scholarly journals Immune Response in Pneumocystis Infections According to the Host Immune System Status

2021 ◽  
Vol 7 (8) ◽  
pp. 625
Author(s):  
Eléna Charpentier ◽  
Sandie Ménard ◽  
Catherine Marques ◽  
Antoine Berry ◽  
Xavier Iriart
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Immune Status ◽  
Pneumocystis Pneumonia ◽  
Favourable Outcome ◽  
Lung Damage ◽  
Host Immune System ◽  
M1 Macrophage ◽  
Immune Deficiencies ◽  
The Impact

The host immune response is critical in Pneumocystis pneumonia (PCP). Immunocompetent hosts can eliminate the fungus without symptoms, while immunodeficient hosts develop PCP with an unsuitable excessive inflammatory response leading to lung damage. From studies based on rodent models or clinical studies, this review aimed to better understand the pathophysiology of Pneumocystis infection by analysing the role of immune cells, mostly lymphocytes, according to the immune status of the infected host. Hence, this review first describes the immune physiological response in infected immunocompetent hosts that are able to eliminate the fungus. The objective of the second part is to identify the immune elements required for the control of the fungus, focusing on specific immune deficiencies. Finally, the third part concentrates on the effect of the different immune elements in immunocompromised subjects during PCP, to better understand which cells are detrimental, and which, on the contrary, are beneficial once the disease has started. This work highlights that the immune response associated with a favourable outcome of the infection may differ according to the immune status of the host. In the case of immunocompetency, a close communication between B cells and TCD4 within tertiary lymphocyte structures appears critical to activate M2 macrophages without much inflammation. Conversely, in the case of immunodeficiency, a pro-inflammatory response including Th1 CD4, cytotoxic CD8, NK cells, and IFNγ release seems beneficial for M1 macrophage activation, despite the impact of inflammation on lung tissue.

scholarly journals Cannabis and Inflammatory Mediators

2020 ◽  
Vol 27 (1) ◽  
pp. 16-24
Author(s):  
Marcelo G. Lima ◽  
Vitor S. Tardelli ◽  
Elisa Brietzke ◽  
Thiago M. Fidalgo
Keyword(s):  
Multiple Sclerosis ◽  
Immune Response ◽  
Inflammatory Response ◽  
Healthy Volunteers ◽  
Inflammatory Mediators ◽  
Inflammatory Markers ◽  
Cannabis Use ◽  
Pubmed Database ◽  
Inflammatory Activation ◽  
The Impact

<b><i>Introduction:</i></b> Although the recreational cannabis use is expressive worldwide, the literature about medical potential of cannabis extracts, including its anti-inflammatory properties, remains inconclusive. <b><i>Methods:</i></b> We screened all articles, published on the PubMed database, on inflammatory mediators and any information about cannabis use from 1980 to March 2019. <b><i>Results:</i></b> Six studies were included, and the main findings were as follows: (i) among healthy volunteers and cannabis users, cannabinoids seemed to decrease the inflammatory response, thus decreasing the immune response, which led to a higher risk of infections; (ii) among patients with multiple sclerosis, cannabinoids seemed to have little impact on the inflammatory markers’ levels. <b><i>Discussion:</i></b> Although cannabis use can produce immune inflammatory suppression in healthy people, this effect is not robust enough to change inflammatory mediators’ levels in situations of highly dysfunctional inflammatory activation. Nevertheless, the impact of cannabinoids in clinical outcomes of these conditions remains to be determined.

scholarly journals Microglia: Agents of the CNS Pro-Inflammatory Response

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1717 ◽  
Author(s):  
José A. Rodríguez-Gómez ◽  
Edel Kavanagh ◽  
Pinelopi Engskog-Vlachos ◽  
Mikael K.R. Engskog ◽  
Antonio J. Herrera ◽  
...  
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Neurodegenerative Diseases ◽  
Current Knowledge ◽  
Reactive Microglia ◽  
Holistic View ◽  
Human Microglia ◽  
Positron Emission ◽  
New Research ◽  
The Impact

