Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-0934, Japan
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ABSTRACT |
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Fifteen years have passed since the first description of interleukin (IL)-8/CXCL8 as a potent neutrophil chemotactic factor. Accumulating evidence has demonstrated that various types of cells can produce a large amount of IL-8/CXCL8 in response to a wide variety of stimuli, including proinflammatory cytokines, microbes and their products, and environmental changes such as hypoxia, reperfusion, and hyperoxia. Numerous observations have established IL-8/CXCL8 as a key mediator in neutrophil-mediated acute inflammation due to its potent actions on neutrophils. However, several lines of evidence indicate that IL-8/CXCL8 has a wide range of actions on various types of cells, including lymphocytes, monocytes, endothelial cells, and fibroblasts, besides neutrophils. The discovery of these biological functions suggests that IL-8/CXCL8 has crucial roles in various pathological conditions such as chronic inflammation and cancer. Here, an overview of its protein structure, mechanisms of production, and receptor system will be discussed as well as the pathophysiological roles of IL-8/CXCL8 in various types of lung pathologies.
inflammation; angiogenesis; chemokine; neutrophil
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INTRODUCTION |
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INTERLEUKIN (IL)-8 was first purified and molecularly cloned as a neutrophil chemotactic factor from lipopolysaccharide-stimulated human mononuclear cell supernatants (109, 166). Since then, a family of structurally related cytokines has been identified. Because most of them exhibit chemotactic activity for a limited spectrum of leukocytes, they are now called chemokines (chemotactic cytokines) (12, 103). Chemokines are low-molecular-weight proteins with cysteines at well-conserved positions, exhibiting a basic charge and an affinity for heparin. It is, therefore, believed that chemokines efficiently bind to proteoglycans on vascular endothelium cells and to extracellular matrix proteins in the tissues (12). Chemokine receptors comprise a large branch of the rhodopsin family of cell-surface G protein-coupled receptors with seven-transmembrane domains (122). High-affinity binding to target cells and subsequent signaling and functional effects of chemokines are mediated by these receptors.
Chemokines are divided into four subgroups, CXC, CC, CX3C with four to six cysteines, and C chemokines with only two, corresponding to the second and fourth cysteines in the other groups. CXC and CX3C chemokines are distinguished by the presence of one (CXC) and three (CX3C) intervening amino acids, respectively, whereas the first two cysteines are adjacent in CC chemokines. A novel nomenclature system has been proposed for chemokines and their receptors (122, 169). Systematic chemokine names are based on their cysteine subclass roots, followed by "L" for "ligand". The numbers correspond generally to the same number used in the corresponding gene nomenclature. Because most chemokine receptors are restricted to a single chemokine subclass, the nomenclature system of chemokine receptors is rooted by the chemokine subclass specificity, followed by "R" for "receptor" and the number. According to this nomenclature system, IL-8 is now called CXCL8.
CXC chemokines can be further subclassified into Glu-Leu-Arg
(ELR)+ and ELR CXC chemokines, based
on the presence or absence of tripeptide motif ELR of the
NH2 terminus before the first cysteine. This classification
correlates with the functional differences. ELR+ CXC
chemokines bind CXCR1 and/or CXCR2 with a high affinity and have a
potent chemotactic effect, particularly on neutrophils (4,
121), and exhibit potent angiogenic activity (148).
It is presumed that growth-related proteins (GRO; CXCL1, 2, and 3) substitute for the functions of IL-8 in mice and rats, both of which
lack the ortholog of human IL-8/CXCL8 and CXCR1. Thus although we will
mainly discuss IL-8/CXCL8, we will refer to other ELR+ CXC
chemokines, particularly GROs.
