Tumor necrosis factor α, protein gene product 9.5, matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 presence in congenital intra-abdominal adhesions in children under one year of age

IntroductionThe regulatory role of cytokines and extracellular matrix remodeling factors in congenital intra-abdominal adhesions has not yet been defined. The aim of this study was to assess the presence and relative distribution of tumor necrosis factor α (TNF-α), protein gene product 9.5 (PGP 9.5), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in adhesions.Material and methodsTNF-α, PGP 9.5, MMP-2 and TIMP-2 were detected using immunohistochemical methods and their relative distribution was evaluated by means of the semiquantitative counting method. The results were analyzed using non-parametric statistical methods.ResultsA moderate number of TNF-α positive macrophages and fibroblasts was found. A positive correlation was observed between the immunoreactive structures for TNF-α and PGP 9.5. A positive reaction for PGP 9.5 was observed in nerve fibers and shape modified fibroblasts. In control group tissues, positive structures were seen in significantly higher counts for PGP 9.5. Few to moderate numbers of MMP-2 positive macrophages, epithelioid cells, fibroblasts and endotheliocytes were detected. There was no significant difference between the groups. A positive reaction for TIMP-2 was seen in fibroblasts, macrophages and endotheliocytes. In control group tissues, positive structures were found in significantly higher counts for TIMP-2.ConclusionsThe positive correlation between the immunoreactive structures for TNF-α and PGP 9.5 suggests that nerve in-growth into intraabdominal adhesions might be induced by TNF-α and PGP 9.5 could have a role in maintaining inflammation. The down-regulation of PGP 9.5 suggests that pathogenesis of congenital intraabdominal adhesions may be related to hypoxia induced damage. The imbalance between MMP-2 and TIMP-2 may prove tissue fibrosis as a response to congenital peritoneal adhesions.

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MMP-2 Plays an Important Role During the Early Acute Developmental Phase of Oligofructose-Induced Equine Laminitis

Bulletin of the Veterinary Institute in Pulawy ◽

10.1515/bvip-2015-0022 ◽

2015 ◽

Vol 59 (1) ◽

pp. 149-153 ◽

Cited By ~ 1

Author(s):

Xinran Li ◽

Renli Jiang ◽

Guanying Wang ◽

Yue Li ◽

Xiaojing Fan ◽

...

Keyword(s):

P38 Mapk ◽

Plasma Concentrations ◽

Clinical Signs ◽

Tissue Inhibitor Of Metalloproteinase ◽

Matrix Metalloproteinase 2 ◽

Developmental Phase ◽

Tnf Α ◽

Mitogen Activated Protein ◽

Factor Α ◽

Necrosis Factor

Abstract The study was conducted on 24 Mongolian horses, with oligofructose-induced equine laminitis (10 g/kg b.w.). The objective of the study was to investigate the relationships among matrix metalloproteinase 2 (MMP-2), P38 mitogen-activated protein kinases (P38 MAPK), tissue inhibitor of metalloproteinase 2 (TIMP-2), lipopolysaccharides (LPS), and tumour necrosis factor-α (TNF-α) during acute developmental phase of laminitis, and to determine whether there are any characteristic tendencies. Moreover, plasma concentrations of LPS and TNF-α were measured in order to determine the time of leukocytes’ activation. Eleven of the 12 horses showed clinical signs of laminitis. The contents of MMP-2 and P38 MAPK increased significantly from 8 h to 64 h, and the content of TIMP-2 decreased significantly at the same time. Plasma LPS concentrations increased significantly between 8 h and 20 h and reached a peak of 0.024 ± 0.009 EU/mL (equivalent to 3.04 ± 1.19 pg/mL) at 12 h. TNF-α concentration increased between 20 h and 36 h. This data indicates that MMP-2 plays an important role during the early acute developmental phase of oligofructose-induced equine laminitis.

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The Effects of Rice Husk Liquid Smoke in Porphyromonas gingivalis-Induced Periodontitis

European Journal of Dentistry ◽

10.1055/s-0041-1727554 ◽

2021 ◽

Author(s):

Theresia Indah Budhy ◽

Ira Arundina ◽

Meircurius Dwi Condro Surboyo ◽

Anisa Nur Halimah

Keyword(s):

