Global longitudinal strain as a biomarker in diabetic cardiomyopathy. A comparative study with Gal-3 in patients with preserved ejection fraction / Deformación longitudinal global como un biomarcador en miocardiopatía diabética. Estudio comparativo con galectina-3 en pacientes con fracción de eyección preservada

Abstract: Objectives: To establish a relationship between global longitudinal strain (GLS) and Galectin-3 in pre-clinical heart failure in diabetic patients. Galectin-3 is a biomarker in heart failure with depressed ejection fraction (HFdEF). The hypothesis is presented that Galectin-3 is related to GLS and can detect left ventricular dysfunction in heart failure with preserved ejection fraction. Methods: Galectin-3 and GLS were measured in 121 asymptomatic individuals: 14 diabetics with mild depressed ejection fraction (mdEF) (LVEF 47.0 ± 6.9); 76 diabetics with preserved ejection fraction (LVEF 61 ± 5.5), and 31 controls (61.7 ± 5.1). Results: Galectin-3 was elevated in all diabetics vs controls (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = .003). It was also elevated in mdEF (3.76 ± 1.12 ng/ml vs 2.78 ± 0.9 ng/ml; p = .009) and pEF subjects (3.41 ± 1.40 ng/ml vs 2.78 ± 0.9 ng/ml; p = .058), respectively, vs controls. No difference in Gal-3 was found between diabetic groups (p = .603). Diabetics had lower GLS than controls (-18.5 ± 3.9 vs -20 ± 2.6; p = .022). Diabetics with mdEF had lower GLS than those with pEF (-13.3 ± 3.41 vs -19 ± 3.2; P<.001). There was no difference in GLS with pEF compared to controls (-19.4 ± 3.2 vs -20 ± 2.6; p = .70). Conclusions: Galectin-3 is elevated in diabetic patients with mdEF, and is associated with a diminished GLS. GLS could be an early marker of left ventricular dysfunction as well as evidence of diabetic cardiomyopathy.

Resumen: Objetivos: Establecer una asociación entre deformación longitudinal global (DLG) y galectina-3 en insuficiencia cardiaca preclínica en pacientes diabéticos. Galectina-3 es un biomarcador en insuficiencia cardiaca con fracción de eyección deprimida. Nuestra hipótesis es que la DLG y galectina-3 correlacionan y pueden detectar disfunción ventricular en insuficiencia cardiaca con FEVI preservada. Métodos: Se midieron galectina-3 y DLG en 121 individuos asintomáticos: 14 diabéticos con FEVI deprimida leve (FEdl) (FEVI 47 ± 6.9); 76 diabéticos con FEVI preservada (FEp) (FEVI 61 ± 5.5) y 31 sujetos controles (FEVI 61.7 ± 5.1). Resultados: Galectina-3 se encontró elevada en todos los diabéticos vs controles (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = 0.003). Está elevada en sujetos con FEdl (3.76 ± 1.12 vs 2.78 ± 0.9 vs ng/ml p = 0.009) y FEp (3.41 ± 1.40 vs 2.78 ± 0.9 ng/ml p = 0.058), respectivamente vs controles; no encontramos diferencia en galectina-3 en ambos grupos de diabéticos (p = 0.603). Los diabéticos tienen menor DLG que los controles (-18.5 ± 3.9 vs -20 ± 2.6; p = 0.022). Los diabéticos con FEdl tienen DLG más disminuida que aquellos con FEp (-13.3 ± 3.41 vs -19 ± 3.2; p < 0.001). No existe diferencia en DLG con FEp y controles (-19.4 ± 3.2 vs -20 ± 2.6; p = 0.70). Conclusiones: Galectina-3 está elevada en diabéticos con FEdl y correlaciona DLG disminuida. DLG podría ser un marcador temprano de disfunción ventricular y evidencia en miocardiopatía diabética.

