LINC01119 encapsulated by cancer-associated adipocytes-derived exosomes promotes M2 polarization of macrophages to induce immune escape in ovarian cancer in a 3D co-culture cell-based model

Introduction In the present study, we sought to clarify the role of LINC01119 delivered by cancer-associated adipocytes (CAAs)-derived exosomes (CAA-Exo) and its mechanistic actions in ovarian cancer (OC). Materials and methods The expression of LINC01119 was determined in OC, and the relationship between LINC01119 expression and the prognosis of OC patients was analyzed. Besides, 3D co-culture cell models were constructed using green fluorescent protein-labeled OC cells and red fluorescent protein-labeled mature adipocytes. Mature adipocytes were co-cultured with OC cells to induce CAA. Macrophages treated with CAA-Exo were co-cultured with SKOV3 cells following ectopic expression and depletion experiments of LINC01119 and SOCS5 to detect M2 polarization of macrophages, PD-L1 level, proliferation of CD3+ T cells, and cytotoxicity of T cells to SKOV3 cells. Results LINC01119 was elevated in the plasma Exo of OC patients, which was related to shorter overall survival in OC patients. LINC01119 expression was increased in CAA-Exo, which could upregulate SOCS5 in OC. Finally, CAA-Exo carrying LINC01119 induced M2 polarization of macrophages to promote immune escape in OC, as evidenced by inhibited CD3+ T cell proliferation, increased PD-L1 level, and attenuated T cell toxicity to SKOV3 cells. Conclusion In conclusion, the key findings of the current study demonstrated the promoting effects of CAA-Exo containing LINC01119 mediating SOCS5 on M2 polarization of macrophages and immune escape in OC (AU)

Induction of killing of Mycobacterium avium subsp. hominissuis in macrophages by cytokine stimulated innate-like lymphoid cells is negatively affected by the pathogen / Inducción de la destrucción de Mycobacterium avium subsp. hominissuis en macrófagos por células linfoides de tipo innato estimuladas por citoquinas se ve afectado negativamente por el patógeno

Mycobacterium avium subsp. hominissuis (MAH) is a common environmental bacterium that causes infection in immunocompromised patients such as those with HIV/AIDS, or patients with chronic lung disease such as cystic fibrosis. There are many strains of MAH with varying levels of virulence. Infection with MAH strains 100 and 104 has been associated with different immune responses in mice and outcome of the disease. While MAH 100 infection tends to be cleared from mice, MAH 104 is virulent and grows in host tissue. What is currently unknown are the mechanisms related to this difference in host defense and virulence. Our hypothesis is that differences in circulating innate lymphocytes response are associated with increased protection from infection. Innate lymphoid cells (ILC) are lymphoid cells with an important role in regulation of innate immune systems. ILCs can be categorized into three subpopulations ILC1, ILC2, and ILC3 based on their cytokine production and regulatory transcription factors. Investigation was carried out on how macrophage anti-MAH response change depending on activation by primary mouse lymphocytes activated with IL-12, IL-33, and IL-23, triggering differentiation into ILC-like subpopulations. Our results do not affirm the role of any one ILC subpopulation in macrophage anti-M. avium ability. Our findings instead support the conclusion that MAH infection of macrophages suppresses the stimulatory function of ILCs.(AU)

Study of hydrogen sulfide biosynthesis in synovial tissue from diabetes-associated osteoarthritis and its influence on macrophage phenotype and abundance

Type 2 diabetes (DB) is an independent risk factor for osteoarthritis (OA). However, the mechanisms underlying the connection between both diseases remain unclear. Synovial macrophages from OA patients with DB present a marked pro-inflammatory phenotype. Since hydrogen sulphide (H2S) has been previously described to be involved in macrophage polarization, in this study we examined H2S biosynthesis in synovial tissue from OA patients with DB, observing a reduction of H2S-synthetizing enzymes in this subset of individuals. To elucidate these findings, we detected that differentiated TPH-1 cells to macrophages exposed to high levels of glucose presented a lower expression of H2S-synthetizing enzymes and an increased inflammatory response to LPS, showing upregulated expression of markers associated with M1 phenotype (i.e., CD11c, CD86, iNOS, and IL-6) and reduced levels of those related to M2 fate (CD206 and CD163). The co-treatment of the cells with a slow-releasing H2S donor, GYY-4137, attenuated the expression of M1 markers, but failed to modulate the levels of M2 indicators. GYY-4137 also reduced HIF-1α expression and upregulated the protein levels of HO-1, suggesting their involvement in the anti-inflammatory effects of H2S induction. In addition, we observed that intraarticular administration of H2S donor attenuated synovial abundance of CD68+ cells, mainly macrophages, in an in vivo model of OA. Taken together, the findings of this study seem to reinforce the key role of H2S in the M1-like polarization of synovial macrophages associated to OA and specifically its metabolic phenotype, opening new therapeutic perspectives in the management of this pathology. (AU)