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MOLECULAR AND CELLULAR BIOLOGY OF IL-8/CXCL8 |
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Protein structure. The CXCL8 cDNA encodes a 99-amino acid precursor protein with a signal sequence, which is cleaved to yield mainly 77- or 72-residue mature protein (109). CXCL8 is further processed at the NH2 terminus yielding different truncation analogs (77-, 72-, 71-, 70-, 69-amino acid forms). The truncation is caused by proteases that are released from CXCL8-secreting cells or by accessory cells (65, 124, 129, 167), and the occurrence of the NH2-terminal forms depends on the producer cells and culture conditions (153-155). The two major forms are 77- and 72-amino acid proteins with a minor 69-amino acid protein. In vitro, fibroblasts and endothelial cells predominantly produce the 77-amino acid form, whereas leukocytes mainly secrete 72- or 69-amino acid forms. These three forms exhibit neutrophil chemotactic activities with distinct potencies: 69- > 72- >77-amino acid form. In vivo, the 77-amino acid form is rapidly cleaved to yield a 72-amino acid form (86).
Nuclear magnetic resonance spectroscopy and X-ray crystallography have revealed that CXCL8, in a concentrated solution and crystallized state, occurs as a homodimer consisting of two identical subunits (14). The monomer contains a disordered NH2 terminus, followed by a loop region, three antiparallelMechanisms of production.
CXCL8 can be produced by leukocytic cells (monocytes, T cells,
neutrophils, and natural killer cells) and nonleukocytic somatic cells
(endothelial cells, fibroblasts, and epithelial cells) (12, 115,
116, 128). CXCL8 production is not constitutive but inducible by
proinflammatory cytokines such as IL-1 and tumor necrosis factor (TNF)- (109). Moreover, CXCL8 production can be induced
by bacteria (e.g., Helicobacter pylori, Pseudomonas
aeruginosa) (5, 44), bacterial products [e.g.,
lipopolysaccharide (LPS)] (12, 128), viruses (e.g.,
adenovirus, respiratory syncytial virus, cytomegalovirus, rhinovirus)
(6, 33, 75, 119), and viral products (e.g., X protein of
human hepatitis virus B, Tax protein of human T cell-leukemia type I
virus) (105, 113). This may result in elevated CXCL8 concentrations in body fluids with microbial infection.
Receptor system. CXCL8 binds to two distinct receptors, CXCR1 and CXCR2, with a similar high affinity (68, 123). CXCR1 and CXCR2 consist of 350 and 360 amino acids, respectively. They are membrane-bound molecules composed of seven-transmembrane domains and coupled to G proteins at the COOH-terminal portion and possibly the third intracellular loop (120, 122). CXCR1 and CXCR2 possess high-sequence homology exceeding 80% at the amino acid level, except in their NH2-terminal portions, and can bind some ELR+ CXC chemokines. Because of the differences in their NH2-terminal portion, their binding specificities differ; CXCR2 binds CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, and CXCL7 with high affinity, whereas only CXCL6 also binds CXCR1, but with a lower affinity than CXCL8 (122).
After ligand binding, human CXCL8 receptors are internalized and subsequently recycled and reappear on the cell surface rapidly within 60 min (140). The inhibition of recycling reduced CXCL8-mediated chemotaxis. Moreover, ligand binding activates pertussis toxin-sensitive and receptor-coupled G proteins, particularly G
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Biological activities.
Accumulating evidence indicates that CXCL8 is involved in the whole
process of leukocyte transmigration into tissues. CXCL8 is internalized
by endothelial cells abluminally, transcytosed to luminal surface, and
presented to the neutrophils (111). There, CXCL8 induces
the shedding of L-selectin, regulates the expression of
2-integrins (CD11b/CD18 and CD11c/CD18) and complement
receptor type 1 (CR1/CD35) on neutrophils, and alters the avidity of
the constitutively expressed integrin molecules (32, 43,
70). CXCL8 promotes adhesion of neutrophils to plastic,
extracellular matrix proteins, and unstimulated as well as
cytokine-stimulated endothelial monolayers through interaction with
CD11b/CD18 (32). CXCL8 stimulates neutrophil migration
across endothelium (70), pulmonary epithelium
(117), and fibroblasts (26) (see Fig. 2).