Changes in the Immuno-Expression of Galectins -1, -3 and -7 in Relation to the Biological Behavior of Lip Squamous Cell Carcinoma

Objective: To evaluate the expression through immunohistochemistry of galectins -1, - 3 and -7 in cases of lip squamous cell carcinoma (SCC) in association with clinical data and morphological parameters proposed by Bryne (1998). Material and Methods: Thirty paraffin-embedded SCC cases were submitted to histological sections. Two independent pathologists performed the analysis of galectins -1, -3 and -7 through light microscopy evaluating the presence or absence of marking and intensity. The expressions of these proteins were submitted to statistical analysis (chi-square test, Fisher's exact test and Binomial test for the comparison of proportions). Results: Positive expression of galectins -1 and -3 was observed in 93.3% and 43.3% of cases, respectively. However, there was no statistically significant association between these proteins and the clinical variables used. Galectin-7 immuno-expression was present in all cases evaluated and showed statistical significance between marked cell type (parenchyma cells) and regional metastasis and between marked cell type (parenchyma cells) and histological gradation. Conclusion: Changes in the galectins -1, -3 and -7 expression suggest the participation of these proteins in the regulation of cellular functions and that the immuno-expression of these proteins can act as a marker of the biological behavior of lip squamous cell carcinoma.

Galectin-8 promotes migration and proliferation and prevents apoptosis in U87 glioblastoma cells

BACKGROUND: Glioblastoma is one of the most aggressive cancers of the brain. Malignant traits of glioblastoma cells include elevated migration, proliferation and survival capabilities. Galectins are unconventionally secreted glycan-binding proteins that modulate processes of cell adhesion, migration, proliferation and apoptosis by interacting with beta-galactosides of cell surface glycoproteins and the extracellular matrix. Galectin-8 is one of the galectins highly expressed in glioblastoma cells. It has a unique selectivity for terminally sialylated glycans recently found enhanced in these highly malignant cells. A previous study in glioblastoma cell lines reported that Gal-8 coating a plastic surface stimulates two-dimensional motility. Because in other cells Gal-8 arrests proliferation and induces apoptosis, here we extend its study by analyzing all of these processes in a U87 glioblastoma cell mode.l METHODS: We used immunoblot and RT-PCR for Gal-8 expression analysis, recombinant Gal-8 produced in a bacteria system for Gal-8 treatment of the cells, and shRNA in lentivirus transduction for Gal-8 silencing. Cell migration as assessed in transwell filters. Cell proliferation, cell cycle and apoptosis were analyzed by FACS. RESULTS: Gal-8 as a soluble stimulus triggered chemotactic migration of U87 cells across the polycarbonate filter of transwell chambers, almost as intensively as fetal bovine serum. Unexpectedly, Gal-8 also enhanced U87 cell growth. Co-incubation of Gal-8 with lactose, which blocks galectin-glycan interactions, abrogated both effects. Immunoblot showed Gal-8 in conditioned media reflecting its secretion. U87 cells transduced with silencing shRNA in a lentiviral vector expressed and secreted 30-40 % of their normal Gal-8 levels. These cells maintained their migratory capabilities, but decreased their proliferation rate and underwent higher levels of apoptosis, as revealed by flow cytometry analysis of cell cycle, CFSE and activated caspase-3 staining. Proliferation seemed to be more sensitive than migration to Gal-8 expression levels. CONCLUSIONS: Gal-8, either secreted or exogenously enriched in the media, and acting through extracellular glycan interactions, constitutes a strong stimulus of directional migration in glioblastoma U87 cells and for the first time emerges as a factor that promotes proliferation and prevents apoptosis in cancerous cells. These properties could potentially contribute to the exaggerated malignancy of glioblastoma cells.

