scholarly journals Resolution in an ‘over-inflamed’ era

2017 ◽  
Vol 39 (4) ◽  
pp. 4-7
Author(s):  
Mauro Perretti ◽  
Trinidad MonteroMelendez
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammation ◽  
Pharmacological Intervention ◽  
Acute Inflammatory Response ◽  
Moderate Pain ◽  
Antiinflammatory Drugs ◽  
Protective Mechanisms ◽  
Life Saving ◽  
Common Perception

Unlike other pathologies, inflammation is a condition that all individuals experience in their lives. Toothache, sunburn, a twisted ankle or cutting your hand while slicing bread, they all evoke what we call an acute inflammatory response. This type of response normally displays the cardinal signs of inflammation originally described by Aulus Cornelius Celsus: redness, swelling, heat and pain. Acute inflammation does not normally require any therapeutic intervention other than perhaps a painkiller, as it resolves, with the damage being naturally repaired. Inflammation is also at the root of many other diseases in a more ‘silent’ way as the cardinal signs of inflammation are not so evident. It is now appreciated that inflammatory mechanisms and processes contribute to the pathogenesis of a number of conditions including obesity, cancer, rheumatoid arthritis, atherosclerosis and diabetes. These are examples of chronic inflammation, arising either by the persistence of the injurious element causing it, or by a defect in our endogenous natural protective mechanisms grouped under the terminology of pro-resolving mechanisms. A common perception, likely to have been enhanced by the large variety of nonprescription antiinflammatory drugs available to anyone experiencing mild-to-moderate pain, is that inflammation is something harmful that must be stopped. In the next sections we will discuss on the protective life-saving role of the inflammatory response, the existence of our own body's resolutive mechanisms that regulate it and on when and why we need a pharmacological intervention to treat inflammation.

scholarly journals Acute inflammation and hematological response in Nile tilapia fed supplemented diet with natural extracts of propolis and Aloe barbadensis

2015 ◽  
Vol 75 (2) ◽  
pp. 491-496 ◽  
Author(s):  
G. Dotta ◽  
J. Ledic-Neto ◽  
ELT. Gonçalves ◽  
A. Brum ◽  
M. Maraschin ◽  
...  
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Nile Tilapia ◽  
Acute Inflammation ◽  
Leukocyte Count ◽  
Acute Inflammatory Response ◽  
Swim Bladder ◽  
Aloe Barbadensis ◽  
Natural Extracts ◽  
Number Of Cells

This study evaluated the acute inflammatory response induced by carrageenin in the swim bladder of Nile tilapia supplemented with the mixture of natural extracts of propolis and Aloe barbadensis (1:1) at a concentration of 0.5%, 1% and 2% in diet during 15 days. Thirty-six fish were distributed into four treatments with three replicates: fish supplemented with 0.5% of admix of extracts of propolis and Aloe (1:1) injected with 500 µg carrageenin; fish supplemented with 1% of admix of extracts of propolis and Aloe (1:1) injected with 500 µg carrageenin; fish supplemented with 2% of admix of extracts of propolis and Aloe (1:1), injected with 500 µg carrageenin and unsupplemented fish injected with 500 µg carrageenin. Six hours after injection, samples of blood and exudate from the swim bladder of fish were collected. It was observed an increase in the leukocyte count in the swim bladder exudate of fish supplemented with extracts of propolis and Aloe injected with carrageenin. The most frequent cells were macrophages followed by granular leukocytes, thrombocytes and lymphocytes. Supplementation with propolis and Aloe to 0.5% caused a significant increase in the number of cells on the inflammatory focus mainly macrophages, cells responsible for the phagocytic activity in tissues, agent of innate fish immune response.

Role of miR-146a in regulation of the acute inflammatory response to monosodium urate crystals

2015 ◽  
Vol 74 (4) ◽  
pp. 786-790 ◽  
Author(s):  
Nicola Dalbeth ◽  
Bregina Pool ◽  
Odette M Shaw ◽  
Jacquie L Harper ◽  
Paul Tan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Monosodium Urate ◽  
Monosodium Urate Crystals ◽  
Urate Crystals

scholarly journals Computational modelling of the inflammatory response in trauma, sepsis and wound healing: implications for modelling resilience

