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Neutrophil Infiltration

Neutrophil Infiltration refers to the migration and accumulation of neutrophils, a type of white blood cell, to a specific site or tissue in response to an inflammatory stimulus.
This process plays a crucial role in the innate immune response, helping to clear infections and facilitate tissue repair.
Neutrophil Infiltration can be observed in a variety of pathological conditions, including infections, autoimmune disorders, and cancer.
Undestanding the underlying mechanisms and modulation of Neutrophil Infiltration is an active area of research with important implications for developing targeted therapies.

Most cited protocols related to «Neutrophil Infiltration»

The model presented here is an extension of a previous ABM that captured cellular interactions leading to granuloma formation during infection with Mtb (38 (link)). The model is considered hybrid since we incorporated both discrete entities (cells) and continuous entities (chemokines, TNF and Mtb) that interact simultaneously. ABMs are developed based on four considerations: an environment, agents that reside there, the rules that describe the agents and their interactions, and the timescales on which events are defined.
The environment represents a 2 mm × 2 mm section of lung parenchyma as a 100 × 100 square 2-dimensional lattice with individual micro-compartments scaled to the approximate size of a single macrophage: 20 μm in diameter (39 (link)). Discrete agents move on the lattice and respond to their environment based on rules reflecting known biological activities. Bacteria and effector molecules can reside anywhere on the lattice and undergo diffusion when appropriate.
Caseation represents inflammation of, and damage to, the lung parenchyma from macrophage cell death. We note a change of terminology to “caseation” from “necrosis” in previous work (38 (link)), as strict necrosis within the granuloma is now believed to be caused by substantial neutrophil infiltration and death, while caseation is likely initiated by macrophage death (unpublished data, JLF). In the ABM, caseation is defined to occur when a threshold number of activated or infected macrophage deaths take place in a micro-compartment. A final environmental feature is designation of spaces as vascular sources.
We include two types of discrete agents in the model: macrophages and T cells. As previously (20 (link), 38 (link)), macrophage agents are either resting (Mr, uninfected), infected (Mi; have taken up bacteria), chronically infected (Mci; are unable to clear their intracellular bacterial load), or activated (Ma; can effectively kill bacteria). In contrast to our previous study (38 (link)), where a single T cell class captured all cell behaviors, here we represent three distinct T cell subpopulations based on function: the Tγ class captures CD4+ and CD8+ pro-inflammatory T cells; Tc represent cytotoxic T cells; and Treg represent regulatory T cells. In this representation, all T cells in a particular class have identical function; this is simpler than in vivo, but we capture enough detail in this representation for a qualitative representation of known T cell effects.
In addition to the discrete entities, extracellular bacteria, diffusing effector molecules (CCL2, CCL5, CXCL9/10/11 and TNF) are agents (concentrations) that are tracked continuously over time. The chemokine model used here is a simplification that was chosen to include a ligand for each key chemokine receptor, while minimizing the distinct chemokine classes represented to save on computation.
Cells respond to signals in the surrounding environment according to rules that represent known activities in vivo. During simulations, each agent responds depending on its state. Examples of rules include uptake of bacteria, macrophage activation by T cells, secretion of cytokines and chemokines, etc. For a full list of rules, see Supplement 1.