Assessment of Galectin-3 Polymorphism in Subjects with Chronic Chagas Disease / Avaliação do Polimorfismo da Galectina-3 em Indivíduos com Doença de Chagas Crônica

AbstractBackground:Galectin-3, a β-galactoside binding lectin, has been described as a mediator of cardiac fibrosis in experimental studies and as a risk factor associated with cardiovascular events in subjects with heart failure. Previous studies have evaluated the genetic susceptibility to Chagas disease in humans, including the polymorphisms of cytokine genes, demonstrating correlations between the genetic polymorphism and cardiomyopathy development in the chronic phase. However, the relationship between the galectin-3 single nucleotide polymorphism (SNP) and phenotypic variations in Chagas disease has not been evaluated.Objective:The present study aimed to determine whether genetic polymorphisms of galectin-3 may predispose to the development of cardiac forms of Chagas disease.Methods:Fifty-five subjects with Chagas disease were enrolled in this observational study. Real-time polymerase chain reaction (PCR) was used for genotyping the variants rs4644 and rs4652 of the galectin-3 gene.Results:For the SNP rs4644, the relative risk for the cardiac form was not associated with the genotypes AA (OR = 0.79, p = 0.759), AC (OR = 4.38, p = 0.058), or CC (OR = 0.39, p = 0.127). Similarly, for the SNP rs4652, no association was found between the genotypes AA (OR = 0.64, p = 0.571), AC (OR = 2.85, p = 0.105), or CC (OR = 0.49, p = 0.227) and the cardiac form of the disease.Conclusion:Our results showed no association between the different genotypes for both SNPs of the galectin-3 gene and the cardiac form of Chagas disease. (Arq Bras Cardiol. 2015; [online].ahead print, PP.0-0).

ResumoFundamento:A galectina-3, uma lectina de ligação à β-galactosidase, foi descrita como um mediador de fibrose cardíaca em estudos experimentais e um fator de risco associado com eventos cardiovasculares em indivíduos com insuficiência cardíaca. Estudos prévios avaliaram a susceptibilidade genética para doença de Chagas em humanos, incluindo polimorfismos dos genes de citocinas, demonstrando correlações entre o polimorfismo genético e o desenvolvimento de cardiomiopatia na fase crônica. No entanto, a relação entre polimorfismos de nucleotídeo único (single nucleotide polymorphism, SNP) e variações fenotípicas na doença de Chagas ainda não foi avaliada.Objetivo:O presente estudo teve como objetivo determinar se os polimorfismos genéticos da galectina-3 podem predispor ao desenvolvimento de formas cardíacas da doença de Chagas.Métodos:Cinquenta e cinco indivíduos com doença de Chagas foram incluídos neste estudo observacional. A genotipagem das variantes rs4644 e rs4652 do gene da galectina-3 foi realizada por PCR (reação em cadeia de polimerase).Resultados:Para o SNP rs4644, não houve associação entre o risco relativo para a forma cardíaca e os genótipos AA (OR = 0,79, p = 0,759), AC (OR = 4,38, p = 0,058), ou CC (OR = 0,39, p = 0,127). Similarmente, para o SNP rs4652, não foi encontrada associação entre os genótipos AA (OR = 0,64, p = 0,571), AC (OR = 2,85, p = 0,105), ou CC (OR = 0,49, p = 0,227) e a forma cardíaca da doença.Conclusão:Nossos resultados não mostraram associação entre os diferentes genótipos para ambos SNPs do gene da galectina-3 e a forma cardíaca da doença de Chagas. (Arq Bras Cardiol. 2015; [online].ahead print, PP.0-0).

Galectins and collectinis expression are increased in Haemonchus contortus-infected corriedale sheep / Aumento da expressão gênica de colectinas e galectinas em ovinos corriedale infectados por Haemonchus contortus

Galectins and collectins are proteins classified in the lectin family that have the ability to recognize molecular patterns associated with pathogens. Studies on cattle have demonstrated high expression of these proteins during infection with gastrointestinal nematodes. The aim of this study was to investigate whether the level of Haemonchus contortus infection would alter the expression of galectins (Gal11 and Gal14) and collectins (SPA and CGN) in sheep. Twelve Corriedale sheep exposed to natural infection with nematodes were divided into two groups: group 1 (G1, n = 7) and group 2 (G2, n = 5), with low and high parasite burdens, respectively, based on fecal egg counts and abomasal parasite counts. The fecal egg counts and abomasal parasite counts were significantly different (p < 0.05) between the groups. Galectin and collectin gene expression was observed in all sheep abomasal samples. However, animals with lower infection levels showed lower expression of the genes Gal14, SPA and CGN (p < 0.05). Expression of lectins was associated with the abomasal H. contortus burden, thus suggesting that these proteins may have a role in controlling of this infection.

