly, we found that tumor cell RAGE rather than neutrophil RAGE is important for the killing process. We further identified neutrophil Cathepsin G as the neutrophil component interacting with tumor cell RAGE. Cathepsin G-deficient neutrophils show impaired ability to kill tumor cells, suggesting that RAGE-Cathepsin G interaction is required for neutrophil cytotoxicity. These data unravel new aspects of neutrophil anti-tumor activity and identify a novel role for RAGE and Cathepsin G in neutrophil-mediated cytotoxicity.