Publication 2009
As-A 2 Bacteria Biopharmaceuticals Blood Vessel CCL2 protein, human CCL5 protein, human CD8-Positive T-Lymphocytes Cell Communication Cells Chemokine Chemokine Receptor CXCL9 protein, human Cytokine Cytotoxic T-Lymphocytes Dietary Supplements Granuloma Hybrids Infection Inflammation Ligands Lung Macrophage Macrophage Activation Macrophages, Alveolar Necrosis Neutrophil Infiltration Population Group Protoplasm Regulatory T-Lymphocytes secretion T-Lymphocyte
Animals were anesthetized and perfused transcardially with PBS, followed by zinc formalin. Lungs were fixed in zinc formalin. For routine histology, tissue sections (~4 μm each) were stained with hematoxylin and eosin. The following criteria were used for scoring edema, hyaline membrane formation and necrotic cellular debris: 0- none; 1-uncommon detection in <5% lung fields (200x); 2- detectable in up to 33% of lung fields; 3- detectable in up to 33-66% of lung fields; 4- detectable in >66% of lung fields. For scoring neutrophil infiltration: 0- within normal limits; 1-scattered PMNs sequestered in septa; 2- #1 plus solitary PMNs extravasated in airspaces; 3-#2 plus small aggregates in vessel and airspaces. For scoring mononuclear infiltrates, thrombosis and hemorrhage: 0-none; 1- uncommon detection in <5% lung fields (200x); 2- detectable in up to 33% of lung fields; 3- detectable in up to 33-66% of lung fields; 4- detectable in >66% of lung fields.
For SARS-CoV-2 antigen detection, slides were incubated with blocking reagent (10% normal goat serum x 30 minutes) followed by rabbit monoclonal antibody against SARS-CoV2 N protein (1:20,000 dilution x 60 minutes, #40143-R019, Sino Biological US Inc., Wayne, PA, USA), then incubated with Rabbit Envision (Dako) and diaminobenzidine (Dako) as chromogen. Tissues were examined and scored in a post-examination method of masking by a boarded experimental pathologist32 . Ordinal scores for lesion parameters were assigned using the following tiers: 0 = within expected limits; 1 - uncommon, <5%; 2 - detectable in 5-33%; 3 - detectable in 34-66% and 4 - detectable in >66% of lung fields (200x objective magnification).
Publication 2020
1-(1-pyrrolidinylmethyl)-2-naphthol Animals Antigens azo rubin S Biopharmaceuticals Blood Vessel Cells Edema Eosin Formalin Goat Hemorrhage Hyalin Substance isononanoyl oxybenzene sulfonate Lung Monoclonal Antibodies Necrosis Neutrophil Infiltration nucleoprotein, Measles virus Rabbits SARS-CoV-2 Serum Severe Acute Respiratory Syndrome Technique, Dilution Thrombosis Tissue, Membrane Tissues Zinc
Preterm labor was diagnosed by the presence of at least two regular uterine contractions every 10 min associated with cervical changes in patients with a gestational age between 20 and 36 6/7 weeks. Acute histologic chorioamnionitis was diagnosed according to previously described criteria [148 (link),149 (link)]. Funisitis was diagnosed when neutrophil infiltration was detected into the umbilical vessel walls or Wharton’s jelly using previously reported criteria [150–152 (link)]. Intra-amniotic inflammation was diagnosed when the AF IL-6 concentration was ≥2600 pg/ml (≥2.6 ng/ml), as determined by ELISA [46 (link),87 (link),117 (link),153 (link)]. MIAC was defined according to the results of AF culture. Intra-amniotic infection was defined as a combination of MIAC with intra-amniotic inflammation.
Publication 2015
Amnion Blood Vessel Chorioamnionitis Enzyme-Linked Immunosorbent Assay Funisitis Gestational Age Infection Inflammation Neck Neutrophil Infiltration Patients Premature Obstetric Labor Umbilicus Uterine Contraction Wharton Jelly
The lung tissue was fixed in 10% formalin and then embedded in paraffin. Later, the tissue blocks were cut into 5-μm sections, placed onto glass slides and stained with hematoxylin and eosin (H&E), dehydrated, and mounted. Morphologic examinations in these tissues were evaluated by light microscopy in a blinded fashion. To examine the extent of lung injury, we considered its five pathological features, such as (i) presence of exudates, (ii) hyperemia/congestion, (iii) intra-alveolar hemorrhage/debris, (iv) cellular infiltration, and (v) cellular hyperplasia. The severity of each of these pathological features was evaluated by a score indicating 0 as absent/none, 1 as mild, 2 as to show moderate, and finally 3 for severe injury. Compilations of these values obtained from individual pathological features represent the lung injury score [7 (link),32 (link)].