Colectinas e galectinas são proteínas da família das lectinas que possuem a capacidade de reconhecer padrões moleculares associados aos patógenos. Estudos em bovinos têm demonstrado a alta expressão dessas proteínas durante a infecção por nematoides gastrintestinais. O objetivo deste estudo foi investigar se o nível de infecção de Haemonchus contortus altera a expressão de colectinas (SPA e CGN) e galectinas (Gal11 e Gal14) de ovinos. Doze ovinos da raça Corriedale expostos a infecção natural com nematoides foram separados em dois grupos: grupo 1 (G1, n=7) com menor grau de parasitismo; e grupo 2 (G2, n=5) com maior grau, a partir da contagem do número de parasitos recuperados do abomaso e OPG. A contagem de OPG e de parasitos recuperados do abomaso dos grupos G1 e G2 apresentaram diferença estatística (p<0,05). A expressão dos genes de colectinas e galectina foi observada em todas as amostras de abomaso dos ovinos, porém animais com menor grau de infecção apresentaram menor expressão dos genes de Gal14, SPA e CGN (p<0,05). A expressão de lectinas foi associada ao número de H. contortus encontrados no abomaso de ovinos, indicando um possível papel dessas proteínas no controle da infecção.

Envolvimento das galectinas na angiogênese tumoral em modelo de melanoma murino e associação com o microambiente tumoral via receptores toll-like / Involvement of galectins in tumor angiogenesis in a murine melanoma model and association with tumor microenvironment through toll-like receptors

O melanoma é a forma mais letal entre os cânceres de pele. Essa neoplasia freqüentemente apresenta-se resistente a abordagens terapêuticas. A angiogênese associada ao tumor representa um crítico passo da tumorigênese, resultado da ação de diferentes citocinas e fatores de crescimento como VEGF produzidos no microambiente tumoral. As galectinas extracelulares participam de múltiplos processos biológicos incluindo angiogênese tumoral e metástases, sua interação com as células presentes no microambiente tumoral pode ocorrer via receptores toll-like sugerindo seu envolvimento nos processos pro-inflamatórios e na secreção de citocinas. Recentemente mostramos que a ausência de gal-3 no estroma e parênquima tumoral diminui a angiogênese por interferir na resposta de macrófagos via VEGF e/ou TGFbeta1. Entretanto, o envolvimento de galectinas extracelulares na angiogênese e na modulação do sistema imune no microambiente tumoral ainda não está esclarecido. Assim, este estudo visa buscar respostas ao envolvimento das galectinas no crescimento tumoral e angiogênese contribuindo ao combate do melanoma maligno. Nossos resultados mostram a participação das galectinas 1 e 3 no crescimento tumoral e seu envolvimento com macrófagos via receptores toll-like, além de coordenarem a modulação do perfil de polarização de macrófagos derivados da medula óssea de camundongos wild-type. Dessa forma, podemos inferir que essas galectinas agem como coordenadoras de mudança de perfil dos macrófagos, uma vez que inibidas extracelularmente promovem uma diminuição do crescimento tumoral em camundongos wild-type, inoculados com células de melanoma murino e uma manutenção do perfil de macrófagos M1 in vitro. Assim, concluimos que as galectinas 1 e 3 extracelulares são importantes para o crescimento tumoral de melanomas murinos pois promovem o crescimento tumoral e são coordenadoras da mudança do perfil de macrófagos.

