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PubMed2005

In vivo IL-10 gene delivery suppresses airway eosinophilia and hyperreactivity by down-regulating APC functions and migration without impairing the antigen-specific systemic immune response in a mouse model of allergic airway inflammation.

IL-10 is an immunosuppressive cytokine. Although previous studies have reported that exogenous delivery of IL-10 reduced airway inflammation in experimental allergic airway inflammation, the mechanism of action has not been fully clarified. In this report, we elucidated a mechanism of action of IL-10 in vivo. BALB/c mice were immunized and aerosol challenged with OVA-Ag. We delivered the IL-10 gene to the mice before systemic sensitization or during aerosol Ag challenge by administering an IL-10-producing plasmid vector. Not only presensitization delivery of IL-10, as reported, but also delivery during inflammation strongly suppressed the development of airway eosinophilia and hyperreactivity. Presensitization delivery suppressed the Ag-specific Th2-type immune response in both the lung and spleen. In contrast, delivery in the effector phase suppressed the Th2 response only in the lung, whereas that in the spleen was not affected. IL-10 gene delivery did not induce the development of a regulatory phenotype of T cells or dendritic cells; rather, it suppressed the overall functions of CD11c(+) APCs of the lung such as Ag-presenting capacity, cytokine production, and transportation of OVA-Ag to lymph nodes, thus attenuating Th2-mediated allergic airway inflammation. Further, IL-10 revealed a distinct immunosuppressive effect in the presence of Ag and APCs. These results suggest that suppression of APC function in the lung, the site of immune response, played a critical role in the IL-10-mediated suppression of Ag-induced airway inflammation and hyperreactivity. Therefore, if delivered selectively, IL-10 could site specifically suppress the Ag-specific immune response without affecting systemic immune responses.

Aerosols↗
PubMed2007

Protectin D1 is generated in asthma and dampens airway inflammation and hyperresponsiveness.

Protectins are newly identified natural chemical mediators that counter leukocyte activation to promote resolution of inflammation. In this study, we provide the first evidence for protectin D1 (PD1, 10R,17S-dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid) formation from docosahexaenoic acid in human asthma in vivo and PD1 counterregulatory actions in allergic airway inflammation. PD1 and 17S-hydroxy-docosahexaenoic acid were present in exhaled breath condensates from healthy subjects. Of interest, levels of PD1 were significantly lower in exhaled breath condensates from subjects with asthma exacerbations. PD1 was also present in extracts of murine lungs from both control animals and those sensitized and aerosol challenged with allergen. When PD1 was administered before aeroallergen challenge, airway eosinophil and T lymphocyte recruitment were decreased, as were airway mucus, levels of specific proinflammatory mediators, including IL-13, cysteinyl leukotrienes, and PGD(2), and airway hyperresponsiveness to inhaled methacholine. Of interest, PD1 treatment after aeroallergen challenge markedly accelerated the resolution of airway inflammation. Together, these findings provide evidence for endogenous PD1 as a pivotal counterregulatory signal in allergic airway inflammation and point to new therapeutic strategies for modulating inflammation in asthmatic lung.

Animals↗
PubMed2002

Influence of mild hypothermia on inducible nitric oxide synthase expression and reactive nitrogen production in experimental stroke and inflammation.

Mild hypothermia is neuroprotective, but the reasons are not well known. Inflammation contributes to ischemic damage; therefore, we examined whether the protection by hypothermia may be attributable to alterations in the inflammation. We examined whether hypothermia might alter the inflammatory cell-associated inducible nitric oxide synthase (iNOS) and subsequent nitric oxide (NO) and peroxynitrite generation in experimental stroke and inflammation. Rats underwent 2 hr of middle cerebral artery occlusion (MCAO). Brain inflammation was modeled by intravenous lipopolysaccharide (LPS) (2 mg/kg) injection. Temperature was maintained at 33 degrees C for 2 hr immediately after MCAO and LPS injection, delayed 2 hr after MCAO or maintained at 38 degrees C. Cultured microglia were activated with LPS and then incubated at 33 or 37 degrees C. Both intraischemic and delayed mild hypothermia attenuated infarct size by 40% (p < 0.05). Immunohistochemistry was performed to identify cell type, iNOS, and peroxynitrite. The majority of iNOS- and peroxynitrite-positive cells were activated microglia-macrophages, and mild hypothermia significantly decreased the numbers of immunoreactive cells at 72 hr by >50% (p < 0.05). After ischemia, mild hypothermia decreased NO production by 40%. Similarly, hypothermia attenuated NO and iNOS in LPS-injected rats, as well as in cultured microglia. Aminoguanidine, an iNOS inhibitor, also attenuated infarct size and NO in ischemic and inflammation models. We conclude that mild hypothermia significantly inhibits the inflammatory response by affecting microglial iNOS-NO generation. Therapies directed against microglia or their activation may be useful in treating stroke.