Extracellular vesicular lncRNA FAL1 promotes hepatocellular carcinoma cell proliferation and invasion by inducing macrophage M2 polarization

Current evidence finds that circulating exosomal lncRNA focally amplified lncRNA on chromosome 1 (FAL1) promotes the progression of hepatocellular carcinoma (HCC). However, the underlying mechanism of serum extracellular vesicular FAL1 in HCC progression remains elusive. Here, we extracted extracellular vesicles (EVs) from serum samples of HCC patients and healthy volunteers, and found that FAL1 was highly enriched in the serum EVs of HCC patients. Then, macrophages were treated with EVs alone or together with small interfering RNA against FAL1 (si-FAL1). The data indicated that FAL1-enriched EVs induced macrophage M2 polarization, while silencing FAL1 in macrophages antagonized the role of EVs. Moreover, HepG2 cells were co-cultured with the conditioned macrophages, and co-culturing with EVs-incubated macrophages promoted HepG2 cell proliferation, invasion, cell cycle progression, and colony formation, and inhibited cell apoptosis and sorafenib sensitivity, while interfering FAL1 in macrophages reversed these effects. Consistently, ectopic expression of FAL1 in macrophages also induced macrophage M2 polarization, and co-culture of FAL1-overexpressing macrophages with HepG2 cells facilitated the malignant progression of HepG2 cells. Furthermore, co-culturing HepG2 cells with EVs-incubated macrophages activated the Wnt/β-catenin signaling pathway, and treatment with a Wnt/β-catenin pathway inhibitor IWP-2 partially neutralized the effect of EVs-incubated macrophages on HepG2 cell malignant behaviors. Additionally, FAL1 enriched EVs-incubated macrophages markedly increased mouse xenograft tumor growth. In conclusion, extracellular vesicular lncRNA FAL1 promotes macrophage M2 polarization and further activates the Wnt/β-catenin signaling pathway in HCC cells, thus promoting HCC progression. (AU)

HSF1 expression in tumor-associated macrophages promotes tumor cell proliferation and indicates poor prognosis in esophageal squamous cell carcinoma

Purpose Tumor-associated macrophages (TAMs), are crucial for the survival and development of tumor cells. Heat shock factor 1 (HSF1) is a potent, complex carcinogenesis modulator, and esophageal cancer (EC) patients have a bad prognosis when HSF1 is highly expressed. HSF1's clinical importance and biological role in TAMs are still unknown. Methods The HSF1 expression profile and patient survival information were analyzed from the TCGA database. The infiltration of different types of immune cells in EC was evaluated based on HSF1 gene expression by Sangerbox 3.0. Immunochemistry was employed to assess HSF1 protein expression in 134 individuals with esophageal squamous cell carcinoma (ESCC), proceeded by association with clinicopathological variables. The role of macrophage-driven HSF1 were observed using HSF1-knockdown THP1 cells. Results High level of HSF1 have a poorer prognosis in individuals with EC. The expressing level of HSF1 was positively related to infiltration of M2 macrophages (P < 0.05). The expression of HSF1 in macrophages was an independent factor for DFS (P = 0.002) and OS (P = 0.002) in ESCC cases. HSF1 was up-regulated in IL-4 stimulation THP1 cells in a time-dependent manner. Under the heat stimulation condition, THP1-derived macrophages were more sensitive than tumor cells. Compared to IL-4 induced-THP1 cells control, the HSF1 knockdown in THP1 cell inhibited the growth and proliferation of ESCC cells. Conclusions The up-regulation of HSF1 was more rapid and could affect the proliferation of tumor cells in IL4-induced macrophages. The expression of HSF1 in TAMs can also serve as a marker for ESCC prognosis (AU)