Melanoma is the most aggressive form of skin cancer. This tumor often presents itself resistant to therapeutic approaches. The tumor-associated angiogenesis is a critical step in tumorigenesis and the result of the action of several cytokines and growth factors such as VEGF produced in the tumor microenvironment. The extracellular galectins participate in multiple biological processes including tumor angiogenesis and metastasis, their interaction with cells present in the tumor microenvironment may occur via toll-like receptors suggesting their involvement in pro-inflammatory processes and the secretion of cytokines. We have recently shown that the absence of Gal-3 the stroma and tumor parenchyma decreases angiogenesis by interfering with the macrophage response by VEGF and / or TGFbeta1. However, the involvement of extracellular galectins on angiogenesis modulation of the immune system in the tumor microenvironment is not yet clear. This study aims is to find answers to the involvement of galectins on tumor growth and angiogenesis contributing to the study of the malignant melanoma. Our results demonstrate the involvement of galectin 1 and 3 on tumor growth and its involvement in macrophage by toll-like receptors pathway, and coordinating the modulation of the polarization profile in wild-type mice bone marrow derived macrophages. Therefore, we show these galectins act as coordinators of macrophages profile change, since inhibited extracellularly promote a reduction in tumor growth in wild-type mice inoculated with murine melanoma cells and macrophages M1 maintenance of profile in vitro. Thus, we conclude that galectins 1 and 3 extracellular are important for tumor growth of murine melanomas because they promote tumor growth and are coordinators of change macrophages profile.

Galectin-8 binds to LFA-1, blocks its interaction with ICAM-1 and is counteracted by anti-Gal-8 autoantibodies isolated from lupus patients

Galectin-8 belongs to a family of mammalian lectins that recognize glycoconjugates present on different cell surface components and modulate a variety of cellular processes. A role of Gal-8 in the immune system has been proposed based on its effects in immune cells, including T and B lymphocytes, as well as the presence of anti-Gal-8 autoantibodies in the prototypic autoimmune disease systemic lupus erythematosus (SLE). We have previously described that Gal-8 induces apoptosis in activated T cells interacting with certain β1 integrins and this effect is counteracted by the anti-Gal-8 autoantibodies. Given that Gal-8 can potentially interact with several glycoproteins, here we analyzed the β2 integrin Lymphocyte Function-Associated Antigen-1 (LFA-1), which is involved in leukocyte cell adhesion and immunological synapses. We show by GST-pull down assays that Gal-8 interacts with LFA-1 and this interaction is inhibited by anti-Gal-8 autoantibodies isolated from SLE patients. In cell adhesion assays, Gal-8 precluded the interaction of LFA-1 with its ligand Intracellular Adhesion Molecule-1 (ICAM-1). These results suggest that Gal-8 can exert immunosuppressive action not only by inducing apoptosis in activated T cells but also by negatively modulating the crucial function of LFA-1 in the immune system, while function-blocking autoantibodies counteract these effects.

Avaliação imuno-histoquímica das galectinas 1, 3, 4 e 7 e, carcinoma epidermóide de língua / Imuno-histoquímica evaluation of galectinas 1, 3, 4 and 7 in carcinoma epidermóide of language

Diversos estudos são desenvolvidos com o intuíto de se estabelecer parâmetros para determinar o comportamento biológico do carcinoma epidermóide oral, tendo em vista que esta neoplasia apresenta altas taxas de morbidade e mortalidade. O objetivo do presente trabalho foi realizar uma análise clínica, morfológica e imuno-histoquímica através da expressão das galectinas 1, 2, 3 e 7 em 65 casos de carcinoma epidermóide de língua, correlacionando essa expressão à parâmetros clínicos (desfecho da doença, metástase, estadiamento clínico) e morfológicos analisados e a expressão das galectinas 1, 3, 4 e 7 foram submetidos a análise estatística (teste do Qui), observando-se que os mesmos podem ser utilizados como indicadores do comportamento biológico do carcinoma epidermóide de língua. A galectina 1 foi expressa em 87,7 por cento dos casos, apresentando correlação estatisticamente significativa com a metástase (p=0,033) e o estadiamento clínico (p=0,016), localizando-se principalmente no citoplasma das células estromais. A imunomarcação da galectina 3, em 87,7 por cento dos casos, correlacionou-se com a...