Growth Factor ◽

Porphyromonas Gingivalis ◽

Rice Husk ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Control Group ◽

Proliferation Markers ◽

Liquid Smoke ◽

Tnf Α ◽

Factor Α

Abstract Objectives The purpose of this study is to analyze the effects of rice husk liquid smoke in Porphyromonas gingivalis-induced periodontitis in the inflammatory and proliferation marker such as nuclear factor kappa β (NF-kB), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), transforming growth factor-β (TGF-β), fibroblast growth factor 2 (FGF2), collagen type 1 (COL-1) expression, and the number of macrophages, lymphocytes, and fibroblasts. Materials and Methods Rice husk liquid smoke is obtained by the pyrolysis process. Porphyromonas gingivalis-induced periodontitis in 20 μL phosphate-buffered saline containing 1 × 109 CFU was injected into the lower anterior gingival sulcus of Wistar rats. The periodontitis was then treated with 20 μL/20 g body weight of rice husk liquid smoke once a day for 2 and 7 days, respectively. After treatment, the bone and lower anterior gingival sulcus were analyzed with immunohistochemistry and hematoxylin–eosin staining. Results The treatment of periodontitis with rice husk liquid smoke showed a lower NF-kB, TNF-α, and IL-6 expression and a higher TGF-β, FGF2, and COL-1 expression than the control after treatment for 2 and 7 days (p < 0.05), respectively. The number of macrophages and fibroblasts was also higher when compared with the control group (p < 0.05), but the number of lymphocytes was lower than the control (p < 0.05). Conclusion Rice husk liquid smoke showed its effects on Porphyromonas gingivalis-induced periodontitis with a decrease in inflammatory markers and an increase in proliferation markers. The development of a rice husk liquid smoke periodontitis treatment is promising.

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Association of Tumor Necrosis Factor-α -308G>A, -238G>A and -376G>A polymorphisms with recurrent pregnancy loss risk in the Greek population

Fertility Research and Practice ◽

10.1186/s40738-021-00101-x ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Sofoklis Stavros ◽

Despoina Mavrogianni ◽

Myrto Papamentzelopoulou ◽

Evaggelos Basamakis ◽

Hend Khudeir ◽

...

Keyword(s):

Pregnancy Loss ◽

Recurrent Pregnancy Loss ◽

Pcr Amplification ◽

Greek Population ◽

Control Group ◽

Increased Risk ◽

Tnf Α ◽

Caucasian Women ◽

Factor Α ◽

And Control

Abstract Background Promoter region SNPs in TNF-α have been studied in association with Recurrent Pregnancy Loss (RPL) occurrence in various populations. Among them, −238G > A, −308G > A and − 376G > A have been frequently investigated for their potential role in recurrent abortions. The aim of the present study is to evaluate the correlation among TNF-α 238, TNF-α 308 and TNF-α 376 polymorphisms and recurrent pregnancy loss risk in Greek women. Methods This study included 94 Caucasian women with at least two miscarriages of unexplained aetiology, before the 20th week of gestation. The control group consisted of 89 Caucasian women of proven fertility, with no history of pregnancy loss. DNA samples were subjected to PCR amplification using specific primers. Sanger sequencing was applied to investigate the presence of TNF-α 238, TNF-α 308, TNF-α 376 polymorphisms in all samples. Results The TNF-α 238 and TNF-α 308 variants were both detected in RPL and control groups (7.45% vs 4.49 and 45.16% vs 36.73%, respectively), but with no statistically significant association (p-value 0.396 and 0.374, respectively). The TNF-α 376 variant was not detected at all in both control and RPL groups. When TNF-α 238 and TNF-α 308 genotypes were combined no association with RPL was detected (p-value = 0.694). In subgroup analysis by parity, RPL patients carrying the A allele reported less previous births. Conclusions This is the first study demonstrating TNF-α 238 and TNF-α 308 gene expression and the absence of TNF-α 376 variant in Greek women with RPL. However, no association emerged between each polymorphism studied and the occurrence of recurrent pregnancy loss. Accordingly, TNF-α -308G > A, −238G > A and -376G > A variants are not considered genetic markers for identifying women at increased risk of recurrent pregnancy loss in the Greek population.

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The Immuno modulatory Changes of Patients with Tuberculosis.

International Journal of Research in Pharmaceutical Sciences ◽

10.26452/ijrps.v9ispl1.1386 ◽

2018 ◽

Vol 9 (SPL1) ◽

Author(s):

Rafal J Al-Saigh ◽

Hussam Al-Humadi

Keyword(s):

