Human blood monocytes, but not alveolar macrophages, reveal increased CD11b/CD18 expression and adhesion properties upon receptor-dependent activation

Lundahl, Joachim; Halldén, Gunilla; Sköld, C. Magnus

doi:10.1183/09031936.96.09061188

Cited by 34 publications

(33 citation statements)

References 37 publications

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“…The expression of adhesion molecules on AM and Mo has been studied earlier with conflicting results [18, 19, 20, 21], which partly are contradictory to the results of the present study [12, 22]. However, flow-cytometric comparisons have been done without due consideration of the strong and varying AM autofluorescence.…”

Section: Discussioncontrasting

confidence: 54%

Modulation of Adhesion Molecule Profiles on Alveolar Macrophages and Blood Leukocytes

et al. 1999

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Background: Cell adhesion molecules are believed to be essential for blood cell recruitment to the lung and for the movement of alveolar macrophages (AM) within the lung. Objective: To investigate the expression pattern of L-selectin and β₂ integrins on blood leukocytes and AM, including AM of various maturity. Methods: Flow cytometry was used to study the expression of L-selectin (CD62L) and of the β₂ integrins CD11a, CD11b, and CD11c on AM (including density-defined subpopulations), monocytes (Mo), polymorphonuclear neutrophils (PMN) and lymphocytes (Ly) sampled from healthy individuals, during incubation with and without lipopolysaccharide (LPS). Results: A significantly different modulation pattern of β₂ integrins and L-selectin was demonstrated on Mo and AM, cells of the same differentiation lineage. In contrast to AM, Mo had a marked ability to respond to LPS stimulation by increased expression of CD11a, CD11b and CD11c and decreased expression of L- selectin. These molecules were expressed to a similar degree on AM, whereas the basal levels of CD11b and L-selectin were considerably higher on Mo than on AM. A significantly different expression of CD11a as well as differences in the regulation of L-selectin during incubation were also demonstrated between density-defined subpopulations of AM. CD11a could not be upregulated on PMN, otherwise the modulation patterns of CD11b, CD11c and L-selectin were similar to that on Mo. The expression of CD11a on Ly was 3- to 6-fold higher than on Mo, PMN and AM. The level of CD11b decreased significantly upon incubation (uninfluenced by LPS stimulation), and CD11c was hardly expressed on Ly. The level of L-selectin on Ly was higher than on Mo, AM and PMN and was not decreased during incubation. Conclusion: Developmental origin, degree of cell differentiation (maturity) as well as different environmental conditions all heavily influence the expression and modulation pattern of β₂ integrins and L-selectin on leukocytes and Mo-derived AM.

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Section: Discussioncontrasting

confidence: 54%

Modulation of Adhesion Molecule Profiles on Alveolar Macrophages and Blood Leukocytes

et al. 1999

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“…We tested monocytes in "whole blood" samples after lysis of the erythrocytes, thus reducing stimulation of cells by the isolation procedure to a minimum. Monocytes release Mac-1 from preexisting vesicles after stimulation, which results in a rapid increase in surface expression (48). Therefore, isolation procedures may influence expression levels of Mac-1 on monocytes.…”

Section: Discussionmentioning

confidence: 99%

Increased Serum Levels of MRP-8/14 in Type 1 Diabetes Induce an Increased Expression of CD11b and an Enhanced Adhesion of Circulating Monocytes to Fibronectin

et al. 2004

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The recruitment of monocytes from the bloodstream is crucial in the accumulation of macrophages and dendritic cells in type 1 diabetic pancreases. Adhesion via integrins to endothelium and extracellular matrix proteins, such as fibronectin (FN), and the production of myeloid-related protein (MRP)-8, -14, and -8/14 by recently transmigrated monocytes are thought to be instrumental in such recruitment. We determined the FN-adhesive capacity and integrin expression of monocytes of type 1 and type 2 diabetic patients and related them to the subjects' serum levels of MRP-8, -14 and -8/14. Monocytes of type 1 diabetic patients displayed an increased adhesion to fibronectin in comparison with type 2 patients and healthy control subjects but had a normal expression of the FN binding integrins CD29, CD49a, CD49d, and CD49e (although CD11b and CD18 expression was increased). MRP-8/14, which was increased in the sera of type 1 diabetic patients, induced healthy donor monocytes to adhere to FN and upregulate CD11b expression in a dosage-dependent manner. The observed MRP-induced increased adhesion of monocytes to FN and upregulation of CD11b most likely contributed to a facilitated accumulation of monocytes and monocyte-derived cells at the site of inflammation, in this case the pancreatic islets.