Autoanticuerpos anti-galectina-8 en pacientes con lupus eritematoso sistémico / Antibodies against galectin-8 in patients with systemic lupus erythematosus

Background: The family of lectins known as galectins (galectins 1-14) are involved in the regulation of the immune system and in oncogenesis. During a search for antigens recognized by antibodies produced by a patient with systemic lupus erythematosus (SLE) we found reactivity against galectin-8, for which autoantibodies have not been previously described. Aim: To determine the frequency of autoantibodies against galectin-8 in lupus patients compared with healthy controls. Patients and Methods: Galectin-8 was purified from a bacterial expression system and used in immunoblot assays as antigen to screen the sera of 55 SLE patients and matched controls. Disease activity was evaluated using the Mexican Modification of the Systemic Lupus Erythematosus Disease Activity Index (MEX-SLEDAI). Results: Reactivity against galectin-8 was detected in 30% of SLE patients, compared to 7% of controls (p=0.003). We could not detect any particular SLE manifestation associated to the presence of these autoantibodies. Conclusions: This is the first description of autoantibodies against galectin-8. Its higher frequency in patients with SLE suggests a pathogenic role. Further studies are needed to determine their clinical relevance.

Interacción entre proteínas y glicanos en la regulación fisiológica de las células T / How do protein-glycan interactions regulate T-cell physiology?

Recent evidence indicates that protein-glycan interactions play a critical role in different events associated with the physiology of T-cell responses including thymocyte maturation, T-cell activation, lymphocyte migration and T-cell apoptosis. Glycans decorating T-cell surface glycoproteins can modulate T-cell physiology by specifically interacting with endogenous lectins including selectins and galectins. These endogenous lectins are capable of recognizing sugar structures localized on T-cell surface glycoproteins and trigger different signal transduction pathways leading to differentiation, proliferation, cell cycle regulation or apoptosis. Protein-carbohydrate interactions may be controlled at different levels, including regulated expression of lectins during T-cell maturation and differentiation and the spatio-temporal regulation of glycosyltransferases and glycosidases, which create and modify sugar structures present in T-cell surface glycoproteins. This article briefly reviews the mechanisms by which protein-carbohydrate interactions modulate immunological processes such as T-cell activation, migration and apoptosis.

Las interacciones entre proteínas y glicanos juegan un papel fundamental en numerosos eventos de la regulación de la fisiología del sistema inmune, como maduración tímica, activación, migración y apoptosis de células T. Los carbohidratos son capaces de modular la fisiología linfocitaria a través de la interacción específica con lectinas endógenas como selectinas y galectinas. Estas lectinas endógenas son capaces de reconocer estructuras sacarídicas localizadas en glicoproteínas de la superficie celular y regular procesos tan diversos como proliferación, diferenciación y ciclo celular. Existen diversos niveles de control de la interacción entre lectinas y azúcares; en primer lugar podemos mencionar la expresión regulada de estas lectinas durante el desarrollo de una respuesta inmune, y en segundo lugar la regulación espacio-temporal de la actividad de glicosiltranferasas y glicosidasas cuya función es crear y modificar los azúcares específicos para estas lectinas. Existen evidencias de que la expresión y actividad de estas enzimas se regulan en forma positiva o negativa durante diferentes eventos del desarrollo, ejecución y finalización de la respuesta inmune. En este artículo se analizarán los mecanismos a través de los cuales las interacciones entre lectinas con sus carbohidratos específicos modulan en forma específica diversos procesos fisiológicos, como maduración de timocitos, migración linfocitaria, activación y diferenciación de células T y apoptosis.

