ABSTRACT
Flexor tendon tenosynovitis is an entrapment of the flexor tendons at its entrance to the pulley system. Because there is a high incidence of this pathology, it should be well known by physicians, rheumathologists and orthopaedic surgeons. On this paper we present a literature review, analyzing the anatomic facts, biomechanics, diagnosis, classification, therapeutic options and we propose some general recommendations for physicians.
Subject(s)
Humans , Tenosynovitis/etiology , Tenosynovitis/epidemiology , Trigger Finger Disorder/diagnosis , Trigger Finger Disorder/therapy , Tenosynovitis/classification , Biomechanical Phenomena , Incidence , Neutrophil Infiltration , Trigger Finger Disorder/surgery , AnatomyABSTRACT
Abstract Purpose: To evaluate the effects of infliximab on the inflammation of the colonic mucosa devoid from fecal stream. Methods: Twenty-four rats were submitted to a Hartmann's procedure. They remained for 12 weeks with the fecal derivation to development of diversion colitis on excluded colorectal stump. After this period, they were divided into 3 groups: one group received intervention with saline (2.0 mL / week), other group infliximab at doses of 5 mg/kg/week and the other 10 mg/kg/week for five consecutively weeks. Concluded the intervention period, the animals were euthanized to remove colon segments with and without fecal stream. Colitis was diagnosed by histological analysis and the degree of inflammation by validated score. The neutrophilic infiltrate was evaluated by tissue expression of myeloperoxidase identified by immunohistochemical. The tissue content of myeloperoxidase was measured by computer-assisted image analysis. Results: The inflammatory score was high in colonic segments without fecal stream. The intervention with infliximab reduced the inflammatory score in excluded colonic segments. The content of myeloperoxidase was reduced in colonic segments of animals treated with infliximab mainly in high concentrations. Conclusion: Intervention with infliximab reduced the inflammation and the neutrophil infiltrate in colonic segments devoid of the fecal stream.
Subject(s)
Animals , Male , Gastrointestinal Agents/pharmacology , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Colitis/drug therapy , Infliximab/pharmacology , Time Factors , Image Processing, Computer-Assisted , Gastrointestinal Transit/drug effects , Immunohistochemistry , Reproducibility of Results , Rats, Wistar , Colitis/pathology , Colon/drug effects , Colon/pathology , Peroxidase/analysis , Neutrophil Infiltration/drug effects , Feces , Intestinal Mucosa/drug effects , Intestinal Mucosa/pathologyABSTRACT
BACKGROUND/AIMS: The aim of this study was to determine the risk factors of multiple gastric polyps according to the histological classification of gastric polyps. METHODS: Subjects with multiple gastric polyps (at least three) during endoscopy were enrolled prospectively. They were assigned to a fundic gland polyp (FGP) group and hyperplastic polyp (HP) group based on a histological classification of gastric polyps. Helicobacter pylori (H. pylori) was confirmed by its histology. Serum gastrin was measured using the radioimmunoassay method. A questionnaire was taken regarding the intake of proton pump inhibitor and nonsteroidal anti-inflammatory drugs, alcohol, smoking history, and diet. RESULTS: Among the 60 subjects enrolled from 2015 to 2018 at Seoul National University Bungdang Hospital, 47 and 13 subjects were assigned to the FGP and HP groups, respectively. The H. pylori infection rate was 12.8% in the FGP group, which is lower than that in the HP group (69.2%, p<0.001). The gastrin level was higher in the HP group (194.7 pg/dL, range 50.6–387.8 pg/dL) than in the FGP group (57.4 pg/dL, range 24.8–79.0 pg/dL) (p=0.007). Histologically, neutrophil infiltration in the antrum and body of the stomach were higher in the HP group than in the FGP group (p=0.022 and p=0.030, respectively). In contrast, monocyte infiltration in the antrum and body of the stomach were higher in the FGP group than in the HP group (p=0.018 and p<0.001, respectively). CONCLUSIONS: HPs arise from inflammation caused by H. pylori. On the other hand, the FGP was not associated with H. pylori or environmental factors.
