Cell signaling underlying the pathophysiology of pneumonia

2006 ◽  
Vol 291 (3) ◽  
pp. L297-L300 ◽  
Author(s):  
Alice S. Prince ◽  
Joseph P. Mizgerd ◽  
Jeanine Wiener-Kronish ◽  
Jahar Bhattacharya
Keyword(s):  
Cell Signaling ◽  
Bacterial Virulence ◽  
Innate Immune ◽  
Tnf Receptor ◽  
Cytokine Induction ◽  
Signaling Mechanisms ◽  
Innate Immune Mechanism ◽  
Specific Receptors ◽  
Alveolar Capillary

The symposium addressed the burgeoning interest in fundamental mechanisms underlying the onset of pneumonia. Bacteria exploit the lung's innate immune mechanism, resulting in pathophysiological cell signaling. As a consequence inflammation develops, leading to pneumonia. New mechanisms have been identified by which bacteria or bacterial products in the airway induce cross-compartmental signaling that leads to inflammatory consequences. The speakers addressed activation of the transcription factor, NF-κB occurring as a consequence of bacterial interactions with specific receptors, such as the Toll-like receptors and the TNF receptor 1 (Prince), or as a consequence of cytokine induction (Mizgerd). Also considered were mechanisms of bacterial virulence in the clinical setting (Wiener-Kronish) and the role of alveolar-capillary signaling mechanisms in the initiation of lung inflammation.

scholarly journals THE ROLE OF SYNAPSIN I IN INTRACELLULAR SIGNALING MECHANISMS UNDERLIES EXERCISE-INDUCED IMPROVEMENT IN SOCIAL MEMORY: A SYSTEMATIC REVIEW

2017 ◽  
Vol 10 (9) ◽  
pp. 88
Author(s):  
Ria Margiana ◽  
Akmal Primadian Suprapto
Keyword(s):  
Cell Signaling ◽  
Intracellular Signaling ◽  
Laboratory Experiments ◽  
Biological Function ◽  
Social Memory ◽  
Synapsin I ◽  
Signaling Mechanism ◽  
Signaling Mechanisms ◽  
Exercise Induced

  Objective: Intracellular signaling mechanism is an important biological function, as scholars continue to seek new ways of improving social memory. Researchers have conducted several studies on the role of synapsin I in intracellular signaling mechanism. This study assessed the empirical evidence that shows the role of synapsin I in intracellular signaling mechanism with the aim of achieving exercise-induced improvement in social memory.Methods: Nine previously conducted researches were reviewed in this paper. The included studies were controlled laboratory experiments involving mice as the subjects.Results: Although the studies included were done in different timelines, the researchers agreed in unison that synapsin I plays a crucial role in cell signaling. The outcome of the practical studies was vital in understanding function and physiology of human cells, which is fundamental in science and human anatomy.Conclusion: In particular, the findings shows how exercise can improve social memory by triggering the intracellular signaling mechanism. The limited number of studies addressing the topic of intracellular cell signaling suggests that more study is needed to provide more evidence on the issue.

scholarly journals Cytokinin Sensing in Bacteria

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 186
Author(s):  
Samar Kabbara ◽  
Baptiste Bidon ◽  
Jaafar Kilani ◽  
Marwan Osman ◽  
Monzer Hamze ◽  
...  
Keyword(s):  
Cell Signaling ◽  
Host Plant ◽  
Plant Hormones ◽  
Cellular Signaling ◽  
Phytopathogenic Bacteria ◽  
Signaling Mechanisms ◽  
Plant Chemicals ◽  
First Time ◽  
Broad Role

Although it has long been known that bacteria detect and react to plant chemicals to establish an interaction, the cellular signaling mechanisms involved in these perception processes have hitherto remained obscure. Some exciting recent advances in the field have described, for the first time, how some phytopathogenic bacteria sense the host plant hormones, cytokinins. These discoveries not only advance the understanding of cell signaling circuitries engaged in cytokinin sensing in non-plant organisms, but also increase our knowledge of the broad role of these ancient molecules in regulating intra- and interspecific communications.

scholarly journals Role of Specialized Pro-Resolving Mediators in Modifying Host Defense and Decreasing Bacterial Virulence

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6970
Author(s):  
Julianne M. Thornton ◽  
Kingsley Yin
Keyword(s):  
Host Defense ◽  
Host Response ◽  
Tissue Repair ◽  
Defense Mechanisms ◽  
Neutrophil Migration ◽  
Bacterial Virulence ◽  
Innate Immune ◽  
Bioactive Fatty Acids ◽  
Insight Into