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ROLES OF IL-8 IN PULMONARY DISEASES |
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Bacterial infection. CXCL8 is frequently detected at sites of infections. This may be because various types of microbes and their products can induce CXCL8 protein production in a variety of cell lines in vitro (115). Moreover, several lines of evidence suggest that neutrophils are recruited by endogenously produced CXCL8 to infection sites to eradicate inciting microbes. CXCL8 can enhance the in vitro intracellular killing of Mycobacterium fortuitum (126) and Candida albicans by neutrophils (45). Lung-specific transgenic expression of mouse CXCL1 induces neutrophil accumulation in the bronchi and terminal bronchioles (101) but enhances resistance to Klebsiella pneumoniae infection (152). Moreover, CXCR2-deficient mice show an enhanced susceptibility to mucosal and systemic C. albicans infection with reduced neutrophil infiltration into the infected tissues (15). In an acute pyelonephritis model caused by Escherichia coli infection, neutrophils cannot transverse the mucosal barrier and eventually accumulate under the epithelium in CXCR2-deficient mice (54, 63). Subepithelial neutrophil entrapment finally results in renal scarring. In Listeria monocytogenes infection, CXCR2-deficient mice often develop chronic infection, compared with wild-type mice (37). These observations suggest that CXCL8 and its related molecules (CXCL1, CXCL2, and CXCL3) play a crucial role in regulating the processes of eradication of invasive bacteria, which are restricted to local sites.
Intrapleural injection of LPS into rabbits induces a massive infiltration of neutrophils into pleural cavity (23). The administration of an anti-CXCL8 antibody reduces neutrophil infiltration in this model, implicating CXCL8 as a key mediator in endotoxin-induced pleurisy (Table 1). Intravenous injection of LPS into a normal human volunteer causes a rapid increase in plasma CXCL8 levels, peaking at 2 h and returning to baseline levels within 5 h after LPS injection (106). Moreover, an elevation in plasma CXCL8 levels precedes neutrophil accumulation and activation, as shown by an elevated neutrophil-derived elastase level (135). Similar results are also observed in patients with sepsis (56, 64). In lethal and sublethal sepsis induced by infusing primates with live E. coli and LPS, respectively, CXCL8 is detected in the circulation. The CXCL8 levels are higher in animals with lethal bacteremia than in those with sublethal endotoxemia (156). However, the administration of an anti-CXCL8 antibody only marginally improved survival in endotoxin-induced acute lethality in Propionibacterium acnes-primed rabbits (72). Thus it remains elusive on the pathogenic roles of CXCL8 in endotoxemia.
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Viral infection.
Various types of viruses and viral products can induce CXCL8 production
in a wide variety of cell types (33, 105, 107, 113, 119,
132) at the transcriptional level. In most cases, viruses and
viral products can activate both NF-B and AP-1, which results in
rapid CXCL8 gene transcription. However, the involvement of additional
transcription factors is suggested in respiratory syncytial
virus-induced IL-8 gene transcription (33).
Acute respiratory distress syndrome. Acute respiratory distress syndrome (ARDS) is identified as an acute respiratory failure associated with a nonhydrostatic pulmonary edema (19). The involvement of neutrophils in ARDS has been documented by several groups (146), and elevated bronchioalveolar lavage fluid (BALF) concentrations of CXCL8 and granulocyte colony-stimulating factor correlated with increased neutrophil numbers in BALF (3). Moreover, CXCL8 levels in BALF were increased in ARDS patients and correlated with the development of ARDS in at-risk patient groups (46). Kurdowska and colleagues (95) claimed that CXCL8 in BALF was associated with anti-CXCL8 autoantibodies and that there was a significant correlation between the concentrations of CXCL8:anti-CXCL8 complex and the onset of ARDS. These clinical observations implicate CXCL8 in the pathogenesis of ARDS.
This hypothesis is supported by results on several animal models. In acid aspiration- and endotoxemia-induced ARDS in rabbits, CXCL8 is produced in the lungs (53, 165). In both models, the abrogation of CXCL8 activity reduces neutrophil infiltration as well as tissue damage. These effects may be explained by the assumption that locally produced CXCL8 can suppress neutrophil apoptosis (48) and induce neutrophil migration into the lungs and damages to lung tissues, including alveolar epithelial barrier function (112).Reperfusion injury and transplantation. Reperfusion injury occurring after a transient ischemic episode frequently causes greater injury than the ischemia itself (55, 161) and is frequently observed in myocardial infarction, cerebral infarction, and transplanted organs. Reperfusion of blood flow results in reoxygenation of ischemic tissue, leading to the generation of ROI such as hydrochloric acid and hydrogen oxide (110). These generated ROI damage every component in tissue, including nucleic acids, membrane lipids, enzymes, and receptors. Reperfusion injury is characterized by the adherence and emigration of neutrophils into postcapillary venules (51). Depletion of neutrophils or the prevention of neutrophil adherence with antibodies to leukocyte adhesion molecules abolished reperfusion-induced vascular dysfunction (69, 89). These results imply that neutrophil infiltration has a crucial role in the establishment of reperfusion injury.