Expressão das proteínas galectinas-1, -3 e anexina 1 em células inflamatórias: estudo em modelos in vivo e in vitro de inflamação aguda / Expression of galectin-1, -3 and annexin 1 in imflammatory cells: a study of in vivo and in vitro modesls of acute inflammation

Objetivos: Investigar o efeito do tratamento farmacológico das proteínas (Gal-1) e -3 (Gal-3) no recrutamento dos leucócitos durante a reação i aguda, e a expressão das galectinas e da anexina 1 (ANXA1) nas células inflamatórias utilizando uma combinação de modelos experimentais in vivo e in vitro. Métodos: No estudo in vivo, ratos Sprague-Dawley foram tratados pela injeção intravenos ou Gal-3 (3 μg/kg), seguida da aplicação de carragenina (1,5 mg/kg) e da lavados peritoniais, para as análises quantitativa e de Western blotting. Para indução da peritonite experimental, os animais receberam injeção intraperitonial de carragenina e foram sacrificados após 0, 4, 24 e 48 horas. No modelo in vitro, os neutrófilos humanos de voluntários sadios e as células endoteliais da linhagem Ea.hy926 foram utilizados no ensaio de transmigração induzido pela IL-8. Na análise imunocitoquímica, fragmentos do mesentério e amostras de sangue dos ratos, obtidos após peritonite experimental, foram processados e a expressão das Gal-1 e -3, monitoradas pelos anticorpos policlonais de coelho anti-Gal-1 e -3. Nos neutrófilos humanos e nas células endoteliais, a expressão da ANXA1 foi investigada pelos anticorpos policlonais de cabra anti-ANXA1 LCS3 (reconhecedor das isoformas intacta e clivada da proteína ANXA1) e LCPS1 (específico para a região N-terminal da proteína intacta),bem como pela anti-Gal-1 e -3. Resultados: No modelo in vivo de inflamação, após 4 horas da resposta inflamatória, observamos no mesentério mastócitos desgranulados e intensa migração leucocitária e, ao término de 24 e 48 horas, aumento do número de macrófagos. O tratamento dos animais com a Gal-1 diminuiu (~50 por cento) o recrutamento dos leucócitos para a cavidade peritonial após 4 horas, enquanto o tratamento com o anticorpo rabbit anti-Gal-1, depois de 48 horas, aumentou o número de leucócitos na cavidade. Neste mesmo período, a expressão da Gal-3 foi detectada no lavado peritonial pela análise de Western blotting. A análise imunocitoquímica demonstrou que, na fase inicial da inflamação do mesentério, a expressão das proteínas Gal-3 e -1 diminuiu nos mastócitos e neutrófilos transmigrados, respectivamente, ao passo que nas fases tardias, uma alta imunorreatividade da Gal-3 foi observada nos mastócitos e macrófagos e da Gal-1 nos neutrófilos transmigrados e também nos macrófagos. No modelo in vitro de transmigração celular, a interação neutrófilo-endotélio produziu um aumento da ANXA1 clivada em todos os compartimentos intracelulares dos neutrófilos aderidos, principalmente na membrana plasmática, detectada pela quantificação da imunorreatividade dos anticorpos LCS3 e LCPS1. Nestas células, observamos ainda um aumento na expressão da Gal-3, enquanto a imunorreatividade da Gal-1 diminuiu (~50 por cento) nos neutrófilos transmigrados em relação às células que não migraram. As células endoteliais, após a transmigração dos neutrófilods, apresentaram altos níveis na membrana plasmática das proteínas ANXA1(detectada pelo anticorpo LCS3) e Gal-3. Conclusões: As alterações nas concentrações e localizações das proteínas investigadas nas células inflamatórias, tanto no modelo in vivo como in vitro, sugerem um mecanismo de equilíbrio intracelular dos seus papéis pró(Gal-3) e antiinflamatório (Gal-1 e ANXA1) para a homeostase da resposta inflamatória aguda.