Gr-1 is a 21- to 25-kDa myeloid differentiation protein and also known as Ly-6G/Ly-6C. This myeloid differentiation antigen is a glycosylphosphatidylinositol (GPI)-linked protein expressed on granulocytes and macrophages. In the bone marrow, expression levels of Gr-1 directly correlate with granulocyte differentiation and maturation [33 (link)]. To examine neutrophil infiltration in lungs we performed immunohistochemistry using anti-Gr-1 Ab (BioLegend, San Diego, CA, USA; Catalog No.: 108413) as described previously [7 (link)]. In brief, 10% formalin-fixed, paraffin-embedded lung tissues were dewaxed in xylene and rehydrated in a graded series of ethanol. The slides were heated in 0.92% citric acid buffer (Vector Laboratories, Burlingame, CA) at 95°C for 30 min. After cooling to room temperature, the slides were incubated with 2% H2O2 in 60% methanol and blocked in 2% normal rabbit serum/Tris-buffered saline. Anti-Gr-1 antibody (BioLegend) was then applied and incubated overnight. Vectastain ABC reagent and DAB kit (Vector Laboratories) were used to detect the immunohistochemical reaction. Slides were counterstained with 4′, 6-diamidino-2-phenylindole and examined under a phase contrast light microscope (Eclipse Ti-S; Nikon, Melville, NY, USA). Gr-1-positive staining cells were counted in 10 visual fields/section at × 200 magnification, and averaged number was calculated.
Publication 2015
Antibodies, Anti-Idiotypic Bone Marrow Buffers Cells Citric Acid Cloning Vectors Differentiation Antigens Eosin Ethanol Exudate Formalin Glycosylphosphatidylinositols Granulocyte Hemorrhage Hyperemia Hyperplasia Immunohistochemistry Injuries Light Microscopy link protein Lung Lung Injury Macrophage Methanol Microscopy, Phase-Contrast Neutrophil Infiltration Normal Saline Paraffin Paraffin Embedding Peroxide, Hydrogen Physical Examination Proteins Rabbits Serum Tissues Xylene
Gestational age was determined by the last menstrual period and confirmed by ultrasound examination, or by ultrasound examination alone if the sonographic determination of gestational age was not consistent with menstrual dating. Preterm PROM was diagnosed using a sterile speculum examination with documentation of pooling of AF in the vagina in association with a positive nitrazine test and/or positive ferning tests when necessary. Clinical chorioamnionitis was diagnosed when maternal temperature was ≥37.8 °C and two or more of the following criteria were present: uterine tenderness, malodorous vaginal discharge, maternal leukocytosis (>15,000 cells/mm3), maternal tachycardia (>100 beats/min), or fetal tachycardia (>160 beats/min) [59 (link)–61 (link)]. The diagnosis of acute histologic chorioamnionitis was made on the basis of the presence of acute inflammatory changes in the examination of the extra-placental chorioamniotic membrane roll and/or chorionic plate of the placenta using criteria previously described [62 (link),63 (link)]. Funisitis was diagnosed when neutrophil infiltration was detected in the umbilical vessel walls or Wharton’s jelly using criteria previously reported [64 (link),65 (link)]. Intra-amniotic inflammation was diagnosed when AF IL-6 determined ELISA concentration was ≥2,600 pg/ml [36 (link),39 (link),46 (link)]. MIAC was defined according to the results of AF culture. Intra-amniotic infection was defined as a combination of MIAC with intra-amniotic inflammation.