The pleiotropic mode and molecular mechanism of macrophages in promoting tumor progression and metastasis

Macrophages are the most abundant immune cells in primary and metastatic tumor tissues. Studies have shown that macrophages mainly exhibit a tumor-promoting phenotype and play a key role in tumor progression and metastasis. Therefore, many macrophage-targeted drugs have entered clinical trials. However, compared to preclinical studies, some clinical trial results showed that macrophage-targeted therapy did not achieve the desired effect. This may be because most of what we know about macrophages comes from in vitro experiments and animal models, while macrophages in the more complex human microenvironment are still poorly understood. With the development of technologies such as single-cell RNA sequencing, we have gained a new understanding of the origin, classification and functional mechanism of tumor-associated macrophages. Therefore, this study reviewed the recent progress of macrophages in promoting tumor progression and metastasis, aiming to provide some help for the formulation of optimal strategies for macrophage-targeted therapy (AU)

FoxO4 mediates macrophage M2 polarization by promoting LXA4R expression in an ovalbumin-induced allergic asthma model in mice

Background: Asthma imposes a heavy burden due to its high prevalence. Forkhead box O4 (FoxO4) proteins participate in the modulation of cell progression. However, the role and mechanism of FoxO4 in asthma remains uncharted. Methods: An allergic asthma model was constructed by the induction of ovalbumin and interleukin (IL)-4 in mice and monocyte/macrophage-like Raw264.7 cells, respectively. The role and mechanism of FoxO4 in asthma was determined by pathological staining, immunofluorescence assay, measurement of inflammatory cells in the blood, reverse transcription quantitative polymerase chain reaction (RT-qPCR), Western blot analysis, and flow cytometry. Results: Ovalbumin treatment triggered an obvious inflammatory cell infiltration with a prominent increase in F4/80+ cell numbers. The relative messenger RNA (mRNA) and protein expressions of FoxO4 were increased in both ovalbumin-induced mice and interleukin-4 (IL-4)-induced Raw264.7 cells. Inhibition of FoxO4 via AS1842856 reduced inflammatory cell infiltration, the number of Periodic Acid Schiff+ (PAS+) goblet cells, the numbers of inflammatory cells in the blood, and the airway resistance in ovalbumin-induced mice. Besides, interference of FoxO4 decreased the number of F4/80+CD206+ cells, and the relative protein expressions of CD163 and Arg1 in vivo and in vitro. Mechanically, suppression of FoxO4 diminished the relative mRNA and protein expressions of LXA4R in both ovalbumin-induced mice and IL-4-induced Raw264.7 cells. Overexpression of LXA4R reversed the outcomes caused by repression of FoxO4, including airway resistance, the number of F4/80+ cells, the proportion of CD206+ cells in ovalbumin-induced mice, and the proportion of F4/80+CD206+ cells in IL-4-induced Raw264.7 cells. Conclusion: FoxO4/LXA4R axis mediated macrophage M2 polarization in allergic asthma (AU)

Cancer cell-derived exosomal LINC00313 induces M2 macrophage differentiation in non-small cell lung cancer

Purpose Non-small cell lung cancer (NSCLC) is the major subtype of lung cancer, which is the leading cause of cancer death worldwide. Tumor-associated macrophages (TAMs) are one of the main non-tumor cells in the tumor microenvironment. Here, we investigated the effect of cancer cell-derived exosomal LINC00313 on the M2 macrophage differentiation in NSCLC and clarified its underlying mechanism. Methods Flow cytometry, Western blotting, ELISA and immunohistochemical staining were performed to identify the macrophage phenotype by detecting the expression of M2 markers. The expression levels of LINC00313 and miR-135a-3p were measured by qRT-PCR, and luciferase reporter assay was used to validate the binding of lncRNA to miRNA, and miRNA to the target gene STAT6. The mouse-xenograft models were established by subcutaneous injection of the NCl-H1299 cells with stable overexpression or knockdown of LINC00313. GW4869 was injected intra-tumorally after tumor implantation. Results It was found that the cancer cells promoted M2 macrophage differentiation by secreting exosomes. LINC00313 was overexpressed in H1299-derived exosomes, and its knockdown abolished the effect of H1299-induced M2 macrophage differentiation. LINC00313 sponged miR-135a-3p to increase the STAT6 expression, resulting in the M2 macrophage differentiation. LINC00313 promoted tumor progression and promoted the expression of M2 markers in isolated tumor macrophages. A novel regulatory mechanism of M2 macrophage differentiation in NSCLC was revealed. It was found that cancer cell-derived exosomal LINC00313 promoted M2 macrophage differentiation in NSCLC by up-regulating STAT6 as miR-135a-3p sponge. Conclusions This study provides a new mechanism and direction to prevent the M2 macrophage differentiation in NSCLC (AU)