Subject(s)
Classification , Cohort Studies , Diet , Endoscopy , Gastrins , Hand , Helicobacter pylori , Inflammation , Methods , Monocytes , Neutrophil Infiltration , Polyps , Prospective Studies , Proton Pump Inhibitors , Proton Pumps , Radioimmunoassay , Risk Factors , Seoul , Smoke , Smoking , StomachABSTRACT
Objective To explore the application of neutrophil migration distance for wound age estimation of skeletal muscles in rats, and to provide methodological basis for follow-up study in future. Methods The skeletal muscle contusion model was established in rats, and the control group and the 2, 4, 6 h post-traumatic groups were set. The law of response of neutrophils that participated in the inflammation after injury was detected by immunohistochemical staining, and the relationship between neutrophil migration distance and injury time was detected by TissueFAXS PLUS software. Results The skeletal muscle was obviously infiltrated with neutrophils 2-6 h after injury. The positive rate of neutrophil was (28.75±0.94)% at 2 h post-traumatic, and reached the peak (45.50±3.63)% at 4 h post-traumatic, then decreased to (31.92±1.56)% at 6 h post-traumatic. The neutrophil migration distances increased with the progress of inflammation, and reached (124.80±12.32) μm, (229.03±21.45) μm and (335.04±16.75) μm at 2 h, 4 h and 6 h, respectively. Conclusion There is a relationship of neutrophil infiltrated number and migration distance and wound age within the 2-6 h after skeletal muscle injury, which could be used for the inference of skeletal muscle wound age.
Subject(s)
Animals , Rats , Contusions/metabolism , Follow-Up Studies , Muscle, Skeletal/pathology , Neutrophil Infiltration , Neutrophils , Rats, Sprague-Dawley , Time FactorsABSTRACT
BACKGROUND/AIMS: The aim of this study was to determine the risk factors of multiple gastric polyps according to the histological classification of gastric polyps.METHODS: Subjects with multiple gastric polyps (at least three) during endoscopy were enrolled prospectively. They were assigned to a fundic gland polyp (FGP) group and hyperplastic polyp (HP) group based on a histological classification of gastric polyps. Helicobacter pylori (H. pylori) was confirmed by its histology. Serum gastrin was measured using the radioimmunoassay method. A questionnaire was taken regarding the intake of proton pump inhibitor and nonsteroidal anti-inflammatory drugs, alcohol, smoking history, and diet.RESULTS: Among the 60 subjects enrolled from 2015 to 2018 at Seoul National University Bungdang Hospital, 47 and 13 subjects were assigned to the FGP and HP groups, respectively. The H. pylori infection rate was 12.8% in the FGP group, which is lower than that in the HP group (69.2%, p<0.001). The gastrin level was higher in the HP group (194.7 pg/dL, range 50.6–387.8 pg/dL) than in the FGP group (57.4 pg/dL, range 24.8–79.0 pg/dL) (p=0.007). Histologically, neutrophil infiltration in the antrum and body of the stomach were higher in the HP group than in the FGP group (p=0.022 and p=0.030, respectively). In contrast, monocyte infiltration in the antrum and body of the stomach were higher in the FGP group than in the HP group (p=0.018 and p<0.001, respectively).CONCLUSIONS: HPs arise from inflammation caused by H. pylori. On the other hand, the FGP was not associated with H. pylori or environmental factors.