Animals↗
PubMed1999

Relationship between mucosal levels of Helicobacter pylori-specific IgA, interleukin-8 and gastric inflammation.

Mucosal IgA is important in local immune defence. Helicobacter pylori induces a specific IgA response in antral mucosa, but its immunopathology is unknown. Interleukin-8 (IL-8) has been suggested to be important in H. pylori-induced inflammation. Current information on the relationship between H. pylori-induced IgA and mucosal inflammation is limited. To investigate possible associations between mucosal-specific IgA, the toxinogenicity of H. pylori, mucosal levels of IL-8 and gastric inflammation, 52 endoscoped patients were studied. These comprised 28 patients with peptic ulcer and 24 with non-ulcer dyspepsia. Of these patients, 38 had H. pylori infection: 28 with peptic ulcer and 10 with non-ulcer dyspepsia. Antral biopsies were taken for histology, H. pylori culture and measurement of mucosal levels of IL-8 (pg/mg) and specific IgA (A450x1000) by ELISA. Mucosal H. pylori IgA was detectable in 35 out of 38 patients with H. pylori infection, with a median (interquartile) level of 220 (147, 531) units. There was no significant difference in mucosal levels of the IgA antibodies between patients infected with cytotoxin-positive or cagA-positive strains of H. pylori and those with toxin-negative or cagA-negative strains. The IgA levels in those patients with severe neutrophil infiltration were lower than in those with mild or moderate infiltration (P<0.05). There was a weak inverse correlation between antral mucosal IgA and IL-8 in infected patients (r=-0.36; P=0.04). H. pylori infection induced a significant local mucosal IgA response in most infected patients. The level of IgA antibodies does not appear to be correlated with the toxinogenicity of H. pylori. However, patients with severe active inflammation appear to have decreased levels of IgA. An inverse correlation between mucosal IL-8 and IgA may suggest that IL-8-induced inflammation compromises the mucosal IgA defence and renders the mucosa susceptible to further damage.

Adult↗
PubMed1999

Suppression of renal inflammation with vitamins A and E in ascending pyelonephritis in rats.

PURPOSE: We evaluated the effects of vitamin A and E supplementation alone or in combination with non-steroidal anti-inflammatory drugs (NSAIDs) on the development of inflammation in an animal model of ascending pyelonephritis. MATERIALS AND METHODS: Ascending pyelonephritis was induced in adult rats by surgical bladder inoculation with P-pili-forming Escherichia coli. Treatment of pyelonephritic rats was initiated at 72 hours post-infection. Treatment groups included no treatment, or a five day regimen of antibiotic only, antibiotic plus vitamins A and E, or antibiotic, vitamins and either of two NSAIDs. Kidneys were harvested at six weeks post-infection and assessed for histopathologic inflammation. RESULTS: Antibiotic treatment of pyelonephritic rats with vitamins A and E alone or in combination with NSAIDs resulted in significantly less kidney inflammation, as compared with untreated rats or rats treated with antibiotic alone. There was no significant difference in inflammation between animals treated with vitamins alone or vitamins plus NSAIDs. CONCLUSIONS: Antibiotic therapy and diet supplementation with vitamins A and E can significantly reduce the inflammation associated with ascending pyelonephritis, suggesting a potential use in the medical management of reflux nephropathy in children.

Animals↗
PubMed1999

Leukocyte entry into sites of inflammation requires overlapping interactions between the L-selectin and ICAM-1 pathways.