ROI can activate NF-Lung injuries due to other physical conditions. Reexpansion of collapsed lung induces increased microvascular permeability and neutrophil infiltration, leading to reexpansion pulmonary edema. CXCL8 is produced by alveolar macrophages and epithelial cells in the reexpanded lung in rabbits (125). Moreover, pretreatment with a neutralizing antibody to CXCL8 reduced microvascular permeability and neutrophil infiltration, indicating the crucial roles of CXCL8 in the establishment of reexpansion lung injury. Smoke inhalation also causes lung endothelial injury and formation of pulmonary edema, due to an increase in alveolar epithelial permeability to protein and reduction in the fluid transport capacity of alveolar epithelium. The pretreatment with a neutralizing anti-CXCL8 antibody significantly reduced the smoke-induced increase in bidirectional transport of protein across the alveolar epithelium and restored alveolar liquid clearance to a normal level (96). Thus CXCL8 has a crucial role in edema formation due to these injuries.
High oxygen concentration contributes to lung disease and concomitant neutrophil infiltration in the newborn. High oxygen concentration synergistically increases TNF-Allergic inflammation and asthma. CXCR2-deficient mice exhibit increased serum IgE levels when they are kept under specific pathogen-free conditions (29). IgE production in allergen-induced pulmonary inflammation is also enhanced in CXCR2-deficient mice compared with wild-type mice (42). These phenotypes may be explained by the observation that CXCL8 selectively inhibits IL-4-induced IgE production (81, 82). Because the treatment of human lungs with IgE results in release of CXCL8 (52), CXCL8 may constitute a negative feedback for IgE production.
Analysis of induced sputum in persistent asthma identifies two different inflammatory patterns (62). The most common pattern is noneosinophilic and is associated with neutrophil influx into the lungs and increased local CXCL8 production. Increases in sputum CXCL8 as well as CCL2 and CCL4 levels precede a late exacerbation of acute asthmatic attack (94). Furthermore, in noninfectious status asthmaticus, neutrophil number and CXCL8 levels in BALF are markedly increased (97). Although the mechanism of CXCL8 production in asthma remains elusive, it is of interest that pulmonary epithelial cells can produce high levels of CXCL8 in the presence of diesel exhaust particles (151), which can contribute to the pathogenesis of asthma (138). Because CXCL8 inhalation has been shown to directly provoke bronchoconstriction in guinea pigs (57), it presumably contributes to the establishment of asthma at various stages directly and indirectly by inducing neutrophil infiltration and activation.Idiopathic pulmonary fibrosis and other diffuse lung diseases. Increased CXCL8 expression by alveolar macrophage is observed in idiopathic pulmonary fibrosis (IPF) (31). CXCL8 levels in both serum and BALF are increased significantly, and serum CXCL8 levels are indicative of the disease activity of IPF (30, 168). In mice, the administration with anti-mouse CXCL2 antibodies attenuates bleomycin-induced pulmonary fibrosis by reducing angiogenesis but not neutrophil infiltration (79). In contrast, CXCL10 also attenuates bleomycin-induced pulmonary fibrosis by inhibiting angiogenesis (78). Because the level of CXCL10 is decreased in IPF tissues (77), the imbalance between CXCL8 and CXCL10 may be responsible for the angiogenesis observed in IPF.