Resveratrol enhanced chemosensitivity by reversing macrophage polarization in breast cancer

BackgroundResveratrol, a naturally occurring polyphenolic compound, has been shown to inhibit cancer growth by targeting several cancer-related signalling pathways. In the tumor microenvironment (TME), tumor-associated macrophages (TAMs) are the most abundant leukocyte population that are associated with poor prognosis in over 80% of breast cancer cases. However, little is known about the effect of resveratrol in the TME.MethodsIn this study, MDA-MB-231(MB231), cisplatin resistance MDA-MB-231 (cisR), and T47D were used to examine the antitumor effect of resveratrol. The effectiveness of resveratrol, together with cisplatin as breast cancer treatment was investigated in vivo. Gene expressions of M1 (iNOS and CXCL10) and M2 (ARG1, CD163 and MRC1) markers in differentiated macrophages derived from THP-1 cells were examined to investigate the effect of resveratrol on TAM polarization in breast cancer progression.ResultsOur results demonstrated that resveratrol significantly reduced cell proliferation and enhanced chemosensitivity in breast cancer cells by inhibiting production of IL-6 and STAT3 activation. Treatment of resveratrol increased CXCL10 (M1 marker) expression. Further, resveratrol decreased IL-6 levels in LPS-treated differentiated macrophages. The use of resveratrol with cisplatin inhibited suppressed tumor growth when compared with cisplatin alone.ConclusionThis study revealed that resveratrol inhibited breast cancer cell proliferation by promoting M1/M2 macrophage polarization ratio and suppressing IL-6/pSTAT3 pathway.

The influence of macrophage polarisation status and IL-6 in breast carcinoma invasion / La influencia del estado de polarización de los macrófagos y la IL-6 en la invasión del carcinoma de mama

Introduction: Breast cancer metastasis accounts for the majority of deaths from breast cancer. The knowledge on IL-6 affecting cancer cell metatastatic behaviour need to be studied.Objectives: This study aim to examine the association of macrophage polarisation status and IL-6 with clinicopathological criteria and lymphovascular invasion (LVI) of breast carcinoma.Material & Method: 81 cases of FFPE breast carcinoma samples were stained with IL6, CD80 (M1 macrophage), CD204 and CD163 (M2 macrophage) and CD68 (pan-macrophage marker). The macrophages count were evaluated based on 3 hotspots of positively stained cells. IL-6 scoring was done using the H-score method.Result: Significant association was observed between CD68 marker with blood vessel invasion (p-value = 0.014), lymphatic vessel invasion (p-value = 0.005), and metastasis (p-value =0.028). CD68 was also significantly associated with CD204 (p = 0.027). CD80 biomarker also showing significant association with patient tumour grade (p-value = 0.054), ER (0.028) and PR (0.010) in patient clinical data and CD204 is significantly associated with ER (0.053) and PR (0.054) patient clinical data. Meanhile, there is no significant association of IL-6 with the patient clinical data.Conclusion: There is no significant association of IL-6 with the patient clinicopathological data obtained in this study while CD68 showed significant correlation with M2 macrophage biomarker and LVI indicating the influence of M1 and M2 macrophage in breast cancer metastatic pathway through blood and lymphatic vessel invasion. (AU)