Leukocyte interactions with vascular endothelium during inflammation depend on cascades of adhesion molecule engagement, particularly during selectin-mediated leukocyte rolling. Leukocyte rolling is also facilitated by members of the integrin and Ig families. Specifically, leukocyte rolling velocities during inflammation are significantly increased in ICAM-1-deficient mice, with ICAM-1 expression required for optimal P- and L-selectin-mediated rolling. Elimination of ICAM-1 expression in L-selectin-deficient mice significantly reduces leukocyte rolling. Whether disrupted leukocyte rolling in L-selectin and ICAM-1 double-deficient (L-selectin/ICAM-1-/-) mice affects leukocyte entry into sites of inflammation in vivo was assessed in the current study by using experimental models of inflammation; thioglycollate-induced peritonitis, chemokine-induced neutrophil migration to the skin, delayed-type hypersensitivity responses, rejection of allogeneic skin grafts, and septic shock. In many cases, the loss of both L-selectin and ICAM-1 expression dramatically reduced leukocyte migration into sites of inflammation beyond what was observed with loss of either receptor alone. In fact, the effects from loss of both L-selectin and ICAM-1 effectively eliminated multiple chronic inflammatory responses in L-selectin/ICAM-1-/- mice. By contrast, the combined loss of L-selectin and ICAM-1 expression had minimal effects on the generation of Ag-specific T cell responses or humoral immunity. Thus, members of the selectin and Ig families function synergistically to mediate optimal leukocyte rolling and entry into tissues, which is essential for the generation of effective inflammatory responses in vivo.

Animals↗
PubMed2000

Evidence of subclinical intestinal inflammation by 99m technetium leukocyte scintigraphy in patients with HLA-B27 positive juvenile onset active spondyloarthropathy.

OBJECTIVE: The concept that gut inflammation is implicated in the pathogenesis of spondyloarthropathies (SpA) has long been considered. Subclinical intestinal inflammation has been reported in adult patients with SpA by histological examination of intestinal biopsies. We assessed the presence of gut inflammation by abdominal 99mTc-hexamethyl propylene amine oxime (99mTc-HMPAO) labeled leukocyte scintigraphy in a group of children and adolescents with HLA-B27 positive SpA without gastrointestinal (GI) symptoms, and correlated the scintigraphic results to disease activity. METHODS: Abdominal scintigraphy with 99mTc-HMPAO labeled leukocytes was performed in 27 HLA-B27 positive children and adolescents with SpA without GI symptoms. Patients were divided into 2 groups according to the presence of active or inactive joint disease: Group A, 17 patients with active disease, and Group B, 10 patients with inactive disease. Patients with positive abdominal scintigraphy underwent complete bowel investigation by means of small bowel barium follow-through, abdominal ultrasound scan, and ileocolonoscopy with mucosal biopsies. RESULTS: Thirteen of 27 patients (48%) had scintigraphy indicating the presence of bowel inflammation. All patients with abnormal scan had active joint disease, whereas no patient with inactive disease had a positive intestinal uptake of labeled leukocytes. Bowel investigation revealed the presence of aspecific mucosal inflammatory changes in the majority of patients with positive scintigraphy. CONCLUSION: The presence of intestinal leukocyte uptake only in patients with active joint disease, even if intestinal inflammatory changes were minimal and clinical gut manifestations were absent, supports the role of gut inflammation in the pathogenesis of joint disease in HLA-B27 positive patients with SpA.

Adolescent↗
PubMed2000

Modulation of acute inflammation and keratocyte death by suturing, blood, and amniotic membrane in PRK.

PURPOSE: To investigate the role of acute inflammation in keratocyte death, which may influence corneal haze after photorefractive keratectomy (PRK). METHODS: Transepithelial PRK was performed on both eyes of 30 rabbits. Twenty-six rabbits were divided into 4 groups receiving autologous blood, suturing alone, suturing with amniotic membrane graft, or no treatment as the control. Twenty-four hours later, the ablated zone was analyzed for keratocyte death by TdT-dUTP terminal nick-end label (TUNEL) staining and transmission electron microscopy, for polymorphonuclear cell (PMN) infiltration by hematoxylin-eosin staining, and for oxygen radical-induced lipid peroxidation by malondialdehyde immunohistochemistry. The remaining four rabbits were subjected to PRK or mechanical scraping and analyzed immediately or after culturing for 24 hours. RESULTS: Compared with the control group where TUNEL-positive keratocytes were found only in the superficial ablated stroma, blood application or suturing caused more and deeper keratocyte death and PMN infiltration (P: < 0.05). The amniotic membrane graft group had less keratocyte death and PMN than the control or the suture group (P: < 0.05 and P: < 0.01, respectively). There was a strong correlation between keratocyte death and PMN infiltration (P: < 0.01, correlation factor = 0.786). Transmission electron microscopy revealed that the majority of keratocyte death was due to necrosis. Amniotic membrane stroma trapped and prevented PMN infiltration into the stroma. Malondialdehyde-modified antigen was found on the ablated surface and around infiltrated PMN. CONCLUSIONS: Transepithelial PRK causes oxygen radical-mediated lipid peroxidation on the superficial stroma and may contribute to superficial keratocyte death even in the absence of inflammation. Mechanical scraping leads to apoptosis without the participation of inflammation. Keratocyte death by necrosis spreads to the deeper part of the stroma and correlates with additional acute inflammation. Amniotic membrane precludes PMN infiltration and decreases lipid peroxidation and keratocyte death. Future studies are needed to discern whether prevention of inflammation-mediated keratocyte necrosis can reduce unwanted scarring caused by PRK.