The pro-inflammatory immune response driven by microglia is a key contributor to the pathogenesis of several neurodegenerative diseases. Though the research of microglia spans over a century, the last two decades have increased our understanding exponentially. Here, we discuss the phenotypic transformation from homeostatic microglia towards reactive microglia, initiated by specific ligand binding to pattern recognition receptors including toll-like receptor-4 (TLR4) or triggering receptors expressed on myeloid cells-2 (TREM2), as well as pro-inflammatory signaling pathways triggered such as the caspase-mediated immune response. Additionally, new research disciplines such as epigenetics and immunometabolism have provided us with a more holistic view of how changes in DNA methylation, microRNAs, and the metabolome may influence the pro-inflammatory response. This review aimed to discuss our current knowledge of pro-inflammatory microglia from different angles, including recent research highlights such as the role of exosomes in spreading neuroinflammation and emerging techniques in microglia research including positron emission tomography (PET) scanning and the use of human microglia generated from induced pluripotent stem cells (iPSCs). Finally, we also discuss current thoughts on the impact of pro-inflammatory microglia in neurodegenerative diseases.

scholarly journals Characterization of a Distinct Host Response Profile to Pneumocystis murina Asci during Clearance of Pneumocystis Pneumonia

2013 ◽  
Vol 81 (3) ◽  
pp. 984-995 ◽  
Author(s):  
Michael J. Linke ◽  
Alan Ashbaugh ◽  
Margaret S. Collins ◽  
Keeley Lynch ◽  
Melanie T. Cushion
Keyword(s):  
Life Cycle ◽  
Inflammatory Response ◽  
Immune Responses ◽  
Host Response ◽  
Cellular Response ◽  
Pneumocystis Pneumonia ◽  
Lung Damage ◽  
Th17 Response ◽  
Content Type ◽  
Chronic Lung Diseases

ABSTRACTPneumocystisspp. are yeast-like fungi that cause pneumocystis pneumonia (PcP) in immunocompromised individuals and exacerbate chronic lung diseases in immunocompetent individuals. ThePneumocystislife cycle includes trophic forms and asci (cyst forms). The cell walls ofPneumocystisasci contain β-1,3-d-glucan, and treatment of PcP with β-1,3-d-glucan synthase inhibitors, such as anidulafungin, results in depletion of asci, but not trophic forms. The pulmonary host response during immune reconstitution (IR)-mediated clearance of PcP in anidulafungin-treated and untreated mice was characterized to identify ascus-specific responses. During IR, similar numbers of trophic forms were present in the anidulafungin-treated and untreated mice; however, asci were only present in the untreated mice. IR resulted in a significant reduction of trophic forms from the lungs in both groups and asci in the untreated group. The presence of asci in untreated mice correlated with increased β-glucan content in the lungs. The untreated mice mounted immune responses associated with a deleterious host inflammatory response, including increased CD8+T cell influx and expression of macrophage inflammatory response markers. A more robust cellular response was also observed in the untreated mice, with increased numbers of macrophages and neutrophils that were associated with greater lung damage. Markers of a Th17 response were also elevated in the untreated mice. These results suggest that the host mounts unique responses to asci and trophic forms. That these 2 life cycle stages provoked distinct host response profiles has significant implications for clearance and interpretation of the host immune responses to PcP.

scholarly journals The influence of the gut microbiota on influenza vaccine-induced immunity

2021 ◽  
Author(s):  
◽  
Anna Mooney
Keyword(s):  
Immune Response ◽  
Gut Microbiota ◽  
Immune Responses ◽  
Influenza Vaccine ◽  
Influenza Vaccination ◽  
Antibody Production ◽  
Host Immune System ◽  
Viral Control ◽  
Nutritional Interventions ◽  
The Impact