Rural Areas ◽

Liver Function Tests ◽

Pulmonary Diseases ◽

Control Group ◽

Chronic Obstructive ◽

Descriptive Data ◽

Tnf Α ◽

Significant Difference ◽

Level Versus ◽

Factor Α

Tuberculosis(TB) is aninfectious disease caused by Mycobacterium tuberculosis. The aim was to investigate the levels of immunomodulatory markers like interluekin-6 (IL-6), tumor necrotizing factor-α (TNF- α),cell differentiation-4 (CD4) and CD8 levels in those patients with active tuberculosis (TB) disease in comparison with control group. 41 Adults diagnosed with TB were included in comparison to 32 healthy individuals at Babylon health center for pulmonary diseases and TB. Descriptive data for patients and control group werecollected by well-trained researcher following a structured questionnaire. In parallel, peripheral blood collected to determine IL-6, TNF- α,CD4 and CD8. Then the assessment for the association between clinical and descriptive data and immunomodulatory markers levels was investigated statistically. The majority of TB patients were males (56%) and 71% were resident in rural areas; 47% of them were living in middle socioeconomic state,moreover,47% of TB cases had diabetes,furthermore,51% had chronic obstructive pulmonary diseases,12% had hypertension and 39% of them had chronic anemia with 47% smokers with no significant difference versus control. Following to that,there was highly increased in IL-6 and TNF-α levels in TB patients versus control (P<0.001),with low CD4 level versus control (P<0.001). While there was no significant change shown in CD8 levels versus control and this might highly be correlated with 30% of abnormal liver function tests among TB patients. A high proportion of TB patients have low CD4 level mostly associated with active disease. Moreover,the increase of IL-6 and TNF-α levels suggests a inverse impact on CD4 level which closely associated with the outcome of the disease.

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Analysis on the Expression and Prognostic Value of LncRNA FAF in Patients with Coronary Heart Disease

BioMed Research International ◽

10.1155/2020/9471329 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Hai Xu ◽

Xiwen Zhang ◽

Kun Yu ◽

Gang Zhang ◽

Yafei Shi ◽

...

Keyword(s):

Risk Factors ◽

Coronary Heart Disease ◽

Heart Disease ◽

Poor Prognosis ◽

Prognostic Value ◽

High Sensitivity ◽

Control Group ◽

Coronary Lesion ◽

Tnf Α ◽

Factor Α

Objective. To investigate the expression and prognostic value of LncRNA FAF in patients with coronary heart disease. Patients and Methods. 97 patients with coronary heart disease who came to our hospital were selected as the research group (RG), and 97 healthy people who came to our hospital for physical examination during the same period were selected as the control group (CG). The serum LncRNA FAF, plasma homocysteine (HCY), lipoprotein A (Lp-a), serum tumor necrosis factor α (TNF-α), and high-sensitivity C-reactive protein (hsCRP) in the two groups of patients were detected, and their correlations were analyzed. Then, the predictive value and risk factors of FAF for poor prognosis of patients with coronary heart disease were analyzed. Results. The expression of LncRNA FAF in the serum of patients in the RG was significantly lower than that in the CG, and the expressions of HCY, Lp-a, TNF-α, and hsCRP were significantly higher than those in the CG (p <0.05). The AUC of FAF in the diagnosis of coronary heart disease was more than 0.9. FAF was negatively correlated with the coronary lesion vessels, HCY, Lp-a, TNF-α, and hsCRP expressions in patients with coronary heart disease ( p < 0.05 ). The ROC of FAF for predicting poor prognosis in patients with coronary heart disease was greater than 0.9. Low expression of FAF; high expressions of HCY, Lp-a, and hsCRP; and increase of coronary lesion vessels were independent risk factors for poor prognosis in patients with coronary heart disease. Conclusions. LncRNA FAF was lowly expressed in the serum of patients with coronary heart disease, and it was of high value in the diagnosis and prediction of poor prognosis of coronary heart disease. It was also an independent risk factor for poor prognosis of patients with coronary heart disease and may be a potential target for diagnosis and treatment of coronary heart disease.

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Temporal response of canine flexor tendon to limb suspension

Journal of Applied Physiology ◽

10.1152/japplphysiol.00051.2010 ◽

2010 ◽

Vol 109 (6) ◽

pp. 1762-1768 ◽

Cited By ~ 17

Author(s):

Yu-Long Sun ◽

Andrew R. Thoreson ◽

Stephen S. Cha ◽

Chunfeng Zhao ◽

Kai-Nan An ◽

...