Amnion↗
PubMed2000

Peri-implant mucosal inflammation and bone loss: clinical and radiographic evaluation of 108 dental implants after 1-year loading.

OBJECTIVE: To evaluate the clinical outcomes, and a possible correlation between peri-implant mucosal inflammation and marginal bone loss, 1 year after restoration in a group of Chinese patients with dental implants. METHODS: Observation of the clinical and radiographic parameters of 108 IMZ and Frialit-2 dental implants in 70 patients. RESULTS: One year after loading, there were no signs of mobility and peri-implant radiolucency in any of the implants. The average bone loss adjacent to implants was 0.63 mm (SD 0.78). The prevalence of peri-implant mucosal inflammation, as indicated by sulcus bleeding index (SBI) of 1.0 or more, was 32.9%. Significant positive correlation was found between mucosal inflammation and bone loss (P < 0.05). 92% of the observed sites had plaque index (PLI) scores greater than 1. CONCLUSIONS: The 1-year outcomes from this patient group indicate that IMZ and Frialit-2 implants provide satisfactory clinical results. One of the etiologic factors of alveolar bone loss around implants seems to be plaque-associated marginal inflammation. Improvement of oral hygiene, elimination of soft tissue inflammation, and proper treatment of periodontal disease of natural teeth are critical for maintaining the implants.

Adolescent↗
PubMed2001

Recombinant human interleukin-11 restores smooth muscle function in the jejunum and colon of human leukocyte antigen-B27 rats with intestinal inflammation.

Recombinant human interleukin (rhIL)-11 has anti-inflammatory and protective effects in models of intestinal mucosal injury. Our aim was to investigate whether oral treatment with rhIL-11 reverses functional abnormalities in intestinal muscle contractility resulting from human leukocyte antigen (HLA)-B27-dependent gut inflammation. Isometric contractions were studied in jejunal and colonic longitudinal muscles. Muscle strips were isolated from HLA-B27 transgenic rats with spontaneous inflammation following treatment with enteric-coated rhIL-11 multiparticulates (500 microg/kg) or placebo multiparticulates given orally every 48 h for 2 weeks. Myeloperoxidase (MPO) activity was measured in intestinal tissue samples and served as an index of inflammation. Colonic damage was also assessed histologically. The HLA-B27 rats receiving placebo had chronic diarrhea, and MPO activity was increased in the jejunum and colon. Intestinal inflammation was associated with a decreased ability of the muscles to generate active tension in response to electrical field stimulation, carbachol, or high KCl. In the jejunum of placebo-treated HLA-B27 rats, concentration-effect curves for carbachol were shifted to lower concentrations yielding a higher EC50. Oral treatment of HLA-B27 rats with rhIL-11 suppressed the symptoms of diarrhea, normalized MPO activity, and improved the colonic damage score. Simultaneously, neurally mediated responses were improved and the maximal tension generated by carbachol or KCl was normalized in the jejunum and colon. The EC50 for carbachol in the jejunum of HLA-B27 rats was also normalized by rhIL-11 treatment. Our data demonstrate that oral administration of enteric-coated rhIL-11 suppresses intestinal inflammation and reverses intestinal smooth muscle dysfunction in HLA-B27 transgenic rats.

Animals↗
PubMed1999

[Kinin generation in acute and chronic airway inflammation].