Subject(s)
Classification , Cohort Studies , Diet , Endoscopy , Gastrins , Hand , Helicobacter pylori , Inflammation , Methods , Monocytes , Neutrophil Infiltration , Polyps , Prospective Studies , Proton Pump Inhibitors , Proton Pumps , Radioimmunoassay , Risk Factors , Seoul , Smoke , Smoking , StomachABSTRACT
Wischnewski spots (WS) are multiple black spots observed in the gastric mucosa at autopsy that are considered a reliable and important feature of hypothermia. Nonetheless, the frequency of WS varies widely. WS were discovered in 20 cases out of 3,493 autopsies (0.57%) conducted between 2001 and 2017 in the Department of Forensic Medicine of the School of Medicine, Kyungpook National University in Korea. This study aimed to investigate the distribution and size of WS in these cases and analyze the respective causes of death. Nine cases that occurred in winter were the same as the nine cases with hypothermia as the cause of death or contributory cause. The post-mortem blood alcohol test was positive in eight cases, with acute or chronic alcoholism determined as the cause of death in two of these cases. There were two cases of acute poisoning by pesticides. Putrefaction was noted in six cases (30%). WS presented in various sizes ranging from pinpoint to more than 5 mm in diameter, and the number of WS varied from 5 to 100. WS distribution was diffuse in four cases (20%) and localized in 13 cases (65%). Microscopic examination showed brown to black pigmentation but no neutrophil infiltration or vital reactions in the WS. Thus, WS are associated with hypothermia and are considered post-mortem alterations with variable appearance, size, and distribution. Hypothermia is an exclusive diagnosis at autopsy that should result from a combined assessment of toxicological tests, circumstance of death, and autopsy findings.
Subject(s)
Humans , Alcoholism , Autopsy , Cause of Death , Diagnosis , Forensic Medicine , Gastric Mucosa , Hypothermia , Korea , Neutrophil Infiltration , Pesticides , Pigmentation , PoisoningABSTRACT
PURPOSE: Atopic dermatitis (AD) is the most common chronic and relapsing inflammatory skin disease with skin barrier defects and altered immune responses. Chronic inflammation leads to irreversible fibrosis in the skin and there is no treatment to completely abolish the inflammation and fibrosis. To prevent or treat the chronic process of AD, it is necessary to develop a murine model of AD that reflects the chronic process to identify the mechanism. The aims of this study were to develop a chronic AD model with a crude extract Aspergillus fumigatus (Af) antigen. METHODS: We applied Af extract (40 µg) epicutaneously to the dorsal skin of BALB/c mice for 5 consecutive days per week during a period of 5 weeks for a chronic AD model, and 5 consecutive days repeatedly with 2 weeks interval for an acute AD model. RESULTS: The clinical score and transepidermal water loss were more increased in the chronic AD model than in the acute AD model. Histologic findings showed that more increased epidermal thickness, neutrophil infiltration and hyperkeratosis in the chronic model than in the acute model. Skin fibrosis was more prominent in the chronic model than in the acute model. The mRNA expression levels of transforming growth factor (TGF)-β, thymic stromal lymphopoietin, and interleukin-33 were increased in the skin of the chronic model compared to the acute model. The levels of total IgE, Af-specific IgE, IgG1, and IgG2a were significantly increased in the chronic model compared to controls. CONCLUSION: The Af-induced chronic AD model showed prominent fibrosis and increased TGF-β expression in the skin, which suggests that these models may be useful in the research for the mechanism of the chronic process in AD.
Subject(s)
Animals , Mice , Aspergillus fumigatus , Aspergillus , Dermatitis, Atopic , Fibrosis , Immunoglobulin E , Immunoglobulin G , Inflammation , Interleukin-33 , Neutrophil Infiltration , RNA, Messenger , Skin , Skin Diseases , Transforming Growth Factors , WaterABSTRACT
Abstract: Adult-onset Still's disease is a systemic inflammatory disorder of unknown etiology, characterized by skin rash, spiking fever, arthralgias or arthritis, and leukocytosis. The typical skin rash is evanescent, salmon-pink, nonpruritic and maculopapular, predominantly on the extremities. It is considered one of the major Yamaguchi's criteria in adult-onset Still's disease. However, atypical skin lesions are also described. Here, a 61-year-old woman with sore throat, spiking fever, polyarthritis and evanescent salmon-pink nonpruritic maculopapular skin rash on the extremities was diagnosed with adult-onset Still's disease. In addition, atypical brown macules on oral mucosa, localized on the inner lips and tongue were also observed. Biopsy revealed a neutrophilic infiltrate. Despite treatment and improvement of the adult-onset Still's disease, the atypical oral mucosal lesions persisted.