Publication 2015
Amnion Blood Vessel Cells Chorioamnionitis Chorion Enzyme-Linked Immunosorbent Assay Fern Test Fetus Funisitis Gestational Age Infection Inflammation Leukocytosis Menstruation Mothers Neutrophil Infiltration Placenta Speculum Sterility, Reproductive Tissue, Membrane Ultrasonography Umbilicus Uterus Vagina Wharton Jelly

Most recents protocols related to «Neutrophil Infiltration»

For histological analyses, the right lung of each mouse was perfused with PBS, inflated with 10% buffered formalin (ThermoFisher Scientific, Waltham, MA, USA), and stored at 4 °C until processing. Slices from each lobe of the right lung were trimmed and sent to the UAB Comparative Pathology Laboratory to be processed, paraffin embedded, sectioned onto slides and stained with hematoxylin and eosin (H and E). Semiquantitative grading of histopathological changes of all lung sections was performed by a board-certified surgical pathologist (L.N.). Severity of lung tissue injury included alveolar, peribronchial inflammation, perivascular neutrophil infiltration, pleuritis and tissue necrosis. Severity of tissue damage from all lung lobes was graded. Grade 0 showed no neutrophil infiltrate in lung tissue; grade 1 showed rare neutrophils in the alveolar, peribronchial or perivascular tissue; grade 2 showed dense neutrophil infiltrate within the alveolar spaces with no injury to alveolar tissue; grade 3 showed dense neutrophil infiltrate within the alveolar space and necrosis of involved alveolar tissue. H-score is a cumulative score, determined by the percentage of tissue area assigned each grade (0–3). Maximum grade was assigned to the most severely damaged lobe, representing the maximum infection per animal. Images of lung sections were taken on a Lionheart FX Automated Imaging microscope (BioTek, Winooski, VT, USA) using 10× objective. Scale bar represents 200 µm.
Publication 2023
Animals Eosin Formalin Infection Inflammation Injuries Lung Lung Injury Microscopy Mus Necrosis Neutrophil Neutrophil Infiltration Operative Surgical Procedures Paraffin Pathologists Pleurisy Tissues
Data from at least three experiments were pooled for each assay. Two-tailed Mann-Whitney U tests were performed with GraphPad Prism 5 software (GraphPad Software, San Diego, CA) for all comparisons described in morphology, biofilm, CAUTI, neutrophils recruitment, qRT-PCR, and catheter coverage experiments. Values represent means ± SEM derived from at least three independent experiments (*P < 0.05; **P < 0.005; ***P < 0.0005; ****P < 0.0001; and ns, difference not significant).
Publication 2023
Biofilms Biological Assay Catheters Neutrophil Infiltration prisma
Female C57BL/6 mice (6–8 weeks) were bred and maintained at the experimental animal center of Soochow University. All animal experiments were approved by the Ethics Committee of Soochow University and conducted in accordance with the Guidelines for the Care and Use of Research Animals established by Soochow University. The streptomycin-pretreated mouse model was established as described previously.40 (link) Mice that fasted for 4 h were administered intragastrically with streptomycin (100 μl of 200 mg/ml solution in sterile water; Sigma, USA). After 24 h, mice were randomly divided into four groups, including control, STM-WT, STM-ΔsopF, and STM-ΔsopF/psopF infection groups. 100 µL of either 5 × 107 colony-forming unit (CFU) S. Typhimurium strains or sterile PBS were used for oral gavage to mice that were fasted for 4 h before infection. Mice were sacrificed using CO2 asphyxiation at indicated time points.
For histopathology, tissue samples were harvested and fixed in 4% paraformaldehyde, processed according to standard procedures for dehydration, paraffin embedding, section cutting, and deparaffinization. The sections were stained with hematoxylin–eosin (Baso, Zhuhai, China) and observed under a light microscope (Olympus, Japan). Total inflammatory scores were assessed based on the following parameters according to previous literature:28 (link) neutrophil infiltration (0, none; 1, slight increase; 2, marked increase), fibrin deposition, submucosal neutrophil margination, submucosal edema, epithelial necrosis, epithelial ulceration (0, absent; 1, present). The percentage of pathological lesions was counted on a total scale of 0–20.