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“…Chronic alcohol ingestion depleted GSH levels in BAL fluid (9) and AMs (10) and caused oxidative stress and AM dysfunction in clinical and animal studies (12,14,37,70). AMs are important to innate and acquired immunity (66) due to their ability to phagocytize and clear apoptotic cells and infectious particles from the lung (47). Chronic ethanol exposure causes AM dysfunction (12) through mechanisms that may involve alcohol-induced oxidative stress (16).…”

Section: Discussionmentioning

confidence: 99%

“…In clinical and animal studies, decreased GSH in the alveolar space is associated with chronic oxidative stress and AM dysfunction (12,14,37,70). AMs are critical in innate and acquired immunity (66) since they phagocytize and clear apoptotic cells and infectious particles (47). The binding and internalization of inactive Staphylococcus aureus by AMs from chronic ethanol-exposed animal models is impaired (12), and oral treatments with GSH precursors L-2-oxothiaxolidine-4-carboxylate (Procysteine; Transcend Therapeutics) or N-acetylcysteine improved AM phagocytosis in vitro (14).…”

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confidence: 99%

Glutathione attenuates ethanol-induced alveolar macrophage oxidative stress and dysfunction by downregulating NADPH oxidases

Yeligar

Harris

Hart

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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-Chronic alcohol abuse increases lung oxidative stress and susceptibility to respiratory infections by impairing alveolar macrophage (AM) function. NADPH oxidases (Nox) are major sources of reactive oxygen species in AMs. We hypothesized that treatment with the critical antioxidant glutathione (GSH) attenuates chronic alcohol-induced oxidative stress by downregulating Noxes and restores AM phagocytic function. Bronchoalveolar lavage (BAL) fluid and AMs were isolated from male C57BL/6J mice (8 -10 wk) treated Ϯ ethanol in drinking water (20% wt/vol, 12 wk) Ϯ orally gavaged GSH in methylcellulose vehicle (300 mg·kg Ϫ1 ·day Ϫ1 , during week 12). MH-S cells, a mouse AM cell line, were treated Ϯ ethanol (0.08%, 3 days) Ϯ GSH (500 M, 3 days or last 1 day of ethanol). BAL and AMs were also isolated from ethanol-fed and control mice Ϯ inoculated airway Klebsiella pneumoniae (200 colony-forming units, 28 h) Ϯ orally gavaged GSH (300 mg/kg, 24 h). GSH levels (HPLC), Nox mRNA (quantitative RT-PCR) and protein levels (Western blot and immunostaining), oxidative stress (2=,7=-dichlorofluorescein-diacetate and Amplex Red), and phagocytosis (Staphylococcus aureus internalization) were measured. Chronic alcohol decreased GSH levels, increased Nox expression and activity, enhanced oxidative stress, impaired phagocytic function in AMs in vivo and in vitro, and exacerbated K. pneumonia-induced oxidative stress. Although how oral GSH restored GSH pools in ethanol-fed mice is unknown, oral GSH treatments abrogated the detrimental effects of chronic alcohol exposure and improved AM function. These studies provide GSH as a novel therapeutic approach for attenuating alcohol-induced derangements in AM Nox expression, oxidative stress, dysfunction, and risk for pneumonia. glutathione; alveolar macrophage; nicotinamide adenine dinucleotide phosphate oxidases; oxidative stress; phagocytic function CHRONIC ALCOHOL ABUSE INCREASES susceptibility to acute respiratory distress syndrome (ARDS) (54), a severe form of lung injury with a 26% mortality rate (23), and increases risk of developing respiratory infections, such as pneumonia (49). ARDS is characterized by the development of pulmonary inflammation and edema in response to aspiration, sepsis, or trauma, resulting in systemic proinflammatory cascade activation (68). Compared with a 22% incidence of ARDS in nonalcoholic patients at risk for lung injury, alcoholic patients have a 43% incidence of ARDS (52). Alcohol predisposes to ARDS development through multiple mechanisms, including oxidative stress (11,33,35,37,52). Furthermore, subjects with a history of alcohol use disorders have a higher prevalence of community-acquired pneumonia (20), resulting in worse clinical outcomes than nonalcoholics. Chronic alcohol ingestion increases oxidative stress, which primes the lung for respiratory infections and injury (34).Chronic alcohol consumption depleted levels of the critical antioxidant glutathione (GSH) in the bronchoalveolar lavage (BAL) fluid of human subjects (53) and in the alveolar macro...

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Human blood monocytes, but not alveolar macrophages, reveal increased CD11b/CD18 expression and adhesion properties upon receptor-dependent activation

Cited by 34 publications

References 37 publications

Modulation of Adhesion Molecule Profiles on Alveolar Macrophages and Blood Leukocytes

Modulation of Adhesion Molecule Profiles on Alveolar Macrophages and Blood Leukocytes

Increased Serum Levels of MRP-8/14 in Type 1 Diabetes Induce an Increased Expression of CD11b and an Enhanced Adhesion of Circulating Monocytes to Fibronectin

Glutathione attenuates ethanol-induced alveolar macrophage oxidative stress and dysfunction by downregulating NADPH oxidases

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