In chronic obstructive pulmonary diseases (COPD), both neutrophils and eosinophils are activated in the airway (16). Sputum CXCL8 levels correlated well with levels of neutrophil activation markers such as neutrophil myeloperoxidase and elastase (66, 163). Moreover, sputum CXCL8 levels were inversely correlated with forced expiratory volume. Because COPD is frequently associated with bacterial respiratory infections, invading bacteria may induce CXCL8 production and eventually neutrophil migration and activation. CXCL8 levels in BALF are increased markedly in diffuse panbronchiolitis (DPB), which is characterized by chronic inflammation of the respiratory bronchioles with leukocyte infiltration (88, 139). Macrolide antibiotics, such as erythromycin and clarithromycin, are effective for the treatment of DPB (139), and a regimen with these macrolide antibiotics is associated with inhibition of CXCL8 production at the transcriptional level (1), suggesting the involvement of CXCL8 in the pathogenesis of DPB. Moreover, microsatellite polymorphism of the human CXCL8 gene is reported to be associated with DPB (50). Thus aberrant CXCL8 production may predispose the patient to the development of DPB. Chloride concentrations in the airway surface fluid overlying respiratory epithelia are elevated in cystic fibrosis when compared with normals. Of interest is that elevated chloride concentration in vitro increased CXCL8 synthesis by neutrophils but decreased their capacity to kill P. aeruginosa (149). This may result in neutrophil-mediated damages to lungs and enhanced susceptibility to bacterial infection in cystic fibrosis.Cancer. The roles of leukocyte infiltration in cancer still remain unclear despite a long history of intensive investigation. There are at least two hypotheses to document the role of tumor-associated leukocytes. On one hand, tumor-associated leukocytes may reflect the host's ineffective attempt to reject the tumors. CXCL8 induces the accumulation of neutrophils, which can directly kill tumor cells (99). On the other hand, tumor-associated leukocytes, particularly macrophages, may be a potential source of growth factors for tumor cells and endothelial cells. Thus chemokines with chemotactic activities for monocytes/macrophages, particularly CCL2, are presumed to be involved in tumor progression by recruiting and activating macrophages to produce growth factors (157). In bronchoalveolar carcinoma, tumor cells are a main source of CXCL8, and neutrophils are located mainly in the alveolar lumen, whereas lymphocytes are exclusively in the alveolar wall. Moreover, the presence of increased numbers of neutrophils in BALF is correlated with CXCL8 levels in BALF and associated with poor outcome (17). Thus proangiogenic CXCL8 may promote tumor progression in bronchiolar carcinoma.
Endothelial cells exhibit chemotaxis in response to CXCL8 as well as other ELR+ CXC chemokines, such as CXCL1, CXCL2, CXCL5, CXCL6, and CXCL7 (87, 147, 148). Moreover, these chemokines are angiogenic in the rat corneal vascularization assay. CXCL8 expression is directly correlated with the degree of neovascularization in some tumor tissues, such as nonsmall cell lung cancer and gastric cancer tissues (84, 145). In contrast, ELR ![]() |
FUTURE PERSPECTIVES |
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In 1987, IL-8/CXCL8 was discovered as a neutrophil chemotactic factor (166). Subsequent studies have revealed that CXCL8 exerts a wide variety of actions on various types of cells, including neutrophils, monocytes, lymphocytes, endothelial cells, and fibroblasts. Studies of models of acute inflammation have established CXCL8 as a key mediator in neutrophil-mediated acute inflammation. However, the absence of CXCL8 and CXCR1 orthologs in mice and rats hinders the clarification on the pathophysiological roles of CXCL8 in other pathological conditions, particularly chronic inflammation and cancer. The elucidation of these issues will be made possible by further careful extrapolation of observations on these pathological conditions in mice and rats. This will undoubtedly lead to the development of novel therapeutics and/or preventive modalities by targeting CXCL8.
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ACKNOWLEDGEMENTS |
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We greatly appreciate Drs. Joost J. Oppenheim, Carole Galligan, and Ying Ying Le (National Cancer Institute-Frederick) for thoughtful comments on the manuscript.
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FOOTNOTES |
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This work is supported in part by grants from the Ministry of Education, Science, and Technology, and Osaka Cancer Research Foundation.
Address for reprint requests and other correspondence: N. Mukaida, Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa Univ., 13-1 Takara-machi, Kanazawa 920-0934, Japan (E-mail: naofumim{at}kenroku.kanazawa-u.ac.jp).
10.1152/ajplung.00233.2002
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