Keyword(s):

Flexor Tendon ◽

Control Level ◽

Tissue Inhibitor Of Metalloproteinase ◽

Matrix Metalloproteinase 2 ◽

Control Group ◽

Temporal Response ◽

Cross Sectional ◽

Clinical Disorders ◽

Catabolic Process ◽

Timp1 Expression

Tendon disuse, or stress deprivation, frequently accompanies clinical disorders and treatments, yet the metabolism of tendons subject to stress deprivation has rarely been investigated systematically. The effects of stress deprivation on canine flexor tendon were investigated in this study. One adult canine forepaw was suspended for 21 or 42 days. Control forepaws were collected from dogs that had no intervention on their limbs and paws. The expression of collagen I and III was not significantly altered in the tendons disused for 21 days but was significantly decreased at 42 days ( P < 0.03). The expression of collagen II, aggrecan, decorin, and fibronectin was significantly decreased in the tendons in the suspended limbs at 21 days ( P < 0.002) and further reduced at 42 days. With stress deprivation, the expression of matrix metalloproteinase 2 (MMP2) was significantly increased ( P < 0.004) at 21 and 42 days. The expression of MMP3 was significantly decreased at 21 and 42 days ( P < 0.03). The expression of MMP13 was not altered with stress deprivation at 21 and 42 days. The expression of MMP14 was significantly increased at 21 days ( P = 0.0015) and returned to the control level at 42 days. Tissue inhibitor of metalloproteinase 1 (TIMP1) expression was decreased after the limbs were suspended for 42 days ( P = 0.0043), but not 21 days. However, TIMP2 expression was not significantly different from control at 21 or 42 days. Furthermore, the cross-sectional area of the stress-deprived tendons at 42 days was decreased compared with the control group ( P < 0.01). The intervention method in this study did not result in any alteration of stiffness of the tendon. Our study demonstrated that stress deprivation decreases the anabolic process and increases the catabolic process of extracellular matrix in flexor tendon.

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The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2019-0331 ◽

2019 ◽

Vol 30 (6) ◽

Author(s):

Junaidi Khotib ◽

Naning Windi Utami ◽

Maria Apriliani Gani ◽

Chrismawan Ardianto

Keyword(s):

Tumor Necrosis Factor ◽

Rat Model ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Control Group ◽

Treatment Groups ◽

Tnf Α ◽

Α Level ◽

Factor Α ◽

Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

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T-614 inhibits human aortic adventitial fibroblast proliferation and promotes interleukin-8 production in vitro

Vascular ◽

10.1177/1708538119880088 ◽

2019 ◽

Vol 28 (3) ◽

pp. 314-320

Author(s):

Weiping Ci ◽

Tian Wang ◽

Taotao Li ◽

Jin Wan

Keyword(s):

Cell Viability ◽

Vascular Wall ◽

Underlying Mechanism ◽

Interleukin 8 ◽

Control Group ◽

Survival Fraction ◽

Tnf Α ◽

Significant Difference ◽

Factor Α

Objectives The effect and underlying mechanism of T-614 (iguratimod) on Takayasu’s arteritis (TA) are unknown. Here, we report the effects of T-614 on cell proliferation and interleukin-8 (IL-8) production in human aortic adventitial fibroblasts (HAAFs) in vitro and explore its initial benefit in terms of vascular wall inflammation and remodeling for patients with TA. Methods HAAFs were cultured with 0, 5, 50, 100, or 250 μg/ml T-614 in the absence or presence of tumor necrosis factor-α (TNF-α) in vitro. Cell viability was determined by a modified MTT assay. Supernatant IL-8 levels were measured by enzyme-linked immunosorbent assays. Results In the presence of TNF-α, compared to that in the control group, cell viability of HAAFs significantly decreased in the 50, 100, and 250 μg/ml T-614 treatment groups (OD value: P < 0.01, P < 0.001, P < 0.001, respectively; survival fraction (SF): P < 0.05, P < 0.001, P < 0.001, respectively). However, there was no significant difference in cell viability between TNF-α-stimulated and unstimulated groups at the same concentration of T-614. In the absence or presence of TNF-α, T-614 suppressed HAAF cell viability dose-dependently (OD value: r = −0.915, P = 0.000; r = −0.926, P = 0.000, respectively; SF: r = −0.897, P = 0.000; r = −0.885, P = 0.000, respectively). Compared to that in the control group, in the absence of TNF-α, IL-8 levels in the 5 and 100 μg/ml T-614-treated groups were significantly higher ( P < 0.05); in the presence of TNF-α, IL-8 levels in the 5, 50, and 100 μg/ml T-614-treated groups were significantly higher ( P < 0.001, P < 0.001, P < 0.01, respectively). Further, there was a negative correlation between supernatant IL-8 levels and T-614 concentration in groups stimulated with TNF-α ( r = −0.670, P = 0.000), but there was no significant correlation between these parameters in groups that were not stimulated with TNF-α. Conclusions In the absence or presence of TNF-α, T-614 can inhibit HAAF proliferation and promote IL-8 production in vitro; therefore, it could be used to prevent adventitial thickening of the aorta and improve vascular remodeling in inflammatory environments in vitro and might provide a new immunotherapeutic intervention for TA.

