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1.
Front Physiol ; 11: 573347, 2020.
Article in English | MEDLINE | ID: mdl-33071827

ABSTRACT

Growing evidence demonstrates a continuous interaction between the immune system and the skeletal muscle in inflammatory diseases of different pathogenetic origins, in dystrophic conditions such as Duchenne Muscular Dystrophy as well as during normal muscle regeneration. Although one component of the innate immunity, the macrophage, has been extensively studied both in disease conditions and during cell or gene therapy strategies aiming at restoring muscular functions, much less is known about dendritic cells and their primary immunological targets, the T lymphocytes. This review will focus on the dendritic cells and T lymphocytes (including effector and regulatory T-cells), emphasizing the potential cross talk between these cell types and their influence on the structure and function of skeletal muscle.

2.
Life Sci ; 88(19-20): 830-8, 2011 May 09.
Article in English | MEDLINE | ID: mdl-21396376

ABSTRACT

AIMS: Granulocyte Colony-Stimulating Factor (G-CSF), which mobilizes hemopoietic stem cells (HSC), is believed to protect HSC graft recipients from graft-versus-host disease by enhancing Th2 cytokine secretion. Accordingly, G-CSF should aggravate Th2-dependent allergic pulmonary inflammation and the associated eosinophilia. We evaluated the effects of G-CSF in a model of allergic pulmonary inflammation. MAIN METHODS: Allergic pulmonary inflammation was induced by repeated aerosol allergen challenge in ovalbumin-sensitized C57BL/6J mice. The effects of allergen challenge and of G-CSF pretreatment were evaluated by monitoring: a) eosinophilia and cytokine/chemokine content of bronchoalveolar lavage fluid, pulmonary interstitium, and blood; b) changes in airway resistance; and c) changes in bone-marrow eosinophil production. KEY FINDINGS: Contrary to expectations, G-CSF pretreatment neither induced nor enhanced allergic pulmonary inflammation. Instead, G-CSF: a) suppressed accumulation of infiltrating eosinophils in bronchoalveolar, peribronchial and perivascular spaces of challenged lungs; and b) prevented ovalbumin challenge-induced rises in airway resistance. G-CSF had multiple regulatory effects on cytokine and chemokine production: in bronchoalveolar lavage fluid, levels of IL-1 and IL-12 (p40), eotaxin and MIP-1a were decreased; in plasma, KC, a neutrophil chemoattractant, was increased, while IL-5 was decreased and eotaxin was unaffected. In bone-marrow, G-CSF: a) prevented the increase in bone-marrow eosinophil production induced by ovalbumin challenge of sensitized mice; and b) selectively stimulated neutrophil colony formation. SIGNIFICANCE: These observations challenge the view that G-CSF deviates cytokine production towards a Th2 profile in vivo, and suggest that this neutrophil-selective hemopoietin affects eosinophilic inflammation by a combination of effects on lung cytokine production and bone-marrow hemopoiesis.


Subject(s)
Chemokines/antagonists & inhibitors , Cytokines/antagonists & inhibitors , Down-Regulation/physiology , Eosinophils/metabolism , Granulocyte Colony-Stimulating Factor/therapeutic use , Growth Inhibitors/physiology , Pneumonia/prevention & control , Respiratory Hypersensitivity/prevention & control , Airway Resistance/immunology , Animals , Bronchoalveolar Lavage Fluid/cytology , Bronchoalveolar Lavage Fluid/immunology , Cell Migration Inhibition/immunology , Chemokines/biosynthesis , Cytokines/biosynthesis , Down-Regulation/drug effects , Eosinophils/cytology , Female , Granulocyte Colony-Stimulating Factor/administration & dosage , Male , Mice , Mice, Inbred C57BL , Pneumonia/immunology , Pneumonia/pathology , Respiratory Hypersensitivity/immunology , Respiratory Hypersensitivity/pathology
3.
J Immunol ; 176(3): 1834-9, 2006 Feb 01.
Article in English | MEDLINE | ID: mdl-16424214

