T cell immunity and phagocytic activity were studied in the blood of patients with IgA nephropathy in order to clarify their roles in the pathogenesis of IgA nephropathy. The percentages of total T lymphocytes, helper T cell and suppressor T cells were significantly reduced in patients. A significantly elevated helper T cell/suppressor T cell ratio in patients showed a predominant reduction in suppressor T cells. There was a significant relationship between histologic findings and helper T cell/suppressor T cell ratio in patients. Natural Killer (NK) cell activity was significantly reduced but the lymphocyte response after phytohemagglutinin (PHA) stimulation was not in patients. ConA-induced suppressor cell activity was not depressed despite of a decrease in suppressor T cells in patients. Phagocytic activity of polymorphonuclear leucocytes (PMNs) ingesting yeasts was significantly reduced in patients. Also an inverse correlation was found between serum IgA levels and phagocytic activity of PMN. It is concluded that suppressor T cell defects, depressed phagocytic activity and impaired NK cell activity may play a role in the pathogenesis of IgA nephropathy.
B-Lymphocytes/immunology ; Glomerulonephritis, IGA/*immunology/pathology ; Humans ; Killer Cells, Natural/immunology ; Neutrophils/immunology ; *Phagocytosis ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology

Behcet's disease is recognized as a systemic inflammatory disease of unknown etiology. The disease has a chronic course with periodic exacerbations and progressive deterioration. Previous reports have shown at least three major pathophysiologic changes in Behcet's disease; excessive functions of neutrophils, vasculitis with endothelial injuries, and autoimmune responses. Many reports suggested that immunological abnormalities and neutrophil hyperfunction may be involved in the etiology and the pathophysiology of this disease. HLA-B51 molecules by themselves may be responsible, in part, for neutrophil hyperfunction in Behcet's disease. T cells in this disease proliferated vigorously in response to a specific peptide of human heat shock protein (hsp) 60 in an antigen-specific fashion. T cells reactive with self-peptides produced Th1-like proinflammatory and/or inflammatory cytokines. This leads to tissue injury, possibly via delayed-type hypersensitivity reaction, macrophage activation, and activation and/or recruitment of neutrophils. These data shed new light on the autoimmune nature of Behcet's disease; molecular mimicry mechanisms may induce and/or exacerbate Behcet's disease by bacterial antigens that have activated T cells which are reactive with self-peptide(s) of hsp. This would lead to positive selection of autoreactive T cells in this disease.
Behcet's Syndrome/pathology ; Behcet's Syndrome/immunology* ; Behcet's Syndrome/etiology ; Chaperonin 60/immunology ; Eye/pathology ; Human ; Neutrophils/physiology ; Skin/pathology ; T-Lymphocytes/physiology

The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NaHS group (P<0.05, P<0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NaHS group were significantly higher than that in control group (P<0.01), while compared with LPS group, LPS + NaHS group showed significantly higher apoptotic rate (P<0.01). These results suggest that NaHS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NaHS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.
Acute Lung Injury ; chemically induced ; immunology ; pathology ; Animals ; Apoptosis ; Disease Models, Animal ; Humans ; Hydrogen Sulfide ; pharmacology ; Lipopolysaccharides ; adverse effects ; Lung ; pathology ; Neutrophils ; immunology ; Rats ; Sulfides ; pharmacology

Aged ; Antibodies, Antineutrophil Cytoplasmic ; blood ; Comorbidity ; Glomerulonephritis ; etiology ; immunology ; physiopathology ; Humans ; Male ; Neutrophils ; pathology ; Thrombotic Microangiopathies ; diagnosis ; physiopathology

Autoimmune pancreatitis (AIP) has two distinct subsets. Type 1 AIP or lymphoplasmacytic sclerosing pancreatitis is systemic disease with the elevation in serum levels of the IgG4. Type 2 AIP, also called duct-centric pancreatitis, features granulocyte epithelial lesions with duct obstruction in the pancreas without systemic involvement. Here, we report a case of type 2 AIP diagnosed by pathology, which is the first report in Korea. The case is a 56-year-old woman who presented with anorexia and vomiting. Computed tomography revealed mass-like lesion in the pancreatic head and the compression of the distal common bile duct and the head portion of the main pancreatic duct. Serum levels of the IgG4 were normal. Histologic examination revealed a dense neutrophil infiltration in the pancreatic parenchyme associated with extensive fibrosis, thereby confirming the diagnosis of type 2 AIP. The abnormalities in the clinical, laboratory, and radiological findings improved after oral steroid treatment.
Autoimmune Diseases/blood/immunology/*pathology ; Female ; Fibrosis ; Humans ; Immunoglobulin G/blood ; Magnetic Resonance Imaging ; Middle Aged ; Neutrophils/immunology ; Pancreas/pathology ; Pancreatitis/*drug therapy/immunology/pathology ; Steroids/*therapeutic use ; Tomography, X-Ray Computed