Subject(s)
Humans , Female , Middle Aged , Still's Disease, Adult-Onset/pathology , Mouth Diseases/pathology , Mouth Mucosa/pathology , Tongue/pathology , Biopsy , Still's Disease, Adult-Onset/diagnosis , Neutrophil Infiltration , Exanthema/pathology , Lip/pathology , Mouth Diseases/diagnosisABSTRACT
Triptolide (TP) induces severe liver injury, but its hepatotoxicity mechanisms are still unclear. Inflammatory responses may be involved in the pathophysiology. Neutrophils are the first-line immune effectors for sterile and non-sterile inflammatory responses. Thus, the aim of the present study was to investigate the neutrophilic inflammatory response in TP-induced liver injury in C57BL/6 mice. Our results showed that neutrophils were recruited and accumulated in the liver, which was parallel to or slightly after the development of liver injury. Neutrophils induced release of myeloperoxidase and up-regulation of CD11b, which caused cytotoxicity and hepatocyte death. Hepatic expressions of CXL1, TNF-α, IL-6, and MCP1 were increased significantly to regulate neutrophils recruitment and activation. Up-regulation of toll like receptors 4 and 9 also facilitated neutrophils infiltration. Moreover, neutrophils depletion using an anti-Gr1 antibody showed mild protection against TP overdose. These results indicated that neutrophils accumulation might be the secondary response, not the cause of TP-induced liver injury. In conclusion, the inflammatory response including neutrophil infiltration may play a role in TP-induced hepatotoxicity, but may not be severe enough to cause additional liver injury.
Subject(s)
Animals , Female , Humans , Mice , Chemical and Drug Induced Liver Injury , Allergy and Immunology , Chemokine CCL2 , Genetics , Allergy and Immunology , Diterpenes , Drugs, Chinese Herbal , Epoxy Compounds , Interleukin-6 , Genetics , Allergy and Immunology , Intracellular Signaling Peptides and Proteins , Genetics , Allergy and Immunology , Liver , Allergy and Immunology , Mice, Inbred C57BL , Neutrophil Infiltration , Neutrophils , Allergy and Immunology , Phenanthrenes , Tripterygium , Chemistry , Tumor Necrosis Factor-alpha , Genetics , Allergy and ImmunologyABSTRACT
Triptolide (TP) induces severe liver injury, but its hepatotoxicity mechanisms are still unclear. Inflammatory responses may be involved in the pathophysiology. Neutrophils are the first-line immune effectors for sterile and non-sterile inflammatory responses. Thus, the aim of the present study was to investigate the neutrophilic inflammatory response in TP-induced liver injury in C57BL/6 mice. Our results showed that neutrophils were recruited and accumulated in the liver, which was parallel to or slightly after the development of liver injury. Neutrophils induced release of myeloperoxidase and up-regulation of CD11b, which caused cytotoxicity and hepatocyte death. Hepatic expressions of CXL1, TNF-α, IL-6, and MCP1 were increased significantly to regulate neutrophils recruitment and activation. Up-regulation of toll like receptors 4 and 9 also facilitated neutrophils infiltration. Moreover, neutrophils depletion using an anti-Gr1 antibody showed mild protection against TP overdose. These results indicated that neutrophils accumulation might be the secondary response, not the cause of TP-induced liver injury. In conclusion, the inflammatory response including neutrophil infiltration may play a role in TP-induced hepatotoxicity, but may not be severe enough to cause additional liver injury.