ABSTRACT

Signaling through exposed phosphatidylserine (PS) is fundamental for the TGFbeta1-dependent, noninflammatory phagocytosis of apoptotic cells. This same mechanism operates in the internalization of amastigotes of Leishmania (L) amazonensis (L(L)a) in a process quoted as apoptotic mimicry. Now we show that the host modulates PS exposure by the amastigotes and, as a consequence, BALB/c mice-derived amastigotes expose significantly more PS than those derived from C57BL/6 mice. Due to this difference in the density of surface PS molecules, the former are significantly more infective than the latter, both in vivo, in F1 (BALB/c x C57BL/6) mice, and in vitro, in thioglycollate-derived macrophages from this same mouse strain. PS exposure increases with progression of the lesion and reaches its maximum value in amastigotes obtained at the time point when the lesion in C57BL/6 mice begins to decrease in size and the lesions in BALB/c mice are still growing in size. Synthesis of active TGFbeta1, induction of IL-10 message, and inhibition of NO synthesis correlate with the amount of surface PS displayed by viable (propidium iodide-negative) infective amastigote. Furthermore, we also show that, similar to what happens with apoptotic cells, amastigotes of L(L)a are internalized by macropinocytosis. This mechanism of internalization is consistent with the large phagolysosomes characteristic of L(L)a infection. The intensity of macrophage macropinocytic activity is dependent on the amount of surface PS displayed by the infecting amastigote.


Subject(s)
Apoptosis/immunology , Leishmania mexicana/growth & development , Molecular Mimicry/immunology , Phosphatidylserines/metabolism , Animals , Cells, Cultured , Host-Parasite Interactions/immunology , Interleukin-10/biosynthesis , Interleukin-10/genetics , Leishmania mexicana/immunology , Macrophages/immunology , Macrophages/metabolism , Macrophages/parasitology , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Nitric Oxide/biosynthesis , Pinocytosis/immunology , RNA, Messenger/metabolism , Transforming Growth Factor beta/genetics , Transforming Growth Factor beta/metabolism , Transforming Growth Factor beta1
4.
Exp Parasitol ; 110(1): 39-47, 2005 May.
Article in English | MEDLINE | ID: mdl-15804377

ABSTRACT

Characterization of infective metacyclic promastigotes of Leishmania spp can be an essential step in several experimental protocols. Metacyclic forms of all Leishmania species display a typical morphology with short, narrow cell body, and an elongated flagellum. This feature suggests that metacyclics can be distinguished from procyclic forms by non-fluorimetric flow cytometric parameters thus enabling the follow-up of their appearance and acquisition of specific properties, during metacyclogenesis in in vitro cultures. Here we describe the flow cytometric parameters of stage-specific promastigotes of Leishmania major, Leishmania donovani, Leishmania amazonensis, and Leishmania braziliensis. Our findings were validated by optical microscopy morphology and specific procyclic labeling with FITC-peanut agglutinin. Furthermore, we show that parasite's distribution in the plot during differentiation in culture is not species specific and that the parasites displaying low forward-angle light scatter (FSC(low)) are three times more infective than the FSC(high) ones. The method here described can be applied to the identification of metacyclics of different Leishmania spp within the whole stationary population.


Subject(s)
Leishmania/growth & development , Animals , Cells, Cultured , Flow Cytometry , Humans , Leishmania/isolation & purification , Leishmania/ultrastructure , Leishmania braziliensis/growth & development , Leishmania braziliensis/isolation & purification , Leishmania braziliensis/ultrastructure , Leishmania donovani/growth & development , Leishmania donovani/isolation & purification , Leishmania donovani/ultrastructure , Leishmania major/growth & development , Leishmania major/isolation & purification , Leishmania major/ultrastructure , Leishmania mexicana/growth & development , Leishmania mexicana/isolation & purification , Leishmania mexicana/ultrastructure , Life Cycle Stages , Macrophages, Peritoneal/parasitology , Mice , Mice, Inbred BALB C , Reproducibility of Results , Species Specificity
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