scholarly journals PPARs in Alveolar Macrophage Biology

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-12 ◽  
Author(s):  
Monica R. Smith ◽  
Theodore J. Standiford ◽  
Raju C. Reddy
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Crucial Role ◽  
Respiratory Function ◽  
Lung Diseases ◽  
First Line ◽  
Phagocytotic Activity

PPARs, most notably PPAR-γ, play a crucial role in regulating the activation of alveolar macrophages, which in turn occupy a pivotal place in the immune response to pathogens and particulates drawn in with inspired air. In this review, we describe the dual role of the alveolar macrophage as both a first-line defender through its phagocytotic activity and a regulator of the immune response. Depending on its state of activation, the alveolar macrophage may either enhance or suppress different aspects of immune function in the lung. We then review the role of PPAR-γand its ligands in deactivating alveolar macrophages—thus limiting the inflammatory response that, if unchecked, could threaten the essential respiratory function of the alveolus—while upregulating the cell's phagocytotic activity. Finally, we examine the role that inadequate or inappropriate PPAR-γresponses play in specific lung diseases.

scholarly journals Sialidase of Glaesserella parasuis augments inflammatory response via desialylation and abrogation of negative regulation of Siglec-5

2021 ◽  
Author(s):  
Yuping Song ◽  
Qicong Pan ◽  
Jing Xiao ◽  
Wenjie Li ◽  
Hui Ma ◽  
...  
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Proinflammatory Cytokines ◽  
Alveolar Macrophages ◽  
Sh2 Domain ◽  
Negative Regulation ◽  
Mitogen Activated Protein Kinase ◽  
Porcine Alveolar Macrophage ◽  
Macrophage Infection

Siglecs are sialic acid-binding immunoglobulin-like lectins that play an important role in tissue homeostasis, immune response, and pathogen infection. Bacterial sialidases act on natural ligands of Siglecs, interfering with the Siglec-mediated immune response. Glaesserella parasuis is a porcine bacterial pathogen that secretes sialidase. However, little is known about the sialidase of G. parasuis and its impact on immune regulation. Here, we used wild-type G. parasuis, a sialidase-deficient mutant, and complimentary strains to investigate the role of sialidase in porcine alveolar macrophage infection. Sialidase induced the release of proinflammatory cytokines, such as interleukin (IL)-1α, IL-6, and tumor necrosis factor alpha, from porcine alveolar macrophages. Moreover, sialidase desialylated the surface of porcine alveolar macrophages and altered the expression of Siglecs (the expression of Siglec-5 was reduced). Furthermore, sialidase led to a reduction in endogenous SH2 domain-containing protein tyrosine phosphatase (SHP-2) recruitment to Siglec-5 and simultaneously activated the inflammatory response via the mitogen-activated protein kinase and nuclear factor kappa light chain enhancer of activated B cell signaling pathways. This desialylation occurred before the release of proinflammatory cytokines, suggesting that the sialidase-induced inflammatory response was followed by reduced recruitment of SHP-2 to Siglec-5. Thus, this study is the first to demonstrate the role of sialidase in the inflammatory response of G. parasuis. This role resulted from the abrogation of negative regulation of Siglec-5 on proinflammatory cytokine release. This study helps to understand the molecular mechanism underlying the inflammatory response induced by sialidase secreted by G. parasuis and the acute inflammation caused by G. parasuis.

RESPIRATORY SYNCYTIAL VIRUS LUNG INFECTION IN INFANTS: IMMUNOREGULATORY ROLE OF INFECTED ALVEOLAR MACROPHAGES

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 391-391
Author(s):  
Leon S. Greos
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Lung Injury ◽  
Alveolar Macrophages ◽  
Lung Infection ◽  
Local Immune Response ◽  
Rsv Infection ◽  
Syncytial Virus

Alveolar macrophages are infected by RSV in vivo and coexpress potent immunomodulatory molecules that potentially regulate local immune response or lung injury caused by RSV infection.