Subject(s)
Animals , Female , Humans , Mice , Chemical and Drug Induced Liver Injury , Allergy and Immunology , Chemokine CCL2 , Genetics , Allergy and Immunology , Diterpenes , Drugs, Chinese Herbal , Epoxy Compounds , Interleukin-6 , Genetics , Allergy and Immunology , Intracellular Signaling Peptides and Proteins , Genetics , Allergy and Immunology , Liver , Allergy and Immunology , Mice, Inbred C57BL , Neutrophil Infiltration , Neutrophils , Allergy and Immunology , Phenanthrenes , Tripterygium , Chemistry , Tumor Necrosis Factor-alpha , Genetics , Allergy and ImmunologyABSTRACT
BACKGROUND/AIMS: Recent findings have demonstrated the occurrence of neutrophil transendothelial migration in the reverse direction (reverse TEM) and that endothelial junctional adhesion molecule C (JAM-C) is a negative regulator of reverse TEM. In this study, we tested the effects of a JAM-C blocking antibody on the resolution of kidney injuries and inflammation in a mouse model of cisplatin-induced acute kidney injury (AKI). METHODS: Cisplatin was administered via intraperitoneal injection. A JAM-C blocking antibody or a control immunoglobulin G was administered intraperitoneal at 1.5 mg/kg, with the injection being delayed until day 4 following cisplatin administration to restrict the effect of antibodies on recovery. RESULTS: After cisplatin injection, serum creatinine and histologic injuries peaked on day 4. Treatment with a JAM-C blocking antibody on days 4 and 5 promoted the functional and histologic recovery of cisplatin-induced AKI on days 5 and 6. Facilitating recovery with a JAM-C blocking antibody correlated with significantly increased circulating intercellular adhesion molecule 1+ Tamm-Horsfall protein+ neutrophils and significantly decreased renal neutrophil infiltration, indicating that facilitating reverse the TEM of neutrophils from the kidney to the peripheral circulation partially mediated the resolution of inflammation and recovery. CONCLUSIONS: These results demonstrated that reverse TEM is involved in the resolution of neutrophilic inflammation in cisplatin-induced AKI and that JAM-C is an important regulator of this process.
Subject(s)
Animals , Mice , Acute Kidney Injury , Antibodies , Cisplatin , Creatinine , Immunoglobulin G , Inflammation , Injections, Intraperitoneal , Junctional Adhesion Molecule C , Junctional Adhesion Molecules , Kidney , Neutrophil Infiltration , Neutrophils , Transendothelial and Transepithelial MigrationABSTRACT
Neutrophilic myositis is a very rare disease histologically characterized by neutrophil infiltration of muscle tissues. We report a case of a 47-year-old man who presented with acute onset of severe swelling and pain on his left shoulder with high fever. He was initially suspected of having cellulitis, but intravenous antibiotics did not improve his symptoms. Similar swelling and pain then developed on both calves. Investigations with magnetic resonance imaging of the lower legs and muscle biopsy led to a diagnosis of neutrophilic myositis. High dose glucocorticoid dramatically improved his symptoms within days. Clinicians need to be aware of this rare disease as a cause of acute febrile myositis mimicking infection.
Subject(s)
Humans , Middle Aged , Anti-Bacterial Agents , Biopsy , Cellulitis , Diagnosis , Fever , Leg , Magnetic Resonance Imaging , Myositis , Neutrophil Infiltration , Neutrophils , Rare Diseases , Shoulder , Sweet SyndromeABSTRACT
Toluene diisocyanate (TDI) exposure can directly activate and damage airway epithelium. Folliculin (FLCN) is a protein expressed by human airway epithelial cells (HAECs) to maintain airway epithelial integrity and survival. This study investigated the involvement of FLCN in the pathogenesis of TDI-induced occupational asthma (OA). Enzyme-linked immunosorbent assay was used to measure serum levels of FLCN in TDI-exposed subjects (93 TDI-OA patients and 119 asymptomatic exposed controls (AEC)), 200 non-occupational asthma (NOA) patients and 71 unexposed healthy normal controls (NCs). Significantly more subjects in the TDI-OA and AEC groups had high serum levels of FLCN compared to those in the NOA group (P=0.002 and P=0.001, respectively), all of which were higher than the NC group (all P<0.001). The serum level of FLCN was positively correlated with TDI exposure duration (r=0.251, P=0.027), but was negatively correlated with asthma duration of TDI-OA patients (r=−0.329, P=0.029). TDI-exposed subjects with high FLCN levels had higher serum levels of total IgE than those with lower levels. The effects of TDI exposure on FLCN production was investigated by treating HAECs (A549 cells) with TDI-human serum albumin conjugate, which showed increased expression and release of FLCN and interleukin-8 from HAECs. Co-culture with peripheral blood neutrophils also induced FLCN expression and release from HAECs. In conclusion, TDI exposure and TDI-induced neutrophil recruitment into the airways can activate and stimulate HAECs to produce FLCN, which could be involved in airway inflammation in workers exposed to TDI.