For bacterial burden measurement, spleen, and liver were harvested and then immersed in 100 µg/ml of amikacin for 1 h. Tissues were homogenized in PBS containing 0.3% Triton (Sigma, USA) for 30 min. CFU values were quantified by plating lysates with appropriate dilutions onto Salmonella-Shigella agar (Hangwei, China), followed by incubation overnight.
For immunofluorescence analysis, ceca samples were fixed with 4% paraformaldehyde at 4°C overnight, processed for paraffin embedding. Tissues were cut into 6-μm transverse sections, followed by deparaffinizing and rehydrating for antigen retrieval. The sections were blocked with 3% BSA for 30 min and then incubated with diluted primary antibodies at 4°C overnight. The antibody against EpCAM (#GB11274) was purchased from Servicebio (Wuhan, China; 1:3000 dilution). The antibody against S. Typhimurium O antigen (#S10820100) was purchased from the Lanzhou Institute of Biological Products Co., Ltd. (Lanzhou, China; 1:200 dilution). Next, the slides were incubated with Cy3 (#GB21303; 1:300 dilution) or Alexa Fluor 488 (#GB25303; 1:400 dilution) conjugated goat anti-rabbit immunofluorescent secondary antibodies purchased from Servicebio (Wuhan, China). The nuclei were stained with DAPI (#G1012) purchased from Servicebio (Wuhan, China). Slides were mounted in Anti-fade mounting medium (#G1401; Servicebio). Images were photographed using a Nikon microscope (ECLIPSE, Ts2R-FL, Tokyo, Japan).
Sample processing for transmission electron microscopy (TEM) was carried out in the School of Biology and Basic Medical Science, Medical College of Soochow University. Ceca samples were fixed in ice-cold 2.5% glutaraldehyde for at least 4 h. Samples were washed twice using 0.1 M phosphate buffer for 15 min at room temperature. Subsequently, the samples were post-fixed in 1% OsO4 for 1 h, dehydrated through an acetone series and embedded in epoxy resin. Ultra-thin sections were stained and observed using a 120 kV Transmission electron microscope (HT7700, Hitachi, Japan).
Publication 2023
Acetone Agar alexa fluor 488 Amikacin Animals, Laboratory Anti-Antibodies Antibodies Antigens Asphyxia Bacteria Biological Products Buffers Cecum Cell Nucleus Cold Temperature DAPI Edema Eosin Epoxy Resins Ethics Committees Females Fibrin Fluorescent Antibody Technique Glutaral Goat Immunoglobulins Infection Inflammation Light Microscopy Liver Mice, House Mice, Inbred C57BL Microscopy Microtomy Necrosis Neutrophil Neutrophil Infiltration O Antigens paraform Phosphates Rabbits Salmonella Shigella Spleen Sterility, Reproductive Strains Streptomycin TACSTD1 protein, human Technique, Dilution Tissues Transmission Electron Microscopy Tube Feeding Ulcer

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Publication 2023
Atrophy Cells Cytoplasm Dilatation Fingers Hemorrhage Heterografts HLA-G Antigen Injections, Intraperitoneal Injuries Kidney Light Microscopy Liver Lung Lymph Node Metastasis Males matrigel Mus Necrosis Neoplasms Neutrophil Infiltration Obstetric Delivery Ovum Implantation Pathologists Safety Spleen Therapies, CAR T-Cell Thomsen-Friedenreich antibodies Tissues Tongue Vacuole Zoletil
The day before sacrificing, the mice were fasted overnight and underwent a glucose tolerance test (GTT) and insulin tolerance test (ITT). Glucose solution (2 g/kg) and insulin (0.75 U/kg) were administered by intraperitoneal injection. Tail blood was collected at 0, 15, 30, 60 and 120 min after glucose administration, and glucose concentrations were measured using a glucometer and test strips (ACCU-CHEK Performa; Roche, United States). Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were determined by using standard kits purchased from Cusabio (Wuhan, China). Hepatic, adipose or serum lipids including triglyceride (TG), free fatty acid (FFA) and cholesterol, were determined by commercial lipids assay kits (abcam, Cambridge, MA, United States) according to the manufacturer’s protocols. Four-hydroxynonenal (4-HNE) level in the liver was measured by colorimetric assay using an ELISA kit (Cusabio, China). Formalin-fixed mouse liver and epididymal white adipose tissues were embedded in paraffin and sliced at 4.5 μm. Hematoxylin and eosin (H&E) staining was used for tissue morphology assessment. Pathology was scored in a blinded manner. Scoring ranges were as follows: Degree of steatosis (0–3), lobular inflammation (0–3), hepatocyte ballooning (0–2). In addition, the NAFLD activity score (NAS) was scored according to the non-alcoholic steatohepatitis (NASH) clinical research network scoring system (Kleiner et al., 2005 (link)). Hepatic lipids were visualized by Oil Red O (ORO) stain (Servicebio, Wuhan, China). Image Pro plus 6.0 was used for ORO staining quantification. Neutrophil infiltration in the liver was assessed by a naphthol AS-D chloroacetate (CAE) kit (Sigma-Aldrich, United States) according to the manufacturer’s directions. Apoptosis was detected by terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL; EMD Millipore, Billerica, MA). CAE and TUNEL positive cells were counted by Image J software (NIH, United States) and expressed as the ratio of positive cells per 1,000 hepatocytes.
Publication 2023
Alanine Transaminase Apoptosis Aspartate Transaminase Biological Assay BLOOD Cells chloroacetate Cholesterol Colorimetry deoxyuridine triphosphate DNA Nucleotidylexotransferase Enzyme-Linked Immunosorbent Assay Eosin Epididymis Formalin Glucose Glucose Tolerance Test Hematoxylin Hepatocyte Immune Tolerance Inflammation Injections, Intraperitoneal In Situ Nick-End Labeling Insulin Lipids Liver Mus Naphthols Neutrophil Infiltration Non-alcoholic Fatty Liver Disease Nonalcoholic Steatohepatitis Nonesterified Fatty Acids Obesity Paraffin Embedding PER1 protein, human Serum solvent red 27 Stains Steatohepatitis Tail Tissues Triglycerides White Adipose Tissue

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More about "Neutrophil Infiltration"

Neutrophil Infiltration, also known as Neutrophil Migration or Neutrophil Accumulation, is a critical process in the body's innate immune response.
Neutrophils, a type of white blood cell, are the first responders to sites of inflammation or infection, playing a crucial role in clearing pathogens and facilitating tissue repair.
The migration and accumulation of neutrophils to a specific site or tissue is triggered by various inflammatory stimuli, such as bacterial or viral infections, autoimmune disorders, and certain types of cancer.
This process is mediated by a complex interplay of chemokines, adhesion molecules, and other signaling pathways that guide the neutrophils to the site of interest.
Researchers studying Neutrophil Infiltration often utilize various techniques and tools, including Hexadecyltrimethylammonium bromide (CTAB) for neutrophil isolation, MPO (Myeloperoxidase) assay kits and detection kits to quantify neutrophil activity, and Prism 6 software for data analysis.
Additionally, fluorescent markers like PE/Cy7 anti-mouse CD45 can be used to identify and track neutrophils in vivo.
Understanding the mechanisms underlying Neutrophil Infiltration and its modulation is an active area of research, with important implications for the development of targeted therapies for a wide range of inflammatory and autoimmune conditions, as well as cancer.
By leveraging the insights gained from these studies, researchers can optimize their research processes and achieve better results with the help of AI-driven platforms like PubCompare.ai.