CD209 (DC-SIGN) – role in the work of the innate immunity and pathogen penetration

2020 ◽  
Vol 1 (9) ◽  
pp. 64-71
Author(s):  
E. A. Klimov ◽  
◽  
E. K. Novitskaya ◽  
S. N. Koval’chuk ◽  
◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Dendritic Cells ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Adhesion Molecule ◽  
Immune Evasion ◽  
Intercellular Adhesion Molecule ◽  
Lectin Receptor

Intercellular adhesion molecule CD209 (DC-SIGN) is a membrane C-type lectin receptor expressed on the surface of dendritic cells and macrophages. CD209 plays an important role in innate immunity. Many studies have shown the possibility of interaction of the CD209 molecule with a number of dangerous pathogens of humans and animals. This review summarizes information on the structure of the CD209 gene and its product, describes the role of the CD209 protein in the immune response, in the migration of dendritic cells from the blood to the tissue, and their interaction with neutrophils. The currently known signaling pathway of activation through the CD209 inflammatory response is presented. The role of CD209 as an endocytic antigen receptor and the participation of the protein in immune evasion of pathogens are discussed. The mechanisms known to date for the development of infections caused by pathogens of various nature in animals are described.

scholarly journals The Role of the Immune Response in the Pathogenesis of Bronchiectasis

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Paul T. King
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Respiratory Tract ◽  
Lower Respiratory Tract ◽  
Therapeutic Potential ◽  
Small Airways ◽  
Upper Respiratory Tract ◽  
Causative Factors ◽  
Triggering Factor

Bronchiectasis is a prevalent respiratory condition characterised by permanent and abnormal dilation of the lung airways (bronchi). There are a large variety of causative factors that have been identified for bronchiectasis; all of these compromise the function of the immune response to fight infection. A triggering factor may lead to the establishment of chronic infection in the lower respiratory tract. The bacteria responsible for the lower respiratory tract infection are usually found as commensals in the upper respiratory tract microbiome. The consequent inflammatory response to infection is largely responsible for the pathology of this condition. Both innate and adaptive immune responses are activated. The literature has highlighted the central role of neutrophils in the pathogenesis of bronchiectasis. Proteases produced in the lung by the inflammatory response damage the airways and lead to the pathological dilation that is the pathognomonic feature of bronchiectasis. The small airways demonstrate infiltration with lymphoid follicles that may contribute to localised small airway obstruction. Despite aggressive treatment, most patients will have persistent disease. Manipulating the immune response in bronchiectasis may potentially have therapeutic potential.

The crucial role of the MyD88 adaptor protein in the inflammatory response induced by Bothrops atrox venom

Toxicon ◽  
2013 ◽  
Vol 67 ◽  
pp. 37-46 ◽  
Author(s):  
Vanessa Moreira ◽  
Catarina Teixeira ◽  
Henrique Borges da Silva ◽  
Maria Regina D'Império Lima ◽  
Maria Cristina Dos-Santos
Keyword(s):  
Inflammatory Response ◽  
Crucial Role ◽  
Adaptor Protein ◽  
Bothrops Atrox ◽  
Myd88 Adaptor Protein

scholarly journals Role of Complement in Multiorgan Failure

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Daniel Rittirsch ◽  
Heinz Redl ◽  
Markus Huber-Lang
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Inflammatory Response ◽  
Complement System ◽  
Multiorgan Failure ◽  
Severe Trauma ◽  
Organ Systems ◽  
Activation Products ◽  
The Complement System

Multiorgan failure (MOF) represents the leading cause of death in patients with sepsis and systemic inflammatory response syndrome (SIRS) following severe trauma. The underlying immune response is highly complex and involves activation of the complement system as a crucial entity of innate immunity. Uncontrolled activation of the complement system during sepsis and SIRS with in excessive generation of complement activation products contributes to an ensuing dysfunction of various organ systems. In the present review, mechanisms of the inflammatory response in the development of MOF in sepsis and SIRS with particular focus on the complement system are discussed.

scholarly journals Depletion of Neutrophils Exacerbates the Early Inflammatory Immune Response in Lungs of Mice Infected withParacoccidioides brasiliensis

