Human Galectin-3 Is a Novel Chemoattractant for Monocytes and Macrophages

Sano, Hideki; Hsu, Daniel K.; Yu, Liang; Apgar, John R.; Kuwabara, Ichiro; Yamanaka, Tohru; Hirashima, Mitsuomi; Liu, Fu‐Tong

doi:10.4049/jimmunol.165.4.2156

Cited by 468 publications

(393 citation statements)

References 67 publications

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“…Galectin-3 has been shown to directly attract human alveolar macrophages in vitro and recruit monocytes in vivo in a mouse air pouch model, as well as attract eosinophils by indirect mechanisms in this in vivo model. 28 However, galectin-3 does not appear to function as a monocyte/macrophage chemoattractant in the murine asthma model, because the amount of monocytes/macrophages in BAL fluid from OVA-challenged gal3 ϩ/ϩ and gal3 Ϫ/Ϫ mice was not significantly different. On the other hand, we have recently shown that galectin-3 plays a critical role in phagocytosis by macrophages through an intracellular mechanism, 49 suggesting that galectin-3 may influence the state of activation of resident airway cells that express galectin-3.…”

Section: Discussionmentioning

confidence: 98%

“…Various extracellular and intracellular activities of galectin-3 have been demonstrated in vitro. 23,24 Examples of extracellular activities are modulation of cell adhesion, [25][26][27] chemoattraction of monocytes/ macrophages (including alveolar macrophages) 28 as well as endothelial cells, 29 and angiogenesis. 29 Other examples include activation of various cell types, such as mast cells, 30 neutrophils, 31 monocytes/macrophages, 32 and lymphocytes, 33 through binding to cell surface glycoconjugates.…”

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confidence: 99%

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Critical Role for Galectin-3 in Airway Inflammation and Bronchial Hyperresponsiveness in a Murine Model of Asthma

Zuberi

Hsu

Kalaycı

et al. 2004

The American Journal of Pathology

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Galectin-3 is a member of a ␤-galactoside-binding animal lectin family. Previous in vitro studies have demonstrated that galectin-3 is involved in a number of activities; however, the roles of this lectin in physiological and pathological processes in vivo remain to be elucidated. Herein, we show, in a murine model of ovalbumin (OVA)-induced asthma that 1) peribronchial inflammatory cells expressed large amounts of galectin-3; 2) bronchoalveolar lavage fluid from OVAchallenged mice contained significantly higher levels of galectin-3 compared to control mice; and 3) macrophages in bronchoalveolar lavage fluid were the major cell type that contained galectin-3. We investigated the role of galectin-3 in the allergic airway response by comparing galectin-3-deficient (gal3 ؊/؊ ) mice and wild-type (gal3 ؉/؉ ) mice. OVA-sensitized gal3 ؊/؊ mice developed fewer eosinophils and lower goblet cell metaplasia, after airway OVA challenge compared to similarly treated gal3 ؉/؉ mice. In addition, the OVA-sensitized gal3 ؊/؊ mice developed significantly less airway hyperresponsiveness after airway OVA challenge compared to gal3 ؉/؉ mice. Finally, gal3 ؊/؊ mice developed a lower Th2 response, but a higher Th1 response, suggesting that galectin-3 regulates the Th1/Th2 response. We conclude that galectin-3 may play an important role in the pathogenesis of asthma and inhibitors of this lectin may prove useful for treatment of this disease.

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

Critical Role for Galectin-3 in Airway Inflammation and Bronchial Hyperresponsiveness in a Murine Model of Asthma

Zuberi

Hsu

Kalaycı

et al. 2004

The American Journal of Pathology

Self Cite

160

154

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“…Thioredoxin is a ubiquitous intracellular enzyme with antioxidant activity 41 . Both galectins [42][43][44] and thioredoxin 45,46 have been shown to stimulate various leukocytes and endothelium ex vivo and when injected in vivo to stimulate inflammation. To what extent these molecules actually contribute to the deathinduced inflammatory response, if at all, is unknown.…”

Section: Intracellular Damps With Proinflammatory Activitymentioning

confidence: 99%

How dying cells alert the immune system to danger

2008

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When a cell dies in vivo the event does not go unnoticed. The host has evolved mechanisms to detect the death of cells and rapidly investigate the nature of their demise. If cell death is a result of natural causes, that is, it is part of normal physiological processes, then there is little threat to the organism. In this situation, little else is done other than removing the corpse. However, if cells have died as the consequence of some violence or disease, then both defence and repair mechanisms are mobilized. The importance of this process to host defence and disease pathogenesis has only been appreciated relatively recently. This article will review our current knowledge of these processes.The immune system was recognized in ancient times and rediscovered by Jenner and Pasteur based on its ability to confer protection upon repeat exposure to a pathogen. Through subsequent studies by Von Behring and others it rapidly became apparent that the immune system had the potential to respond not only to whole microorganisms, but to virtually any molecule that was "foreign" to the host. However, whereas injection of such molecules would often provoke a robust immune response, this did not invariably occur. Immunization protocols improved in the 1920s with the discovery by Ramon and Glenny of immunostimulatory molecules (adjuvants [G]) that could boost immune responses to co-administered antigens. Adjuvants were typically of microbial origin and became widely used to promote the effectiveness of immunizations. In the 1960s, Dresser showed that a foreign protein when highly purified would only elicit an immune response if it was admixed with a microbial adjuvant 1 . Injected by itself, the antigen not only failed to elicit immunity but actually induced a state of tolerance 2 . However, the significance of these observations was not well appreciated and adjuvants remained one of those things that everyone used because they were part of standard operating procedures.In 1989 Janeway put these empirical observations into a conceptual framework 3 (Fig. 1). He proposed that the immune system did not respond to all foreign antigens but only to those that are potentially associated with infection. The underlying idea here was that the immune system evolved to protect organisms against microorganisms and this discrimination between infectious versus noninfectious antigens focused defences on real threats rather than innocuous situations.At this time, it was already recognized that in order to stimulate T cell responses, antigens had to first be acquired and presented on MHC molecules of an antigen presenting cell (APC). Moreover, it was further known that APCs also provided additional costimulatory signals necessary to activate T cells. Janeway incorporated these principles into his model (Fig. 1). He postulated that the discrimination between infectious and noninfectious non-self molecules was made by the APCs of the innate immune system through receptors that would recognize pathogen-associated molecular patterns (PAMP...

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“…This disease process, known as atherothrombosis, can lead to ACS or stroke [17][18][19]. The influence of Gal-3 on both atherosclerotic plaque formation and destabilization has been confirmed in several studies [20][21][22].…”

Section: Galectin-3 and Atherosclerosismentioning

confidence: 99%