Introducción: La metástasis del cáncer de mama representa la mayoría de las muertes por cáncer de mama. Es necesario estudiar el conocimiento sobre la IL-6 que afecta el comportamiento metatastásico de las células cancerosas.Objetivos: Este estudio tiene como objetivo examinar la asociación del estado de polarización de los macrófagos y la IL-6 con los criterios clínico-patológicos y la invasión linfovascular (LVI) del carcinoma de mama.Material y método: 81 casos de muestras de carcinoma de mama FFPE se tiñeron con IL6, CD80 (macrófago M1), CD204 y CD163 (macrófago M2) y CD68 (marcador pan-macrófago). El recuento de macrófagos se evaluó en base a 3 hotspots de células teñidas positivamente. La puntuación de IL-6 se realizó mediante el método de puntuación H.Resultado: Se observó una asociación significativa entre el marcador CD68 con invasión de vasos sanguíneos (valour de p = 0,014), invasión de vasos linfáticos (valour de p = 0,005) y metástasis (valour de p = 0,028). CD68 también se asoció significativamente con CD204 (p = 0.027). El biomarcador CD80 también muestra una asociación significativa con el grado del tumour del paciente (valour p = 0,054), ER (0,028) y PR (0,010) en los datos clínicos del paciente y el CD204 se asocia significativamente con los datos clínicos del paciente ER (0,053) y PR (0,054). Mientras tanto, no existe una asociación significativa de IL-6 con los datos clínicos del paciente.Conclusión: No existe una asociación significativa de IL-6 con los datos clínico-patológicos del paciente obtenidos en este estudio, mientras que CD68 mostró una correlación significativa con el biomarcador de macrófagos M2 y LVI que indica la influencia de los macrófagos M1 y M2 en la vía metastásica del cáncer de mama a través de la invasión de vasos sanguíneos y linfáticos. (AU)

Tumor microenvironment in triple-negative breast cancer: the correlation of tumor-associated macrophages and tumor-infiltrating lymphocytes

Purpose Immune cells such as cytotoxic T cells, helper T cells, B cells or tumor-associated macrophages (TAMs) contribute to the anti-tumor response or pro-tumorigenic effect in triple negative breast cancer (TNBC). The interrelation of TAMs, T and B tumor-infiltrating lymphocytes (TILs) in TNBC has not been fully elucidated. Methods We evaluated the association of tumor-associated macrophages, T and B TILs in TNBC. Results TNBCs with a high CD68+, CD163+ TAMs and low CD4+, CD8+, CD20+ TILs had a significantly shorter relapse-free survival (RFS) and overall survival (OS) than those with low CD68+, CD163+ TAMs and high CD4+, CD8+, CD20+ TILs. TNBCs with high CD68+ TAMs/low CD8+ TILs showed a significantly shorter RFS and OS and a significantly poorer prognosis than those with high CD68+ TAMs/high CD8+ TILs, low CD68+ TAMs/high CD8+ TILs, and low CD68+/low CD8+. TNBCs with high CD163+ TAMs/low CD8+, low CD20 + TILs showed a significantly shorter RFS and OS and a significantly poorer prognosis than those with high CD163+ TAMs/high CD8+ TILs and high CD163+ TAMs /high CD20+ TILs. Conclusions Our study suggests that TAMs further create an optimal tumor microenvironment (TME) for growth and invasion of cancer cells when evasion of immunoreactions due to T and B TILs occurs. In TNBCs, all these events combine to affect prognosis. The process of TME is highly complex in TNBCs and for an improved understanding, larger validation studies are necessary to confirm these findings (AU)

The effect of PD-1 expression on tumor-associated macrophage in T cell lymphoma

Purpose Our study aimed to explore the programmed death 1 (PD-1) expression on tumor-associated macrophage (TAM) in T cell non-Hodgkin lymphoma (T-NHL) and its relationship with lymphoma prognosis. The effect of PD-1 expression on the function of macrophages was also studied. Methods Multispectral image quantitative analysis was applied for detecting PD-1 expression on macrophages in T cell lymphoma tissues. The Kaplan–Meier analysis was performed to evaluate the value of PD-1 expression of TAM in predicting the overall survival of T-NHL. PD-1 overexpression THP-1-derived macrophage was constructed and was cocultured with Jurkat cells to explore the effect of PD-1 on macrophage function. Results In 17 T cell lymphoma cases, the 1-year overall survival rate was significantly lower in patients with higher PD-1 expression on TAMs (0.25 vs 0.86, p < 0.05). After co-cultured with Jurkat cells, classically activated (M1)-related markers on PD-1 overexpressed macrophages were significantly lower than those on controls, while the expressions of alternatively activated (M2) related markers were similar. The PD-1 overexpressed macrophages showed inhibited phagocytosis (4.42% vs 40.7%, p < 0.001) and increased IL-10 secretion (144.48 pg/ml vs 32.32 pg/ml, p < 0.001). Conclusion High PD-1 expression on TAMs in T-NHL may predict poor prognosis. The PD-1 overexpression of macrophages significantly inhibited polarization of M1 macrophages and phagocytosis, and more IL-10 was excreted. These changes may enhance the pro-tumor effects of tumor microenvironmen (AU)