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Paula Andrea Pino-Tamayo ◽  
Juan David Puerta-Arias ◽  
Damaris Lopera ◽  
Martha Eugenia Urán-Jiménez ◽  
Ángel González
Keyword(s):  
Monoclonal Antibody ◽  
Immune Response ◽  
Inflammatory Response ◽  
Paracoccidioides Brasiliensis ◽  
Yeast Cells ◽  
Histopathological Analysis ◽  
Acute Inflammatory Response ◽  
Fungal Load ◽  
Inflammatory Immune Response

Neutrophils predominate during the acute phase of theParacoccidioides brasiliensisinfection. Herein, we determined the role of the neutrophil during the early stages of experimental pulmonary paracoccidioidomycosis using a monoclonal antibody (mAb) specific for neutrophils. Male BALB/c mice were inoculated intranasally with1.5×106or2×106P. brasiliensisyeast cells. The mAb was administered 24 h before infection, followed by doses every 48 h until mice were sacrificed. Survival time was evaluated and mice were sacrificed at 48 h and 96 h after inoculation to assess cellularity, fungal load, cytokine/chemokine levels, and histopathological analysis. Neutrophils from mAb-treated mice were efficiently depleted (99.04%). Eighty percent of the mice treated with the mAb and infected with1.5×106yeast cells died during the first two weeks after infection. When mice were treated and infected with2×106yeast cells, 100% of them succumbed by the first week after infection. During the acute inflammatory response significant increases in numbers of eosinophils, fungal load and levels of proinflammatory cytokines/chemokines were observed in the mAb-treated mice. We also confirmed that neutrophils are an important source of IFN-γand IL-17. These results indicate that neutrophils are essential for protection as well as being important for regulating the early inflammatory immune response in experimental pulmonary paracoccidioidomycosis.

scholarly journals Boosting The Peripheral Immune Response in the Skeletal Muscles Improved Motor Function in ALS Transgenic Mice

2021 ◽  
Author(s):  
Maria Chiara Trolese ◽  
Carlotta Scarpa ◽  
Valentina Melfi ◽  
Paola Fabbrizio ◽  
Francesca Sironi ◽  
...  
Keyword(s):  
Immune Response ◽  
Nervous System ◽  
Inflammatory Response ◽  
Muscle Regeneration ◽  
Skeletal Muscles ◽  
Skeletal Muscle Regeneration ◽  
Limiting Factors ◽  
Disease Stage ◽  
Peripheral Compartment

Abstract Background: Monocyte chemoattractant protein 1 (MCP1/CCL2) is one of the most powerful pro-inflammatory chemokines. However, its signalling is pivotal in driving axonal and muscle regeneration following injury. We previously showed that MCP1 is strongly upregulated in the nervous system of slow-progressing than fast-progressing SOD1G93A mice, which are characterised by a poor immune response that leads to a massive nerve and muscle degeneration.Methods: To assess the MCP1-mediated therapeutic role, we boosted the chemokine along the motor unit of the two SOD1G93A ALS models through a single intramuscular injection of a scAAV9 vector engineered with the Mcp1 gene (scAAV9_MCP1) at the pre-symptomatic disease stage.Results: Our observations revealed that slow-progressing SOD1G93A mice responded positively to the scAAV9_MCP1 injection anticipating the activation of the immune response, which sustained the pro-regenerative programme within nerves and skeletal muscles, eventually slackening the symptoms progression. Conversely, fast-progressing SOD1G93A mice exhibited an adverse response to the treatment, exacerbating the toxic inflammatory response in the periphery, resulting in worsened motor ability late in the disease.Intriguingly, our data suggested a novel pleiotropic role of MCP1 in the nervous system of SOD1G93A mice capable of promoting axon regeneration and modulating neuroinflammation, with the overall effect of preventing neurodegeneration.Conclusions: We provided direct evidence underlying the pivotal role of the immune response in promoting and governing skeletal muscle regeneration and thus the speed of ALS progression. The comparison study performed in fast- and slow-progressing SOD1G93A mice spotlights the nature and temporal activation of the inflammatory response as limiting factors to protect the peripheral compartment and interfere with the disease course tangibly. Altogether, these observations highlight the immune response as a key determinant for disease variability and proffer a reasonable explanation for the failure of systemic immunomodulatory treatments suggesting new potential strategies to hamper ALS progression.

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