<p>Currently, annual vaccination is widely considered the most effective method for preventing and controlling influenza virus infection. However, many individuals mount suboptimal immune responses to vaccination and the factors leading to poor immune responses are yet to be elucidated. Interestingly, it has been proposed that microorganisms that inhabit the intestinal tract, the gut microbiota, can profoundly influence many facets of the host immune system, including the strength of the immune response to influenza vaccination.  In line with these observations, we observed that short-term administration of antibiotics drastically reduced influenza vaccine-specific antibody production. In particular, antibiotic treatment diminished the frequency and activation status of multiple myeloid cell subsets in the draining lymph nodes at steady-state and following vaccination, with associated impairments in B and TFH cell responses.  Composition and function of gut microbiota communities can be rapidly altered through dietary changes. Therefore, the impact of potential prebiotic and probiotic nutritional interventions on the immune response to influenza vaccination and subsequent infection was assessed. No improvement in antibody responses to influenza vaccination was observed following the nutritional interventions studies. However, oral administration of a propolis formulation led to some improvement in viral control following infection.  Collectively, this investigation indicates that alterations in microbial-associated signals leads to severe impairments in cellular responses crucial to humoral immunity and subsequent vaccine-induced antibody production. Furthermore, by altering the gut microbiota through dietary interventions, there is potential to improve immune responses to vaccination.</p>

scholarly journals The influence of the gut microbiota on influenza vaccine-induced immunity

2021 ◽  
Author(s):  
◽  
Anna Mooney
Keyword(s):  
Immune Response ◽  
Gut Microbiota ◽  
Immune Responses ◽  
Influenza Vaccine ◽  
Influenza Vaccination ◽  
Antibody Production ◽  
Host Immune System ◽  
Viral Control ◽  
Nutritional Interventions ◽  
The Impact

<p>Currently, annual vaccination is widely considered the most effective method for preventing and controlling influenza virus infection. However, many individuals mount suboptimal immune responses to vaccination and the factors leading to poor immune responses are yet to be elucidated. Interestingly, it has been proposed that microorganisms that inhabit the intestinal tract, the gut microbiota, can profoundly influence many facets of the host immune system, including the strength of the immune response to influenza vaccination.  In line with these observations, we observed that short-term administration of antibiotics drastically reduced influenza vaccine-specific antibody production. In particular, antibiotic treatment diminished the frequency and activation status of multiple myeloid cell subsets in the draining lymph nodes at steady-state and following vaccination, with associated impairments in B and TFH cell responses.  Composition and function of gut microbiota communities can be rapidly altered through dietary changes. Therefore, the impact of potential prebiotic and probiotic nutritional interventions on the immune response to influenza vaccination and subsequent infection was assessed. No improvement in antibody responses to influenza vaccination was observed following the nutritional interventions studies. However, oral administration of a propolis formulation led to some improvement in viral control following infection.  Collectively, this investigation indicates that alterations in microbial-associated signals leads to severe impairments in cellular responses crucial to humoral immunity and subsequent vaccine-induced antibody production. Furthermore, by altering the gut microbiota through dietary interventions, there is potential to improve immune responses to vaccination.</p>

scholarly journals Ozone as Modulator of Resorption and Inflammatory Response in Extruded Nucleus Pulposus Herniation. Revising Concepts

2021 ◽  
Vol 22 (18) ◽  
pp. 9946
Author(s):  
María de los Ángeles Erario ◽  
Eduardo Croce ◽  
Maria Teresita Moviglia Brandolino ◽  
Gustavo Moviglia ◽  
Aníbal M. Grangeat
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Nucleus Pulposus ◽  
Disc Herniation ◽  
Medical Community ◽  
Spinal Diseases ◽  
Host Immune System ◽  
Ozone Therapy ◽  
Disc Disease ◽  
Inflammatory Phase