Bacterial infection activates the innate immune system as part of the host’s defense against invading pathogens. Host response to bacterial pathogens includes leukocyte activation, inflammatory mediator release, phagocytosis, and killing of bacteria. An appropriate host response requires resolution. The resolution phase involves attenuation of neutrophil migration, neutrophil apoptosis, macrophage recruitment, increased phagocytosis, efferocytosis of apoptotic neutrophils, and tissue repair. Specialized Pro-resolving Mediators (SPMs) are bioactive fatty acids that were shown to be highly effective in promoting resolution of infectious inflammation and survival in several models of infection. In this review, we provide insight into the role of SPMs in active host defense mechanisms for bacterial clearance including a new mechanism of action in which an SPM acts directly to reduce bacterial virulence.

scholarly journals Proteomic Analysis of Low-Grade, Early-Stage Endometrial Carcinoma Reveals New Dysregulated Pathways Associated with Cell Death and Cell Signaling

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 794
Author(s):  
Álvaro López-Janeiro ◽  
Ignacio Ruz-Caracuel ◽  
Jorge L. Ramón-Patino ◽  
Vivian De Los Ríos ◽  
María Villalba Esparza ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Cell Signaling ◽  
Endometrial Carcinoma ◽  
Proteomic Analysis ◽  
Early Stage ◽  
Innate Immune ◽  
Future Research ◽  
Low Grade

Low-grade, early-stage endometrial carcinoma (EC) is the most frequent malignant tumor of the uterine corpus. However, the molecular alterations that underlie these tumors are far from being fully understood. The purpose of this study is to describe dysregulated molecular pathways from EC patients. Sixteen samples of tumor tissue and paired healthy controls were collected and both were subjected to mass spectrometry (MS)/MS proteomic analysis. Gene ontology and pathway analysis was performed to discover dysregulated pathways and/or proteins using different databases and bioinformatic tools. Dysregulated pathways were cross-validated in an independent external cohort. Cell signaling, immune response, and cell death-associated pathways were robustly identified. The SLIT/ROBO signaling pathway demonstrated dysregulation at the proteomic and transcriptomic level. Necroptosis and ferroptosis were cell death-associated processes aberrantly regulated, in addition to apoptosis. Immune response-associated pathways showed a dominance of innate immune responses. Tumor immune infiltrates measured by immunofluorescence demonstrated diverse lymphoid and myeloid populations. Our results suggest a role of SLIT/ROBO, necroptosis, and ferroptosis, as well as a prominent role of innate immune response in low-grade, early-stage EC. These results could guide future research in this group of tumors.

scholarly journals Innate Immune Mechanism of Hemarthrosis in Hemophilia-a Mice

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 1043-1043
Author(s):  
Tomasz W. Kaminski ◽  
Egemen Tutuncuoglu ◽  
Margaret V. Ragni ◽  
Mark T Gladwin ◽  
Prithu Sundd
Keyword(s):  
Research Funding ◽  
Hemophilia A ◽  
Cartilage Degeneration ◽  
Advisory Board ◽  
Innate Immune ◽  
Sterile Inflammation ◽  
Innate Immune Mechanism ◽  
And Cartilage ◽  
Bleeding Severity