Subject(s)
Humans , Asthma , Asthma, Occupational , Coculture Techniques , Enzyme-Linked Immunosorbent Assay , Epithelial Cells , Epithelium , Estrone , Immunoglobulin E , Inflammation , Interleukin-8 , Neutrophil Infiltration , Neutrophils , Serum Albumin , Toluene 2,4-Diisocyanate , TolueneABSTRACT
Interleukin (IL)-17 plays an important role in rhinitis and the level thereof correlates with the severity of disease. However, no mouse model for IL-17-dominant rhinitis has yet been developed. Our objective was to establish a mouse model of IL-17-dominant rhinitis via intranasal application of polyinosinic-polycytidylic acid (abbreviated as Poly(I:C)). Mice were divided into 6 groups (n=8 for each group); 1) 1 negative control group, 2) 1 positive control group (OVA/alum model), 3) 2 Poly(I:C) groups (10 or 100 µg), and 4) 2 OVA/Poly(I:C) groups (10 or 100 µg). The positive control group was treated with the conventional OVA/alum protocol. In the Poly(I:C) and OVA/Poly(I:C) groups, phosphate-buffered saline or an OVA solution plus Poly(I:C) were administered. The OVA/Poly(I:C) groups exhibited significantly greater neutrophil infiltration and increased IL-17/interferon γ expression compared with the other groups. However, the levels of total immunoglobulin E (IgE), OVA-specific IgE, eosinophil infiltration, IL-4, IL-5, IL-6, and IL-10 were significantly lower in the OVA/Poly(I:C) groups than in mice subjected to conventional Th2-dominant OVA/alum treatment (the positive control group). IL-17 and neutrophil measurement, chemokine (C-X-C motif) ligand 1 immunohistochemistry, and confocal microscopy revealed increased numbers of IL-17-secreting cells in the nasal mucosa of the OVA/Poly(I:C) groups, which included natural killer cells, CD4 T cells, and neutrophils. In conclusion, we developed a mouse model of IL-17-dominant rhinitis using OVA together with Poly(I:C). This model will be useful in research on neutrophil- or IL-17-dominant rhinitis.
Subject(s)
Animals , Mice , Chemokine CXCL1 , Eosinophils , Immunoglobulin E , Immunoglobulins , Immunohistochemistry , Interleukin-10 , Interleukin-17 , Interleukin-4 , Interleukin-5 , Interleukin-6 , Interleukins , Killer Cells, Natural , Microscopy, Confocal , Nasal Mucosa , Neutrophil Infiltration , Neutrophils , Ovum , Poly I-C , Rhinitis , T-LymphocytesABSTRACT
PURPOSE: Lipopolysaccharide (LPS) is a cell wall component of Gram-negative bacteria and important for pro-inflammatory mediators. This study aimed to establish a rhinitis model using ovalbumin (OVA) and LPS in order to evaluate the role of interleukin (IL)-17 in the pathogenesis of an LPS-induced non-eosionophilic rhinitis model. METHODS: Mice were divided into 4 groups and each group consisted of 10 mice (negative control group, allergic rhinitis model group, 1-µg LPS treatment group, and 10-µg LPS treatment group). BALB/c mice were sensitized with OVA and 1 or 10 µg of LPS, and challenged intranasally with OVA. Multiple parameters of rhinitis were also evaluated to establish the LPS-induced rhinitis model. IL-17 knockout mice were used to check if the LPS-induced rhinitis model were dependent on IL-17. Eosinophil and neutrophil infiltration, and mRNA and protein expression profiles of cytokine in nasal mucosa or spleen cell culture were evaluated using molecular, biochemical, histopathological, and immunohistological methods. RESULTS: In the LPS-induced rhinitis model, neutrophil infiltration increased in the nasal mucosa, and systemic and nasal IL-17 and interferon-gamma (IFN-γ) levels also increased as compared with the OVA-induced allergic rhinitis model. These findings were LPS-dose-dependent. In IL-17 knockout mice, those phenotypes (neutrophil infiltration, IL-17, and IFN-γ) were reversed, showing IL-17 dependency of LPS-induced rhinitis. The expression of vascular endothelial growth factor (VEGF), an important mediator for inflammation and angiogenesis, decreased in IL-17 knockout mice, showing the relationship between IL-17 and VEGF. CONCLUSIONS: This study established an LPS-induced rhinitis model dependent on IL-17, characterized by neutrophil infiltration and increased expression of IL-17.