Ozone therapy has been used to treat disc herniation for more than four decades. There are several papers describing results and mechanism of action. However, it is very important to define the characteristics of extruded disc herniation. Although ozone therapy showed excellent results in the majority of spinal diseases, it is not yet fully accepted within the medical community. Perhaps it is partly due to the fact that, sometimes, indications are not appropriately made. The objective of our work is to explain the mechanisms of action of ozone therapy on the extruded disc herniation. Indeed, these mechanisms are quite different from those exerted by ozone on the protruded disc herniation and on the degenerative disc disease because the inflammatory response is very different between the various cases. Extruded disc herniation occurs when the nucleus squeezes through a weakness or tear in the annulus. Host immune system considers the nucleus material to be a foreign invader, which triggers an immune response and inflammation. We think ozone therapy modulates this immune response, activating macrophages, which produce phagocytosis of extruded nucleus pulposus. Ozone would also facilitate the passage from the M1 to M2 phase of macrophages, going from an inflammatory phase to a reparative phase. Further studies are needed to verify the switch of macrophages.

scholarly journals The Effects of a Single and a Series of Finnish Sauna Sessions on the Immune Response and Heat Shock Protein Levels in Trained and Untrained Men

2021 ◽  
Author(s):  
Pilch Wanda ◽  
Szarek Marta ◽  
Anna Piotrowska ◽  
Czerwińska-Ledwig Olga ◽  
Sadowska-Krępa Ewa ◽  
...  
Keyword(s):  
Immune Response ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Blood Cells ◽  
Immune Status ◽  
Ambient Temperatures ◽  
Protein Levels ◽  
Leukocyte Populations ◽  
The Impact ◽  
Healthy Males

Abstract The aim of the study was to investigate the effect of a Finnish sauna on the immune status markers. Healthy males (20–25 years old) were divided into gropes: the trained (T; n = 10), and the untrained group (N; n = 10). All participants were subjected to 10 baths (3X15-minute with cooled down for 2 minutes). Blood was collected before the 1st and 10th sauna bath, and 10 minutes after their completion. The levels of: cortisol, Il-6, HSP70, IgA, IgG, IgM and blood cells (WBC), leukocyte populations counts: neutrophils, lymphocytes, eosinophils, monocytes, and basophils were determined. No differences were found in the increase in rectal temperature, cortisol and Ig between groups. In response to the 1st sauna bath, a greater increase in HR was observed in the U group. After the last one, the HR value was lower in the T group. The impact on WBC, CD56+, CD3+, CD8+, IgA, IgG and IgM shows a differences in trained and untrained body responses. It seems that in trained people, the non-specific immune response increases, while in untrained, the specific one. Series of sauna baths can be a way of acclimation to high ambient temperatures for athletes and a solution to improve immune response.

Dog hepatocytes are key effector cells in the liver innate immune response to Leishmania infantum

Parasitology ◽  
2018 ◽  
Vol 146 (6) ◽  
pp. 753-764 ◽  
Author(s):  
A. Rodrigues ◽  
G. Alexandre-Pires ◽  
A. Valério-Bolas ◽  
D. Santos-Mateus ◽  
M. Rafael-Fernandes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Inflammatory Response ◽  
Innate Immune Response ◽  
Leishmania Infantum ◽  
Acute Phase Proteins ◽  
Cell Damage ◽  
Innate Immune ◽  
Canine Leishmaniasis ◽  
The Impact

AbstractHepatocytes constitute the majority of hepatic cells, and play a key role in controlling systemic innate immunity, via pattern-recognition receptors (PRRs) and by synthesizing complement and acute phase proteins. Leishmania infantum, a protozoan parasite that causes human and canine leishmaniasis, infects liver by establishing inside the Kupffer cells. The current study proposes the elucidation of the immune response generated by dog hepatocytes when exposed to L. infantum. Additionally, the impact of adding leishmanicidal compound, meglumine antimoniate (MgA), to parasite-exposed hepatocytes was also addressed. L. infantum presents a high tropism to hepatocytes, establishing strong membrane interactions. The possibility of L. infantum internalization by hepatocytes was raised, but not confirmed. Hepatocytes were able to recognize parasite presence, inducing PRRs [nucleotide oligomerization domain (NOD)1, NOD2 and Toll-like receptor (TLR)2] gene expression and generating a mix pro- and anti-inflammatory cytokine response. Reduction of cytochrome P 450s enzyme activity was also observed concomitant with the inflammatory response. Addition of MgA increased NOD2, TLR4 and interleukin 10 gene expression, indicating an immunomodulatory role for MgA. Hepatocytes seem to have a major role in coordinating liver's innate immune response against L. infantum infection, activating inflammatory mechanisms, but always balancing the inflammatory response in order to avoid cell damage.