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Application of Dexmedetomidine in Cardiopulmonary Bypass Prefilling

Dose-Response ◽

10.1177/1559325820939764 ◽

2020 ◽

Vol 18 (3) ◽

pp. 155932582093976 ◽

Cited By ~ 1

Author(s):

Li Wang ◽

Shaowei Wang ◽

Zhen Xing ◽

Fulong Li ◽

Jinliang Teng ◽

...

Keyword(s):

Cardiopulmonary Bypass ◽

Cardiac Troponin ◽

Troponin I ◽

Serum Levels ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Anesthesia Induction ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

Objective: The purpose of this study was to explore the application of dexmedetomidine (Dex) in cardiopulmonary bypass. Methods: A total of 60 patients undergoing elective cardiopulmonary bypass were divided into control (C) group and Dex group. In the Dex group, appropriate amount of Dex was added into the membrane lung prefilling solution before anesthesia induction, while those in control group were given normal saline. The levels of mean arterial pressure (MAP) and heart rate (HR) at different times were measured. The levels of cardiac troponin I (CTNI), malondialdehyde (MDA), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) at different points (T0/T1/T2/T3/T4) in both groups were measured by enzyme-linked immunosorbent assay kits. Results: The intraoperative and postoperative levels of MAP and HR in the 2 groups were significantly lower than those preoperatively ( P < .05). The levels of MAP and HR in the Dex group were significantly lower than those of the C group ( P < .05). The levels of CTNI/MDA/IL-6/TNF-α at different points in both groups were significantly higher than those at T0 ( P < .05). The serum levels of CTNI, MDA, IL-6, and TNF-α in the Dex group at T1/T2/T3/T4 were significantly lower than those in the C group ( P < .05). The rate of arrhythmia in the Dex group was significantly lower than that in the C group ( P < .05). Conclusion: Dexmedetomidine has a stable effect in cardiopulmonary priming solution.

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The Morphopathogenetic Aspects of Intraabdominal Adhesions in Children under One Year of Age

Medicina ◽

10.3390/medicina55090556 ◽

2019 ◽

Vol 55 (9) ◽

pp. 556

Author(s):

Anna Junga ◽

Māra Pilmane ◽

Zane Ābola ◽

Olafs Volrāts

Keyword(s):

Extracellular Matrix ◽

Growth Factor ◽

Fibroblast Growth Factor ◽

Transforming Growth Factor ◽

Interleukin 4 ◽

Relative Distribution ◽

Fibroblast Growth ◽

Pgp 9.5 ◽

Intraabdominal Adhesions ◽

One Year

Background and Objectives: The morphopathogenesis of adhesions is a complex process, characterized by the accumulation of an extracellular matrix, inflammation and hypoxia. The regulatory role between morphopathogenic factors in adhesions has not yet been defined. The aim was to investigate the appearance of transforming growth factor beta (TGFβ), hepatocyte growth factor (HGF), basic fibroblast growth factor (FGF-2), fibroblast growth factor receptor 1 (FGFR1), vascular endothelial growth factor (VEGF), protein gene product 9.5 (PGP 9.5), chromogranin A (CgA), interleukin-1 alpha (IL-1α), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-8 (IL-8), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), human beta defensine-2 (HBD-2), matrix metaloproteinase-2 (MMP-2) and matrix metaloproteinase-2 tissue inhibitor (TIMP-2) in intraabdominal adhesions. Materials and Methods: The study material was obtained from 49 patients under one year of age with total or partial bowel obstruction. All factors were detected using immunohistochemistry methods and their relative distribution was evaluated by means of the semiquantitative counting method. Results: Intraabdominal adhesions are characterized by increased TGFβ, FGFR1, VEGF and decreased FGF-2, HGF, PGP 9.5, IL-1, IL-4, IL-8, TIMP-2 findings. The most significant changes observed were the remodulation of the extracellular matrix, promotion of neoangiogenesis and the maintenance of a prolonged inflammation. Conclusions: The increase in TGFβ, relative to the decrease of HGF, as well as the disbalance between MMP-2 and TIMP-2 proves an increased fibrosis in intraabdominal adhesions. Less detected FGF-2 and more prominent FGR1 findings points out a compensatory receptor stimulation in response to the lacking same factor. The decrease in PGP 9.5 and the increase in VEGF-positive macrophages indicate hypoxic injury and proves the stimulation of neoangiogenesis. An unpronounced IL-1 and marked IL-10 finding indicate the local tissue protection reaction, the decrease in IL-4 could be the direct cause of giant cells, but the decrease of IL-8 could confirm a delayed chemotaxis of inflammatory cells.

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