OBJECTIVE: To investigate the kinin generation pathways in acute and chronic airway inflammation. METHODS: BALF from patients with acute, chronic airway inflammation and healthy controls were collected. Kinins, Plasma kallikrein, alpha 2-macroglobulin and toluenesulphonyl-arginine methyl ester esterase activity (TAME-ea) in BALF were studied. RESULTS: Kinins and TAME-ea values were significantly higher in the BALF of patients with acute and chronic airway inflammation than those in the controls, but there was no significant difference between acute and chronic groups; PK and alpha 2-M values were significantly higher in the acute group than the in chronic one. Gel filtration revealed the highest TAME-ea peak at about 800,000 in the acute group, corresponding with the first alpha 2-M peak, whereas at about 40,000 in chronic bronchitis. The inhibition test of the TAME-ea showed that the TAME-ea peak at 800,000 was mainly due to PK and the TAME-ea peak at 40,000 was mainly due to TK. CONCLUSIONS: The results indicated that in acute airway inflammation kinins seem to be mainly generated by PK, whereas in chronic inflammation kininogenases other than PK--such as TK--seem to be more important.

Acute Disease↗
PubMed2002

Antigenic mimicry: Onchocerca volvulus antigen-specific T cells and ocular inflammation.

PURPOSE: Molecular mimicry has been suggested to play a role in the development of ocular onchocerciasis. The Onchocerca volvulus antigen Ov39 is cross-reactive with the retinal antigen hr44 and induces ocular inflammation in rats after immunization. This study was undertaken to determine whether Ov39-derived T-cell lines, which proliferate in response to stimulation with hr44, can transfer disease to naive Lewis rats. METHODS: Two separately derived IL-2-dependent CD4(+) T-cell lines, LKOV39 1.8 and LKOV39 4.5, specific to Ov39 were transferred to naïve Lewis rats. A T-cell line specific to the peripheral nerve protein P2 served as a positive control for transfer of disease. Ocular tissues were analyzed by immunohistology, and sera were tested for the presence of antibodies to hr44. RESULTS: Transfer of both T-cell lines caused inflammation of the limbus, iris, and choroid. In addition, LKOV39 1.8, which produced slightly more inflammation, induced activation of retinal microglia. LKOV39 4.5 induced a dose-dependent influx of CD8(+) cells into the limbus and the uvea. Sera from rats that received the T-cell lines had no significant antibody responses to hr44. CONCLUSIONS: These findings indicate that CD4(+) cell lines specific to the antigen Ov39 can induce ocular inflammation in naïve rats and suggest that recruitment of CD8(+) T cells may play a regulatory role. The inflammation is milder than that produced by immunization. The absence of antibody responses to hr44 in the animals receiving the T-cell lines may indicate a role for antibody in the development of ocular onchocerciasis.

Adoptive Transfer↗
PubMed2002

Distribution of chronic prostatitis in radical prostatectomy specimens with up-regulation of bcl-2 in areas of inflammation.

PURPOSE: We examined the anatomical relationship of chronic prostatitis with prostate cancer and benign prostatic hyperplasia (BPH) based on the hypothesis that there may be an association of prostatitis with these other entities that may involve up-regulation of bcl-2. MATERIALS AND METHODS: We examined 40 whole mount radical prostatectomy specimens for the presence and distribution of chronic inflammatory infiltrate. Immunostaining for bcl-2 was done in 10 cases. RESULTS: Chronic prostatitis was identified in all 40 cases with peripheral zone inflammation in 95% and transition zone inflammation in 87.5%. In all cases of transition zone inflammation the infiltrate was noted within and/or around BPH. Inflammatory infiltrate was microscopically associated with prostate cancer in 23 of the 40 cases (57.5%). In these 23 cases, there was no association of inflammation with Gleason score, preoperative prostate specific antigen, positive margins, or seminal vesicle invasion. Patients with BPH unassociated with prostatitis had significantly smaller prostate weight (median 32 gm.) and were younger (mean age 54.4 years) than those with BPH associated with prostatitis (median weight 40 gm. and mean age 61.4 years, p <0.05). Bcl-2 staining was intensified in benign glands within areas of prostatitis in all 10 cases examined. CONCLUSIONS: Chronic prostatitis is a common finding in radical prostatectomy specimens. Inflammation was associated with BPH and cancer but had a greater tendency to be associated with BPH. Bcl-2 was prominently expressed in areas of prostatitis. Our findings indirectly support a potential role for prostatitis in the pathogenesis of BPH.

Aged↗
PubMedDate not supplied

Sinus inflammation associated with contralateral inverted papilloma.

