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.

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.

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 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 Hematopoietic progenitor kinase 1 (HPK1) is required for LFA-1–mediated neutrophil recruitment during the acute inflammatory response

Blood ◽  
2013 ◽  
Vol 121 (20) ◽  
pp. 4184-4194 ◽  
Author(s):  
Sascha M. Jakob ◽  
Robert Pick ◽  
Doris Brechtefeld ◽  
Claudia Nussbaum ◽  
Friedemann Kiefer ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammation ◽  
Neutrophil Recruitment ◽  
Acute Inflammatory Response ◽  
Hematopoietic Progenitor ◽  
Key Points

Key Points Hematopoietic progenitor kinase 1 (HPK1) regulates LFA-1 affinity and thereby controls adhesion and postadhesion functions of neutrophils. Hematopoietic progenitor kinase 1 (HPK1) is critically involved in neutrophil trafficking during acute inflammation.

scholarly journals Fibrin(ogen) mediates acute inflammatory responses to biomaterials.

1993 ◽  
Vol 178 (6) ◽  
pp. 2147-2156 ◽  
Author(s):  
L Tang ◽  
J W Eaton
Keyword(s):  
Inflammatory Response ◽  
Complement Activation ◽  
Acute Inflammation ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Material Surface ◽  
Acute Inflammatory Response ◽  
Host Proteins ◽  
Protein Layer ◽  
Large Numbers

Although "biocompatible" polymeric elastomers are generally nontoxic, nonimmunogenic, and chemically inert, implants made of these materials may trigger acute and chronic inflammatory responses. Early interactions between implants and inflammatory cells are probably mediated by a layer of host proteins on the material surface. To evaluate the importance of this protein layer, we studied acute inflammatory responses of mice to samples of polyester terephthalate film (PET) that were implanted intraperitoneally for short periods. Material preincubated with albumin is "passivated," accumulating very few adherent neutrophils or macrophages, whereas uncoated or plasma-coated PET attracts large numbers of phagocytes. Neither IgG adsorption nor surface complement activation is necessary for this acute inflammation; phagocyte accumulation on uncoated implants is normal in hypogammaglobulinemic mice and in severely hypocomplementemic mice. Rather, spontaneous adsorption of fibrinogen appears to be critical: (a) PET coated with serum or hypofibrinogenemic plasma attracts as few phagocytes as does albumin-coated material; (b) in contrast, PET preincubated with serum or hypofibrinogenemic plasma containing physiologic amounts of fibrinogen elicits "normal" phagocyte recruitment; (c) most importantly, hypofibrinogenemic mice do not mount an inflammatory response to implanted PET unless the material is coated with fibrinogen or the animals are injected with fibrinogen before implantation. Thus, spontaneous adsorption of fibrinogen appears to initiate the acute inflammatory response to an implanted polymer, suggesting an interesting nexus between two major iatrogenic effects of biomaterials: clotting and inflammation.

scholarly journals Ras guanine nucleotide exchange factor RasGRP1 promotes acute inflammatory response and restricts inflammation-contributed cancer cell growth

2021 ◽  
Author(s):  
Cong Wang ◽  
Xue Li ◽  
Changping Yu ◽  
Luoling Wang ◽  
Rilin Deng ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammation ◽  
Mrna Level ◽  
Acute Inflammatory Response ◽  
Guanine Nucleotide ◽  
Nucleotide Exchange ◽  
Cancer Cell Growth ◽  
Guanine Nucleotide Exchange ◽  
Nucleotide Exchange Factor