Subject(s)
Animals , Mice , Cell Culture Techniques , Cell Wall , Eosinophils , Gram-Negative Bacteria , Inflammation , Interferon-gamma , Interleukin-17 , Interleukins , Mice, Knockout , Nasal Mucosa , Neutrophil Infiltration , Ovalbumin , Ovum , Phenotype , Rhinitis , Rhinitis, Allergic , RNA, Messenger , Spleen , Vascular Endothelial Growth Factor AABSTRACT
Abstract BACKGROUND: Chronic urticaria is characterized by transient, pruritic lesions of varying sizes, with central pallor and well-defined edges, with disease duration longer than six weeks. Its cellular infiltrate consists of neutrophils, lymphocytes and eosinophils. There is a subgroup of patients with eosinophilic or neutrophilic urticaria, resistant to the treatment with antihistamines, but that respond to a combination of antihistamine with other drugs. OBJECTIVE: To evaluate the present infiltration in chronic urticaria biopsies and correlate it with the clinical disease activity and response to treatment. METHODS: Forty-one patients with chronic urticaria were classified according to the score of severity of the disease, response to treatment and type of perivascular infiltrate. Inflammatory infiltrates were divided in eosinophilic (46.30%), neutrophilic and mixed. RESULTS: An association was found between the eosinophilic infiltrate and clinical scores of greater severity (p = 0.002). CONCLUSION: This association shows that the eosinophilic inflammatory infiltrates denote high clinical activity, which means more severe and exuberant clinical pictures of the disease.
Subject(s)
Humans , Male , Female , Adult , Urticaria/physiopathology , Urticaria/pathology , Neutrophil Infiltration/physiology , Eosinophils/pathology , Reference Values , Urticaria/therapy , Biopsy , Severity of Illness Index , C-Reactive Protein/analysis , Immunoglobulin E/analysis , Chronic Disease , Cross-Sectional Studies , Treatment Outcome , Statistics, NonparametricABSTRACT
Contexto: O pioderma gangrenoso (PG) é doença inflamatória da pele, com intensa infiltração de neutrófilos, que pode surgir após cirurgia da mama. Há relatos cada vez mais frequentes, considerando o aumento desse procedimento nos dias atuais. Pode se desenvolver espontaneamente, associado ao trauma cirúrgico ou por certas doenças sistêmicas e neoplásicas. A manifestação clínica das úlceras é característica e deve ser lembrada nas evoluções cicatriciais desfavoráveis com intensa reação inflamatória, perdas teciduais, secreção sanguinolenta e/ou purulenta, fundo granuloso e vegetante e bordas solapadas. Relato de caso: Relata-se o caso de paciente que teve pioderma gangrenoso após mastectomia parcial por adenocarcinoma de mama. Respondeu ao corticosteroide e imunossupressor sistêmico e evoluiu com duas recidivas em diferentes situações. Conclusão: O PG pode ocorrer após as cirurgias das mamas, havendo sinais e sintomas que indicam o diagnóstico e o tratamento precoce.
Subject(s)
Humans , Female , Middle Aged , Skin , Breast , Mammaplasty , Pyoderma Gangrenosum , Neutrophil InfiltrationABSTRACT
Abstract Interleukin 17A (IL-17A) is a proinflammatory cytokine responsible for the initiation and propagation of inflammation. One of its actions is the recruitment of neutrophils to the site of infection. The aim of this study was to investigate whether there is association between IL-17A expression and neutrophil infiltration in periapical abscesses and periapical granulomas, as well as to find which type of T lymphocyte effector (CD4+ or CD8+) expresses IL-17A in these lesions. Elastase, CD4, CD8, and IL-17A were analyzed by immunohistochemistry and immunofluorescence, in the biopsies of periapical lesions. Abscess lesions exhibited the highest labeling area for IL-17A (p = 0.011). During double immunofluorescence staining, there were significantly more CD4+/IL-17A+ cells compared to CD8+/IL-17A+ cells, both in the abscesses (p = 0.025) and granulomas (p = 0.011). In conclusion, IL-17A was intensively expressed in periapical abscesses rich in neutrophils. The high percentage of IL-17A in these cases suggests the participation of this cytokine particularly in the acute stages of the inflammatory process of the periapical lesions.