scholarly journals Krueppel-Like Factor 4 Expression in Phagocytes Regulates Early Inflammatory Response and Disease Severity in Pneumococcal Pneumonia

2021 ◽  
Vol 12 ◽  
Author(s):  
Toni Herta ◽  
Aritra Bhattacharyya ◽  
Maciej Rosolowski ◽  
Claudia Conrad ◽  
Corinne Gurtner ◽  
...  
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Disease Severity ◽  
Pneumococcal Pneumonia ◽  
Myeloid Cells ◽  
Polymorphonuclear Neutrophils ◽  
Therapeutic Interventions ◽  
Intensive Care Unit Treatment ◽  
Inflammatory Immune Response ◽  
The Impact

The transcription factor Krueppel-like factor (KLF) 4 fosters the pro-inflammatory immune response in macrophages and polymorphonuclear neutrophils (PMNs) when stimulated with Streptococcus pneumoniae, the main causative pathogen of community-acquired pneumonia (CAP). Here, we investigated the impact of KLF4 expression in myeloid cells such as macrophages and PMNs on inflammatory response and disease severity in a pneumococcal pneumonia mouse model and in patients admitted to hospital with CAP. We found that mice with a myeloid-specific knockout of KLF4 mount an insufficient early immune response with reduced levels of pro-inflammatory cytokines and increased levels of the anti-inflammatory cytokine interleukin (IL) 10 in bronchoalveolar lavage fluid and plasma and an impaired bacterial clearance from the lungs 24 hours after infection with S. pneumoniae. This results in higher rates of bacteremia, increased lung tissue damage, more severe symptoms of infection and reduced survival. Higher KLF4 gene expression levels in the peripheral blood of patients with CAP at hospital admission correlate with a favourable clinical presentation (lower sequential organ failure assessment (SOFA) score), lower serum levels of IL-10 at admission, shorter hospital stay and lower mortality or requirement of intensive care unit treatment within 28 days after admission. Thus, KLF4 in myeloid cells such as macrophages and PMNs is an important regulator of the early pro-inflammatory immune response and, therefore, a potentially interesting target for therapeutic interventions in pneumococcal pneumonia.

Atopic dermatitis: new horizons of therapy

2019 ◽  
Vol 1 (7) ◽  
pp. 29-32 ◽  
Author(s):  
L. S. Kruglova ◽  
E. M. Gensler
Keyword(s):  
Blood Pressure ◽  
Immune Response ◽  
Allergic Rhinitis ◽  
Atopic Dermatitis ◽  
Targeted Therapy ◽  
Inflammatory Response ◽  
Bronchial Asthma ◽  
New Horizons ◽  
The Past

Over the past decades, the first breakthrough milestone in the treatment of severe forms of atopic dermatitis (AD) has been targeted therapy aimed at inhibiting IL-4 and IL-13. This was made possible thanks to advances in the understanding of the pathogenesis of AD, the driver of which is the Th2-type immune response, which also underlies such manifestations of atopy as bronchial asthma, allergic rhinitis, and polynosis. In the case of the Th2-type immune response, cytokines IL-4 and IL-13 are secreted, which are the main promoters of the inflammatory response in AD. Inhibition of IL-4 and IL-13 leads to the prevention of inflammation and is an effective approach to therapy. The use of therapy aimed at inhibition of cytokines allows you to effectively cope with the manifestations of severe and moderately severe blood pressure.

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