AbstractAcute inflammatory response needs to be tightly regulated for promoting the elimination of pathogens and preveting the risk of tumorigenesis, but the mechanism has not been fully elucidated. Here, we report that Ras guanine nucleotide releasing protein 1 (RasGRP1) plays a bifunctional regulator that promotes acute inflammation and inhibits inflammation-associated cancer. At the mRNA level, RasGRP1 strengthens the inflammatory response by functioning as a competing endogenous RNA to specifically promote IL-6 expression by sponging let-7a. In vivo overexpression of the RasGRP1 3’ untranslated region significantly aggravated lipopolysaccharide-induced systemic inflammation and dextran sulphate sodium-induced colitis in IL-6+/+ mice but not in IL-6-/- mice. At the protein level, RasGRP1 restricts the growth of inflammation-contributed cancer cells by impairing EGFR-SOS1-Ras-AKT signalling. Tumour patients with high RasGRP1 expression showed a better clinical outcome than those with low expression. Considering acute inflammation rarely leads to tumorigenesis, this work reveals that RasGRP1 is an essential bifunctional regulator for acute inflammatory response.

scholarly journals Electric Cell-Substrate Impedance Sensing To Monitor Viral Growth and Study Cellular Responses to Infection with Alphaherpesviruses in Real Time

mSphere ◽  
2017 ◽  
Vol 2 (2) ◽  
Author(s):  
Matthew R. Pennington ◽  
Gerlinde R. Van de Walle
Keyword(s):  
Real Time ◽  
Cellular Response ◽  
Cellular Responses ◽  
Cellular Damage ◽  
Impedance Sensing ◽  
Novel Technologies ◽  
Antiviral Therapies ◽  
Mucosal Surfaces ◽  
Cell Substrate ◽  
Hsv 1

ABSTRACT Alphaherpesviruses, including those that commonly infect humans, such as HSV-1 and HSV-2, typically infect and cause cellular damage to epithelial cells at mucosal surfaces, leading to disease. The development of novel technologies to study the cellular responses to infection may allow a more complete understanding of virus replication and the creation of novel antiviral therapies. This study demonstrates the use of ECIS to study various aspects of herpesvirus biology, with a specific focus on changes in cellular morphology as a result of infection. We conclude that ECIS represents a valuable new tool with which to study alphaherpesvirus infections in real time and in an objective and reproducible manner. Electric cell-substrate impedance sensing (ECIS) measures changes in an electrical circuit formed in a culture dish. As cells grow over a gold electrode, they block the flow of electricity and this is read as an increase in electrical impedance in the circuit. ECIS has previously been used in a variety of applications to study cell growth, migration, and behavior in response to stimuli in real time and without the need for cellular labels. Here, we demonstrate that ECIS is also a valuable tool with which to study infection by alphaherpesviruses. To this end, we used ECIS to study the kinetics of cells infected with felid herpesvirus type 1 (FHV-1), a close relative of the human alphaherpesviruses herpes simplex virus 1 (HSV-1) and HSV-2, and compared the results to those obtained with conventional infectivity assays. First, we demonstrated that ECIS can easily distinguish between wells of cells infected with different amounts of FHV-1 and provides information about the cellular response to infection. Second, we found ECIS useful in identifying differences between the replication kinetics of recombinant DsRed Express2-labeled FHV-1, created via CRISPR/Cas9 genome engineering, and wild-type FHV-1. Finally, we demonstrated that ECIS can accurately determine the half-maximal effective concentration of antivirals. Collectively, our data show that ECIS, in conjunction with current methodologies, is a powerful tool that can be used to monitor viral growth and study the cellular response to alphaherpesvirus infection. IMPORTANCE Alphaherpesviruses, including those that commonly infect humans, such as HSV-1 and HSV-2, typically infect and cause cellular damage to epithelial cells at mucosal surfaces, leading to disease. The development of novel technologies to study the cellular responses to infection may allow a more complete understanding of virus replication and the creation of novel antiviral therapies. This study demonstrates the use of ECIS to study various aspects of herpesvirus biology, with a specific focus on changes in cellular morphology as a result of infection. We conclude that ECIS represents a valuable new tool with which to study alphaherpesvirus infections in real time and in an objective and reproducible manner.

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