Senescent thyroid tumor cells promote their migration by inducing the polarization of M2-like macrophages

Purpose An in-depth understanding of the mechanism of thyroid cancer progression will help identify patients with thyroid cancer with a high risk of recurrence and metastasis. Although studies have pointed out that the senescence of thyroid tumor cells may stimulate TAMs and cause a series of changes. However, the role of TAMs in aging thyroid cancer cells is still unknown. The aim of this study was to investigate the function of TAMs in aging thyroid cancer cells. Methods We conducted in vitro model studies based on the K1 cell line to induce tumor cell senescence and study its effect on the differentiation of macrophages, flow cytometry was used to confirm polarization of macrophages, transwell assay was used to confirm changes of invasion and migration of tumor cells. Result Our data indicate that aging thyroid tumor cell lines trigger the polarization of M2-like macrophages, accompanied by increased expression of CCL17, CCL18, IL-18, and TGFβ1. This event is caused by the activation of the NFκB pathway upregulation of CXCL2 and CXCL3 is related. Further studies have shown that differentiated M2-like macrophages promote tumor cell migration (but have no effect on cell proliferation). Conclusion Our study indicating that the interaction between tumor and TAMs also occurs in the advanced stages of thyroid tumors and will lead to faster tumors progress (AU)

Eosinophil: a central player in modulating pathological complexity in asthma

Eosinophils are the major inflammatory cells which play a crucial role in the development of allergic and non-allergic asthma phenotypes. Eosinophilic asthma is the most heterogeneous phenotype where activated eosinophils are reported to be significantly associated with asthma severity. Activated eosinophils display an array of cell adhesion molecules that not only act as an activation marker, suitable for assessing severity, but also secrete several tissue factors, cytokines and chemokines which modulate the clinical severity. Eosinophil activations are also strictly associated with activation of other hetero cellular populations like neutrophils, macrophages, mast cells, and platelets which culminate in the onset and progression of abnormal phenotypes such as bronchoconstriction, allergic response, fibrosis instigated by tissue inflammation, epithelial injury, and oxidative stress. During the activated state, eosinophils release several potent toxic signaling molecules such as major basic proteins, eosinophil peroxidase, eosinophil cationic protein (ECP), and lipid mediators, rendering tissue damage and subsequently leading to allergic manifestation. The tissue mediators render a more complex manifestation of a severe phenotype by activating prominent signaling cross-talk. Here, in the current review with the help of search engines of PubMed, Medline, etc, we have tried to shed light and explore some of the potent determinants regulating eosinophil activation leading to asthma phenotype (AU)

Resistance training and innate immunosenescence of the innate immune system / Entrenamiento de resistencia e inmunosenescencia del sistema inmune innato / Treinamento resistido e imunossenescência do sistema imune inato

Phagocytic cells constitute the first defense line against the diversity of infectious agents. The effects of aging on the immune function - immunosenescence - affect the phagocytic capacity of neutrophils and monocytes/macrophages and result in increased risk to cancer and other diseases. The aim of this review was to assess the functional aspects of the innate system cells in aging. Evidence brought about by this review suggests that resistance training is a useful therapy to mitigate the adverse effects of the innate immune system aging process. Resistance training is consistently recommended as assistent strategy for prevention of the inflamaging and associated chronic diseases, but establishing adequate program is still in demand. In addition, future studies are needed to improve our understanding of the resistance training-induced mechanisms underlying changes in phagocytic activity in the elderly

Las células fagocíticas constituyen la primera línea de defensa contra los agentes infecciosos. Los efectos del envejecimiento sobre la función inmune - inmunosenescencia - afectan la capacidad fagocítica de neutrófilos y monocitos/macrófagos y resultan en riesgo aumentado para el cáncer y otras enfermedades. El objetivo de esta revisión fue evaluar los aspectos funcionales de las células del sistema innato en el envejecimiento. Las evidencias revisadas sugieren que el entrenamiento de resistencia es una terapia útil para atenuar los efectos adversos del proceso de envejecimiento del sistema inmune innato. Se recomienda el entrenamiento de resistencia continuamente como estrategia complementaria para la prevención de la inflamación y de las enfermedades crónicas asociadas, pero hay que establecer el programa adecuado. Además, se necesitan más investigaciones para mejorar nuestra comprensión de los mecanismos modulados por el entrenamiento de resistencia que inducen a los cambios en la actividad fagocítica en las personas mayores