In order to determine the extent to which specific forms of glomerulonephritis (GN) contribute to the pool of crescentic GN, renal tissues from 17 crescentic GN patients were examined with special attention to glomerular and interstitial neutrophil infiltration. Renal tissues from five normal kidneys served as normal controls. Renal biopsy tissues from five patients with postinfectious GN in which crescent formation was not observed were also examined as disease controls. The patients were put into both three groups according to immunofluorescence findings and two groups according to the active or inactive phase of the crescents: group 1 with anti-glomerular basement membrane crescentic GN, one case; group 2 with immune complex crescentic GN, ten cases; and group 3 with pauci-immune crescentic GN, six cases. Four of the nine individuals tested were positive for anti-neutrophil cytoplasmic antibody (44.4%). Glomerular and interstitial neutrophil infiltrations were prominent in both the active and inactive phase groups, compared to normal controls (p<.05). Glomerular neutrophil infiltration was significantly prominent in the active phase group, compared to the inactive phase group (p<.001). In both the active and inactive phase groups, interstitial neutrophil infiltration was prominent, compared to disease control groups (p<.05). These results support the concept of the participation of periglomerular leukocytes in the renal tissue damage of crescentic GN, although the role of neutrophils was not examined.
Adult ; Aged ; Female ; Follow-Up Studies ; Glomerulonephritis/pathology* ; Glomerulonephritis/immunology ; Glomerulonephritis/classification ; Human ; Kidney Glomerulus/pathology* ; Kidney Glomerulus/immunology ; Male ; Middle Age ; Nephritis, Interstitial/pathology* ; Nephritis, Interstitial/immunology ; Neutrophils/physiology*

BACKGROUNDCorticosteroid treatment of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) has been one of the most controversial clinical issues in critical care. Although the administration of high-dose corticosteroids does not benefit patients with early septic shock and ARDS, recent clinical trials have indicated that treatment with relatively low-dose corticosteroids (2 to 3 mg/kg/day of methylprednisolone or equivalent) may improve outcome when used for late ARDS or persistent septic shock. The underlying mechanism was not fully clarified. Whether the administration of corticosteroids can arrest neutrophil-driven organ injury once started remains to be elucidated.

OBJECTIVETo observe the effects of hydrocortisone (HC, 6 mg/kg) on oxygen free radicals (OFR) released by PMN and pulmonary pathological changes in rat ALI model induced by lipopolysaccharide (LPS), to investigate the possible mechanism through which corticosteroids exert protective effect on ALI.

METHODSA rat model of ALI was induced by peritoneal injection of 2 x 10(12) Escherichia coli/kg. Fifty-six rats were randomly divided into three groups: normal control group, LPS group and HC group (6 mg/kg). Samples were collected 2 h, 4 h and 6 h after giving LPS to LPS and HC group (6 h after giving normal saline in normal control group) to measure the level of OFR released by PMN using chemiluminescence method based on lumino, and to compae of pulmonary pathological changes among the three groups.

RESULTSPathological examination with light microscope in LPS group showed thickened pulmonary interstitia, inflammatory cell infiltration, edema and hemorrhage, which were in accordance with the features of ALI. There were significant differences in the release of OFR by PMN among the three groups (P < 0.01). The level of OFR released by PMN in LPS group was significantly higher than that of the control group, and continued to increase during the observation period (2 - 6 h after LPS). The release of OFR by PMN in HC group was significantly suppressed as compared with LPS group, which was peaked at 4 h after LPS injection (to 98.2%); there were also significant differences in the grades of ALI pathologic changes among the three groups (P < 0.01). The grades of ALI pathologic changes in LPS group were significantly increased when compared with the normal control group (P < 0.05) while significantly decreased in HC group as compared with LPS group (P < 0.05).

CONCLUSIONIt was demonstrated in the LPS induced ALI model that OFR might play an important role in onset of ALI. Intervening with HC (6 mg/kg) treatment could ameliorate the lung injury and exert significant and sustained suppression on the release of OFR by PMN, showing that HC has a protective effect on LPS induced ALI and its theraputic effect occurs possibly through suppression on the release of OFR by PMN.