Subject(s)
Humans , Periapical Abscess/metabolism , Periapical Granuloma/metabolism , Periapical Granuloma/pathology , Interleukin-17/analysis , Periapical Abscess/pathology , Reference Values , Biopsy , Immunohistochemistry , Pancreatic Elastase/analysis , CD4-Positive T-Lymphocytes/pathology , CD4-Positive T-Lymphocytes/chemistry , CD4 Antigens/analysis , Fluorescent Antibody Technique , CD8 Antigens/analysis , CD8-Positive T-Lymphocytes/pathology , CD8-Positive T-Lymphocytes/chemistry , Neutrophil InfiltrationABSTRACT
Superficial angiomyxomas (SAMs) are rare benign cutaneous tumors that involve the subcutaneous layer. They are commonly located in the trunk, lower limbs and head or neck of women of reproductive age. SAMs in the vulva of postmenopausal women are especially rare case. Herein, we report a vulvar SAM in a postmenopausal 60-year-old woman. The patient presented with a palpable cutaneous mass in the right labium majora that had appeared 3 months earlier. The mass was slow growing and approximately 5 cm in size and resembled a soft tissue malignancy. It appeared as a well-defined multilocular cystic mass in magnetic resonance images. The preoperative diagnosis was a benign cystic lesion such as an epidermoid cyst. Grossly, the completely excised mass was 6 × 5 cm in size and well circumscribed with a multilocular outer surface, a yellowish-gray gelatinous cut surface, and a smooth rubbery inner surface. Histologic review revealed that the mass contained small to moderate amount of cellular angiomyxoid nodules and bland-looking spindle-shaped to ovoid cells without atypia. Neutrophil infiltration, which is a diagnostic feature of SAMs, was observed. Immunohistochemistry showed expression of CD34, but not of estrogen receptors, progesterone receptors, or desmin in the SAM. The patient has been followed up for 12 months without recurrence.
Subject(s)
Female , Humans , Middle Aged , Desmin , Diagnosis , Epidermal Cyst , Gelatin , Head , Immunohistochemistry , Lower Extremity , Myxoma , Neck , Neutrophil Infiltration , Postmenopause , Receptors, Estrogen , Receptors, Progesterone , Recurrence , Soft Tissue Neoplasms , Vulva , Vulvar NeoplasmsABSTRACT
BACKGROUND/AIMS: Role of autophagy in neutrophil function and the association of autophagy and autophagy related (ATG) gene polymorphisms with asthma susceptibility were suggested. In this study, we investigated the genetic association of ATG5 and ATG7 polymorphisms with asthma risk, severity and neutrophilic airway inflammation. METHODS: We recruited 408 asthma patients and 201 healthy controls. Sputum neutrophil counts were determined by H&E staining. Serum interleukin 8 (IL-8) levels were measured by enzyme-linked immunosorbent assay (ELISA). Genetic polymorphisms of ATG5 (-769T>C, -335G>A, and 8830C>T) and ATG7 (-100A>G and 25108G>C) were genotyped. The functional activities of ATG5 -769T>C and -335G>A variants were investigated by luciferase reporter assays. RESULTS: No associations of ATG5 and ATG7 polymorphisms with asthma susceptibility and severity were found. ATG5 -769T>C and -335G>A were in complete linkage disequilibrium. In the asthma group, GA/AA genotypes at ATG5 -335G>A were associated with higher neutrophil counts in sputum (p T associated with lower FEV1% predicted value (p G and 25108G>C were significantly associated with high serum levels of IL-8 (p < 0.05 for both variants). CONCLUSIONS: Genetic polymorphisms of ATG5 and ATG7 could contribute to neutrophilic airway inflammation in the pathogenesis of adult asthma.