OBJECTIVE: To assess with computerized tomography (CT) the association of unilateral inverted papilloma (IP) and contralateral sinus inflammation. DESIGN: Retrospective analysis of CTfindings in a sample of patients with unilateral IP, a sample with other unilateral sinonasal tumors, and normal controls. PATIENTS AND METHODS: Sixteen patients with unilateral IP comprised the study population. Nine patients with other unilateral sinonasal tumors (five with squamous papilloma, two with squamous cell carcinoma, and one each with adenocarcinoma and large cell carcinoma) were used as a comparison population. Patients undergoing maxillofacial CTfor nontraumatic orbital conditions comprised the control sample (n = 12 sides). Each patient's preoperative CT scan was evaluated with a modified Lund-Mackay scoring system. The scores for the sides opposite the IPs were compared with the sides contralateral to other sinonasal tumors as well as to normal controls. RESULTS: Analysis of all three samples' contralateral sides simultaneously using analysis of variance revealed a difference (p = 0.010). The contralateral sinus scores in IPs tended to be higher than the sides opposite the other sinonasal tumors (mean, 2.66 +/- 1.07 versus 1.18 +/- 0.76; p = 0.06). These in turn were higher than the normal controls (mean, 0.75 +/- 0.48; p < 0.02). CONCLUSIONS: Unilateral IPs are associated with contralateral inflammation as detected by CT. This degree of contralateral inflammation is greater than that seen in other sinonasal tumors. The etiology of this association is unclear. A recent histological review suggested IP is an inflammatory polyp and not a true papilloma. Our data further suggest inflammation may be involved in the pathogenesis of IP. Further work is needed to better understand the pathophysiology and behavior of IP and to define its relationship to sinus inflammation.

Humans↗
PubMed2000

Chronic inflammation in dermoid cysts: a clinicopathologic study of 115 patients.

PURPOSE. To analyze the frequency, pattern, and extent of chronic inflammation in orbital and periorbital dermoid cysts and to correlate these findings with clinical data. PATIENTS AND METHODS. We reviewed the clinical and histopathologic data of 115 consecutive patients with histopathologically confirmed orbital or periorbital dermoid cysts between 1980 and 1998. RESULTS. Sixty-one patients were male and 54 female. Their mean age at the time of surgery was 13 years. The lesion was located superotemporally in 71% of the patients. Patients presented most commonly with a palpable mass without clinical signs of inflammation. The mean cyst volume was 1276 mm(3) (range: 72 to 9900 mm(3)). Histopathologically, 50 lesions (43%) showed chronic granulomatous inflammation of the cyst wall. In 16% of them, the inflammatory response completely replaced the epidermal elements and the normal architecture of the cyst wall. Nine lesions showed spread of granulomatous cell infiltration to the surrounding tissue. Granulomatous inflammation was detected more frequently (p<0.001, chi-square test) with increasing age in patients younger than 30 years, being found in 25% of the patients aged 5 years or younger and in 80% of the patients between 16 and 30 years of age. It was also more common (p<0.001, chi-square test) in cysts larger than 1000 mm(3). CONCLUSION. The frequency of chronic granulomatous inflammation of dermoid cysts and its correlation with patient's age and cyst volume suggest that patients should be operated before the age of five years and that large dermoid cysts (>1000 mm(3)) should be removed early.

Journal Article↗
PubMed2001

[The role of immune cells and inflammatory mediators in pathogenesis of intestinal inflammation].

The initiators of intestinal inflammation are greatly variable, but the mechanisms underlying the immunologically mediated mucosal damage are similar. A great progress in our understanding of the functions of gut-associated lymphoid tissue was achieved because of the advances in immuno-biology and molecular immunology. At the beginning of an inflammation microorganisms and hither to derived products or allergen firstly stimulate and activate the specific and nonspecific immune cells, and then intestine epithelials, macrophages and lymphocytes release various cytokines. These cytokines are able to recruit more immune cells to be activated and more cytokines to be released. A "cascade" is then generated between epithelials, macrophages and lymphocytes. Finally the inflammation in certain area of intestinal tract is generated. The balance between inflammatory factors and anti-inflammatory molecules depends the results of the inflammation. Therefore, the better understanding of the mechanisms on inflammatory and anti-inflammatory factors is helpful for the diagnosis and treatment of intestinal inflammation.

Animals↗
PubMed1992

Spondylarthropathy and gut inflammation: immunopathogenetic mechanisms.