As células fagocitárias constituem a primeira linha de defesa contra agentes infecciosos. Os efeitos do envelhecimento sobre a função imune - imunossenescência - afetam a capacidade fagocítica de neutrófilos e monócitos/macrófagos e resultam em aumento do risco para câncer e outras doenças. O objetivo desta revisão foi avaliar os aspectos funcionais das células do sistema inato durante o envelhecimento. Os estudos revisados sugerem que o treinamento resistido é uma terapia útil para atenuar os efeitos adversos do processo de envelhecimento do sistema imune inato. Recomenda-se que o treinamento resistido seja aplicado continuamente como estratégia complementar para a prevenção da inflamação e doenças crônicas associadas, porém deve-se estabelecer o programa adequado. Ressalta-se ainda que, são necessários mais estudos para melhorar a compreensão sobre os mecanismos modulados pelo treinamento resistido que induzem a alterações na atividade fagocítica em idosos

Interacciones neuroinmunológicas en el ictus / Neuroimmunological interactions in stroke

Introducción: El ictus es una de las principales causas de mortalidad en el mundo y debido al incremento en la expectativa de vida su incidencia va en aumento; sin embargo, el desarrollo de nuevos medicamentos con utilidad clínica ha sido prácticamente nulo, por lo que hasta la fecha el tratamiento de estos pacientes es muy limitado. Desarrollo: La evidencia básica y clínica en el área señala que tras un infarto cerebral se producen una serie de cambios neuroquímicos, entre los que se encuentran: la depleción energética, la producción de radicales libres, la acumulación de calcio, la desregulación de neurotransmisores, la excitotoxicidad, y de manera tardía, la activación del sistema inmune caracterizada como inflamación. Esta respuesta del sistema inmunológico ha mostrado ser un evento central en la progresión de la patología, en el que destaca la participación de las citocinas proinflamatorias como TNF, que aumentan el daño por excitotoxicidad y por acumulación de calcio, favorecen la formación de radicales libres y en general promueven la muerte celular. Por otro lado, algunas citocinas antiinflamatorias como IL-10 e IL-4 han mostrado tener efectos neuroprotectores e incluso favorecen la recuperación de sinapsis y la neurogénesis, haciendo de la modulación de la respuesta inmunológica un área con mucho potencial terapéutico. Conclusiones: El entendimiento de las relaciones entre el sistema inmunológico y el sistema nervioso no solo nos permite entender con mayor profundidad el fenómeno del ictus, sino que también nos ofrece un nuevo arsenal de estrategias diagnósticas, pronósticas y terapéuticas que podrían mejorar la calidad de vida de las personas aquejadas por esta terrible enfermedad

Introduction: Stroke is one of the leading causes of death in the world; its incidence is increasing due to increased life expectancy. However, treatment options for these patients are limited since no clinically effective drugs have been developed to date. Development: According to clinical evidence, a number of neurochemical changes take place after stroke, including energy depletion, increased free radical synthesis, calcium accumulation, neurotransmitter imbalance, excitotoxicity, and, at a later stage, immune system activation leading to inflammation. Immune response has been shown to be a major factor in disease progression. The release of proinflammatory cytokines such as TNF increase brain damage secondary to excitotoxicity and calcium accumulation, and promote free radical synthesis and cell death through various mechanisms. On the other hand, certain anti-inflammatory cytokines, such as IL-10 and IL-4, have been shown to have a neuroprotective effect and even promote neurogenesis and synapse remodeling, which makes immune modulation a promising treatment approach. Conclusions: Understanding the relationship between the immune system and the nervous system not only deepens our knowledge of stroke but also provides new diagnostic, prognostic, and therapeutic strategies that may increase the quality of life of stroke patients

Disseminated aspergillosis in an immunocompetent patient treated with corticosteroids: value of PCR for diagnosis / Aspergilosis diseminada en una paciente inmunocompetente en tratamiento con corticoides: valor de la PCR en el diagnóstico

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