2014 ◽  
Vol 4 (5) ◽  
pp. 20140004 ◽  
Author(s):  
Yoram Vodovotz
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammation ◽  
Computational Modelling ◽  
Data Driven ◽  
Patient Specific ◽  
Cell Tissue ◽  
Organ Systems ◽  
Forward Process

Resilience refers to the ability to recover from illness or adversity. At the cell, tissue, organ and whole-organism levels, the response to perturbations such as infections and injury involves the acute inflammatory response, which in turn is connected to and controlled by changes in physiology across all organ systems. When coordinated properly, inflammation can lead to the clearance of infection and healing of damaged tissues. However, when either overly or insufficiently robust, inflammation can drive further cell stress, tissue damage, organ dysfunction and death through a feed-forward process of inflammation → damage → inflammation. To address this complexity, we have obtained extensive datasets regarding the dynamics of inflammation in cells, animals and patients, and created data-driven and mechanistic computational simulations of inflammation and its recursive effects on tissue, organ and whole-organism (patho)physiology. Through this approach, we have discerned key regulatory mechanisms, recapitulated in silico key features of clinical trials for acute inflammation and captured diverse, patient-specific outcomes. These insights may allow for the determination of individual-specific tolerances to illness and adversity, thereby defining the role of inflammation in resilience.

The cytokine midkine supports neutrophil trafficking during acute inflammation by promoting adhesion via β2 integrins (CD11/CD18)

Blood ◽  
2014 ◽  
Vol 123 (12) ◽  
pp. 1887-1896 ◽  
Author(s):  
Ludwig T. Weckbach ◽  
Anita Gola ◽  
Michael Winkelmann ◽  
Sascha M. Jakob ◽  
Leopold Groesser ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammation ◽  
Acute Inflammatory Response ◽  
Key Points ◽  
Β2 Integrins

Key Points MK promotes PMN recruitment during the acute inflammatory response. MK and β2 integrins (CD11/CD18) cooperate in mediating PMN adhesion during acute inflammation.

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.

The role of TLR2 in the acute inflammatory response induced by Bothrops atrox snake venom

Toxicon ◽  
2016 ◽  
Vol 118 ◽  
pp. 121-128 ◽  
Author(s):  
Vanessa Moreira ◽  
Catarina Teixeira ◽  
Henrique Borges da Silva ◽  
Maria Regina D'Império Lima ◽  
Maria Cristina Dos-Santos
Keyword(s):  
Inflammatory Response ◽  
Snake Venom ◽  
Acute Inflammatory Response ◽  
Bothrops Atrox

scholarly journals Rapid dendritic cell recruitment is a hallmark of the acute inflammatory response at mucosal surfaces.

1994 ◽  
Vol 179 (4) ◽  
pp. 1331-1336 ◽  
Author(s):  
A S McWilliam ◽  
D Nelson ◽  
J A Thomas ◽  
P G Holt
Keyword(s):  
Dendritic Cell ◽  
Inflammatory Response ◽  
Cellular Response ◽  
Acute Inflammation ◽  
Protective Mechanism ◽  
Acute Inflammatory Response ◽  
Normal Epithelium ◽  
General Applicability ◽  
Regional Lymph Nodes ◽  
Mucosal Surfaces

Immunohistochemical analysis of challenge sites such as skin and the peritoneal cavity has identified neutrophils as virtually the sole cellular participants in acute bacterial inflammation, peak influx occurring 24-48 h in advance of mononuclear cell populations associated with adaptive immunity. This study challenges the general applicability of this paradigm. We demonstrate here that the earliest detectable cellular response after inhalation of Moraxella catarrhalis organisms is the recruitment of putative class II major histocompatibility complex-bearing dendritic cell (DC) precursors into the airway epithelium, the initial wave arriving in advance of the neutrophil influx. Unlike the neutrophils which rapidly transit into the airway lumen, the DC precursors remain within the epithelium during the acute inflammatory response where they differentiate, and develop the dendriform morphology typical of resident DC found in the normal epithelium. During the ensuing 48-h period, these cells then migrate to the regional lymph nodes. No comparable DC response was observed after epidermal or intraperitoneal challenge, and it may be that mucosal surfaces are unique in their requirement for rapid DC responses during acute inflammation. We hypothesize that the role of the DC influx during acute inflammation may be surveillance for opportunistic viruses, and that this covert protective mechanism is operative at a restricted number of mucosal tissue sites.

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