In 62% of patients with spondylarthropathy (SpA) we found clinically unsuspected gut inflammation to feature acute or chronic enterocolitis on ileocolonoscopy. A proportion of patients of the latter group had subclinical Crohn's disease as demonstrated clinically, endoscopically, genetically, histologically and immunopathologically. There is a relation between the activity of the gut inflammation and clinical rheumatic symptoms. A pathogenetic mechanism is increased handling of luminal (bacterial or nutritional) antigen, hence inducing T-cell activation and intestinal inflammation. In ileal mucosal biopsies we showed two different cellular events: increased enterocytic expression of class II molecules in active inflammation and an increase of membranous (M) cells overlying lymphocytes in inflamed mucosa. Although the number of intraepithelial lymphocytes was not increased in inflammation, intraepithelial T lymphocytes had protruding processes in close apposition to the tips of epithelial plasma membranes. Lymphocytes crossing the basement membrane were a frequent finding. These features indicate that the intestinal immune response caused by increased antigen processing in the terminal ileum induces an inflammatory immunocascade responsible for the clinical picture of SpA.

Adolescent↗
PubMed2004

[The evolvement of Th1/Th2 imbalance in the process of airway inflammation in a rat asthmatic model].

OBJECTIVE: T lymphocytes play an important role in the development of asthmatic airway inflammation. By observing the production of interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) released by peripheral T lymphocytes in asthmatic rat models, this study was designed to clarify the changes of T lymphocytes during the course of airway inflammation. The influence of dexamethasone pre-treatment on the production of IFN-gamma and IL-4 by T lymphocytes was also investigated in the study. METHODS: Twenty-four rats were divided into the study group (group A) and the control group (group B). In the study group, rats were subdivided into two groups with 8 rats in each group. one group (group A(2)) received pre-treatment with intraperitoneal injection with dexamethasone (10 mg/kg), and another group (group A(1)) did not receive dexamethasone pre-treatment, The control group was matched with the study group with regard to both age and weight. Rats were sensitized and challenged by ovalbumin (OVA), and blood samples were obtained and the percentage of IFN-gamma(+)CD(4)(+), IFN-gamma(+)CD(8)(+) and IL-4(+)CD(4)(+) cells were assessed by intracellular cytokine staining and flow cytometric analysis at 2 h, 4 h, 6 h, 8 h, 10 h, 12 h, 24 h, 36 h, 48 h, 72 h, 6 d, 9 d, 12 d, and 15 d after OVA challenge. RESULTS: In group A(1), the peripheral IFN-gamma(+)CD(4)(+) cells, IFN-gamma(+)CD(8)(+) cells, and IL-4 CD(4)(+) cells increased 2 h after OVA challenge [(5.7 +/- 1.6)%, [(11.5 +/- 5.1)%, (1.66 +/- 0.95)%] compared with group A(2) [(2. 6 +/- 1.3)%, (6.1 +/- 1.8)%, (0.77 +/- 0.37)%, P < 0.05 respectively] and group B [(1.8 +/- 0.7)%, (3.9 +/- 1.5)%, (0.65 +/- 0.12)%, P < 0.05 respectively]. The peripheral IFN-gamma(+)CD(4)(+) cells and IFN-gamma(+) CD(8)(+) cells in group A(1) reached their maximal level at 10 h [(9.9 +/- 4.4)%, (38.7 +/- 6.3)%] compared with group A(2) [(4.9 +/- 1.7)%, (15.7 +/- 8.7)%, P < 0.05 respectively and group B [(1.5 +/- 0.5)%, (6.4 +/- 1.5)%, P < 0.05 respectively], and then decreased afterward. The IL-4(+) CD(4)(+) cells in group A(1) at 10 h after challenge was (2.16 +/- 0.75)%. There was no statistical difference compared with group A(2) [(1.39 +/- 0.77)%, P > 0.05], but it was higher than group B [(0.68 +/- 0.15)%, P < 0.05]. The highest level of IL-4(+) CD(4)(+) cells of group A(1) was observed at 36 h [(4.0 +/- 1.6)%], and there was a statistical difference compared with group A(2) [(1.5 +/- 1.0)%, P < 0.05] and group B [(0.7 +/- 0.3)%, P < 0.05]. CONCLUSIONS: Both IFN-gamma and IL-4 generated by peripheral blood T cells in the rat asthmatic models played a role in the development of airway inflammation. INF-gamma dominated at early stage of the airway inflammation, whereas IL-4 took the major effect at the late stage of inflammation. The production of IFN-gamma and IL-4 by T lymphocytes in the asthmatic model was inhibited significantly by dexamethasone.

Animals↗