Hemarthrosis is a chronic arthropathy responsible for irreversible joint damage, disability, and acute joint pain in hemophilia patients. Hemarthrosis is caused by spontaneous or traumatic bleeding into joints, which when recurrent, leads to synovial inflammation and cartilage degeneration. Although release of erythrocyte-derived damage associated molecular pattern molecules (eDAMPs) is believed to promote sterile inflammation in the synovium, the innate immune mechanism of hemarthrosis remains poorly understood and the current therapy is limited to factor replacement and pain management. Here, we use factor 8 total knock-out (F8TKO) hemophilia A mice (C57BL/6J background) that manifest a complete deletion of the F8 coding region, expressing no detectable F8 mRNA and exhibiting a severe hemophilia phenotype. Right knee joint capsules of F8TKO mice were punctured with a 30-g needle below the patella between the anterior portions of the femur and tibia, followed by assessment of bleeding severity score and histological analysis one-week post injury. Intravital multiphoton excitation fluorescence microscopy of injured synovium was performed to assess the role of thrombo-inflammatory events in promoting hemarthrosis. Neutrophil, platelets, and blood vessels were visualized by intravenous administration of fluorescent anti-Ly6G mAb, anti-CD49b mAb, and dextran, respectively. Protein and mRNA levels of proinflammatory cytokines were measured in plasma, joint, synovium, and cartilage tissue using Real-Time PCR and ELISA, respectively. F8TKO but not wild-type (WT) control (C57BL/6J) mice manifested unresolved joint bleeding, cartilage degeneration and synovitis leading to impaired mobility and high bleeding severity scores. Significantly more recruitment of neutrophils and neutrophil-platelet aggregates as well as elevated IL-1b levels were observed in the synovium of F8TKO compared to WT mice. These results are the first to suggest that sterile inflammation contributing to hemarthrosis in hemophilia involves enhanced neutrophil-platelet recruitment to the synovium. Currently, experiments are underway to identify the role of eDAMPs (heme and hemoglobin) mediated activation of TLR4 and inflammasome pathway in promoting IL-1b generation, neutrophil-platelet aggregation, and progression of joint injury in F8TKO mice Disclosures Ragni: OPKO: Research Funding; Sangamo: Research Funding; Shire/Takeda: Other: Advisory Board, Research Funding; Spark Therapeutics: Other: Advisory Board, Research Funding; Alnylam/Sanofi: Other: Advisory Board, Research Funding; BioMarin: Other: Advisory Board, Research Funding; Bioverativ/Sanofi: Other: Advisory Board, Research Funding. Gladwin:Globin Solutions, Inc: Patents & Royalties: Provisional patents for the use of recombinant neuroglobin and heme-based molecules as antidotes for CO poisoning; Bayer Pharmaceuticals: Other: Co-investigator; United Therapeutics: Patents & Royalties: Co-inventor on an NIH government patent for the use of nitrite salts in cardiovascular diseases .

scholarly journals Metabolite Transporters as Regulators of Immunity

Metabolites ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 418
Author(s):  
Hauke J. Weiss ◽  
Stefano Angiari
Keyword(s):  
Intracellular Signaling ◽  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Signaling Cascades ◽  
Effector Functions ◽  
Immunological Responses ◽  
The Face ◽  
Specific Receptors

In the past decade, the rise of immunometabolism has fundamentally reshaped the face of immunology. As the functions and properties of many (immuno)metabolites have now been well described, their exchange among cells and their environment have only recently sparked the interest of immunologists. While many metabolites bind specific receptors to induce signaling cascades, some are actively exchanged between cells to communicate, or induce metabolic reprograming. In this review, we give an overview about how active metabolite transport impacts immune cell function and shapes immunological responses. We present some examples of how specific transporters feed into metabolic pathways and initiate intracellular signaling events in immune cells. In particular, we focus on the role of metabolite transporters in the activation and effector functions of T cells and macrophages, as prototype adaptive and innate immune cell populations.

scholarly journals Interleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Heike C. Hawerkamp ◽  
Lasse van Geelen ◽  
Jan Korte ◽  
Jeremy Di Domizio ◽  
Marc Swidergall ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
T Helper ◽  
T Helper 1 ◽  
Cytokine Induction ◽  
Tnf Α ◽  
Necrosis Factor

Abstract Tuberculosis-causing Mycobacterium tuberculosis (Mtb) is transmitted via airborne droplets followed by a primary infection of macrophages and dendritic cells. During the activation of host defence mechanisms also neutrophils and T helper 1 (TH1) and TH17 cells are recruited to the site of infection. The TH17 cell-derived interleukin (IL)-17 in turn induces the cathelicidin LL37 which shows direct antimycobacterial effects. Here, we investigated the role of IL-26, a TH1- and TH17-associated cytokine that exhibits antimicrobial activity. We found that both IL-26 mRNA and protein are strongly increased in tuberculous lymph nodes. Furthermore, IL-26 is able to directly kill Mtb and decrease the infection rate in macrophages. Binding of IL-26 to lipoarabinomannan might be one important mechanism in extracellular killing of Mtb. Macrophages and dendritic cells respond to IL-26 with secretion of tumor necrosis factor (TNF)-α and chemokines such as CCL20, CXCL2 and CXCL8. In dendritic cells but not in macrophages cytokine induction by IL-26 is partly mediated via Toll like receptor (TLR) 2. Taken together, IL-26 strengthens the defense against Mtb in two ways: firstly, directly due to its antimycobacterial properties and secondly indirectly by activating innate immune mechanisms.

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