Acute Lung Injury ; etiology ; immunology ; Animals ; Disease Models, Animal ; Free Radicals ; metabolism ; Glucocorticoids ; pharmacology ; Hydrocortisone ; pharmacology ; Lipopolysaccharides ; adverse effects ; Lung ; immunology ; pathology ; Mice ; Neutrophils ; drug effects ; metabolism

Neutrophil adhesion and migration are critical in hepatic ischemia/reperfusion (I/R) injury. Despite very strong preclinical data, recent clinical trials failed to show a protective effect of anti-adhesion therapy in reperfusion injury. Therefore, the aim of this study was to assess the role of CD44 in neutrophil infiltration and liver injury from hepatic I/R. In this study, using a partial hepatic ischemic model in vivo, we determined the potential role of CD44 in neutrophil infiltration and liver injury from I/R. Reperfusion caused significant hepatocellular injury as it was determined by plasma ALT levels and liver histopathology. The injury was associated with a marked neutrophil recruitment and CD44 expression into the ischemic livers. Administration of anti-CD44 antibody to mice reduced the infiltration of neutrophil into the ischemic tissue, associated with liver function preservation. These results support crucial roles of CD44 in neutrophil recruitment and infiltration leading to liver damage in hepatic I/R injury. Moreover, they provide the rationale for targeting to CD44 as a potential therapeutic approach in liver I/R injury.
Alanine Transaminase/blood ; Animals ; Antibodies/immunology/pharmacology ; Antigens, CD44/immunology/metabolism/*physiology ; Cytokines/metabolism ; Disease Models, Animal ; Liver/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology/physiology ; Reperfusion Injury/metabolism/pathology/*prevention & control

Cutaneous nocardiosis, which usually manifests in the form of pustules, abscesses, or subcutaneous nodules, is occasionally found in immunocompromised patients. A 59-yr-old Korean man with myasthenia gravis and thymoma developed nodular skin lesions on his trunk. Histopathologically, abscess formation with a dense infiltrate of neutrophils and many cytophagic histiocytes were observed. Numerous filamentous organisms, which turned out to be Nocardia asteroides by culture, were also found. After sulfamethoxazole-trimethoprim therapy, all of the skin lesions rapidly decreased in size, with a marked diminution of the number of cytophagic histiocytes, and cleared up within four months. On reporting a case of cutaneous nocardiosis showing unusual histopathologic findings, we considered that reactive conditions should be included in the differential diagnosis of the cutaneous cytophagocytosis, and that nocardiosis could be one of the diseases showing reactive cytophagocytosis.
Anti-Bacterial Agents/therapeutic use ; Histiocytes/*immunology ; Humans ; Male ; Middle Aged ; Myasthenia Gravis/complications ; Neutrophils/*immunology ; Nocardia Infections/drug therapy/*immunology/microbiology/pathology ; Nocardia asteroides/drug effects/*immunology/isolation & purification ; Phagocytosis/*immunology ; Skin Diseases, Bacterial/drug therapy/*immunology/microbiology/pathology ; Thymoma/complications ; Thymus Neoplasms/complications ; Treatment Outcome ; Trimethoprim-Sulfamethoxazole Combination/therapeutic use

BACKGROUND: Previous studies have shown that the neutrophil-to-lymphocyte ratio (NLR) has a significant impact on the prognosis of many malignant tumors such as gastric cancer, colorectal cancer and pancreatic cancer, but the study on the prognosis of patients with resectable lung adenocarcinoma is less. The aim of this study is to investigate the correlation between the NLR and the clinicopathologic features of adenocarcinoma of lung patients who underwent radical pneumonectomy. Furthermore, this study aimed to clarify the predictive and prognostic significance of NLR in patients who underwent pneumonectomy for lung adenocarcinoma. METHODS: This study reviewed the medical records of 163 patients with lung adenocarcinoma who underwent pneumonectomy. The receiver operating characteristic (ROC) curve and Youden index were used to determine the cut-off value of the NLR. Survival curves were described by Kaplan-Meier method and compared by Log-rank test. The univariate and multivariate analyses were performed with the Cox proportional hazard model to identify the prognostic factors. RESULTS: When the NLR value was 2.96, the Youden index was maximal, with a sensitivity of 77.5% and a specificity of 75.9%. The 5-year survival rate in the low NLR group was higher than that in the high NLR group (P<0.05). The univariate and multivariate analyses showed that TNM staging and NLR were independent factors in predicting survival rate. CONCLUSIONS The NLR value was a simple and useful tool to predict the prognosis of lung adenocarcinoma after radical pneumonectomy.
Adenocarcinoma ; diagnosis ; immunology ; pathology ; surgery ; Adenocarcinoma of Lung ; Aged ; Cell Count ; Female ; Follow-Up Studies ; Humans ; Kaplan-Meier Estimate ; Lung Neoplasms ; diagnosis ; immunology ; pathology ; surgery ; Lymphocytes ; cytology ; Male ; Middle Aged ; Neoplasm Staging ; Neutrophils ; cytology ; Pneumonectomy ; Prognosis ; ROC Curve ; Retrospective Studies