Localization of IL-1, IL-2, IL-4, IL-8 and TNF in Superficial Bladder Tumors Treated with Intravesical Bacillus Calmette-Guerin

Purpose

Cytokines have been detected in the urine during the first hours after intravesical Bacillus Calmette Guerin (BCG) treatment against superficial bladder cancer. To investigate the long-lasting mucosal inflammatory response, we analyzed intracellular cytokines by immunohistochemistry in biopsies taken 2 weeks after BCG treatment.

Materials and Methods

Tumor biopsies were obtained from 8 patients with noninvasive, papillary transitional cell carcinoma (TCC), and intracellular cytokines were visualized by immunohistochemistry using cytokine-specific monoclonal antibodies.

Results

Interleukin (IL)-1 beta sup + or tumor necrosis factor (TNF)-alpha sup + cells were abundant in tumor and stroma. Interleukin-1 alpha, IL-2, IL-4, IL-8 and TNF-beta were variably expressed, while IL-10 sup + and interferon (IFN)-gamma sup + cells were not detected. Among the few patients studied (5 responders and 3 nonresponders to BCG treatment) no single cytokine or cytokine profile was associated with clinical response to BCG therapy.

Conclusion

We conclude that the in situ cytokine response after BCG treatment is highly complex, since cytokine profiles differed among the 8 patients investigated and between tumor and surrounding tumor-free mucosa. Further studies, investigating larger number of patients, is required to clarify whether cytokine profiles correlate with the clinical response to BCG.     

Diltiazem restores IL-2, IL-3, IL-6, and IFN-gamma synthesis and decreases host susceptibility to sepsis following hemorrhage

Various beneficial effects of calcium channel blockers on cell and organ function following endotoxic shock, organ ischemia, and reperfusion have been reported; however, it is not known whether these agents have any salutary or deleterious effects on immune responses after low-flow conditions. Therefore, the aim of this study was to determine (a) the effect of hemorrhage on lymphocyte IL-2, IL-3, IL-6, and IFN-gamma synthesis, and (b) whether diltiazem has any salutary or adverse effects on these parameters when administered following hemorrhage and resuscitation. To study this, C3H/HeN mice were bled to a mean blood pressure of 35 mm Hg, maintained at that level for 60 min, and resuscitated with shed blood plus twice that volume of Ringer's lactate. Immediately following resuscitation mice received either diltiazem (2400, 800, or 400 micrograms/kg body wt), or an equivalent volume of saline. The mice were sacrificed 24 hr later, splenic lymphocytes were obtained, and their capacity to produce lymphokines was assessed. The results indicated that in the vehicle-treated animals, hemorrhage significantly decreased (P less than 0.05) IL-2, IL-3, IL-6, and IFN-gamma synthesis by 82 +/- 19%, 64 +/- 28%, 71 +/- 11%, and 86 +/- 14%, respectively. However, diltiazem (400 but not 2400 micrograms/kg) treatment after hemorrhage restored lymphocyte capacity to produce IL-2, IL-3, IL-6, and IFN-gamma (P less than 0.05). Additional groups of animals were subjected to sepsis by cecal ligation and puncture 3 days following hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)     

Human lymphokine-activated killer cell activity. Role of IL-2, IL-4, and IL-7.

The T-cell growth factors interleukin 2 (IL-2) and interleukin 7 (IL-7) induce lymphokine-activated killer (LAK) cell activity in short-term cultures of human peripheral blood mononuclear cells. Interleukin 4 (IL-4), another T-cell growth factor, induces LAK cell activity in IL-2-prestimulated lymphocytes only and inhibits LAK cell generation in normal peripheral blood mononuclear cells. Our studies of the processes involved using 21-mer phosphorothioate antisense oligonucleotides to the sequence adjacent to the start codon of IL-2 mRNA or IL-4 mRNA (effective concentration, 5 to 10 mumol/L) and cyclosporine (0.01 to 1.0 microgram/mL) or FK506 (0.01 to 1.0 ng/mL) demonstrate that IL-7-induced LAK cell activity is independent of IL-2 production and is regulated by endogenously generated IL-4. Like IL-2, IL-7 stimulated production of tumor necrosis factor alpha, but we failed to detect interferon gamma in IL-7-stimulated cultures. The implication of this regulatory feedback in IL-7-induced LAK cell generation for clinical applications is discussed.     

The cytokines IL-1beta and IL-1 receptor antagonist, IL-2 and IL-2 soluble receptor-alpha, IL-6 and IL-6 soluble receptor, TNF-alpha and TNF soluble receptor I, and IL10 in drained and systemic blood after major orthopaedic surgery.

OBJECTIVE: To measure the concentration of the cytokines interleukin-1beta (IL-1beta), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumour necrosis factor-alpha (TNF-alpha) and the modulators of their function interleukin-1 receptor antagonist (IL-1Ra), interleukin-2 soluble receptor alpha (IL-2 sRalpha), interleukin-6 soluble receptor (IL-6sR) and soluble tumour necrosis factor receptor I (sTNFR-I) in systemic and drained blood for the first six hours after a major orthopaedic operation. DESIGN: Prospective study. SETTING: University hospital, Oslo. PATIENTS: 8 patients operated on for thoracic scoliosis. MAIN OUTCOME MEASURE: Concentrations of IL-1beta, IL-2, IL-6, IL-10, TNF-alpha, IL-1Ra, IL-2 sRalpha , IL-6sR, and sTNFR-I were measured together with haemoglobin (Hb) concentration, white cell count (WCC), and differential count in arterial and drained blood at wound closure and 1, 2, 4, and 6 hours postoperatively. RESULTS: IL-1beta and IL-6 concentrations increased significantly in drained blood, whereas that of TNF-alpha increased only in arterial blood. The modulating factors IL-1Ra, sTNFR-I, and IL-10 were increased both in arterial and drained blood. IL-6sR had decreased slightly at 6 hours in drained blood. No IL-2 was found and IL-2 sRalpha decreased simultaneously with the haemodilution. In arterial blood there was a granulocytosis and in drained blood a relative lymphocytosis. CONCLUSION: Cytokine responses to surgical trauma include modulating factors such as soluble receptors and receptor antagonists that have different responses systemically and locally.     

Osteoprotegerin, IL-6, IL-1, TNF-alpha and TGF-beta concentrations during acetate-free biofiltration

To ascertain the effect of acetate-free biofiltration (AFB), performed with polyacrilonitrile filters, on serum concentrations of osteoprotegerin (OPG) and other bone-acting cytokines (interleukin (IL) IL-1, IL-6, tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta)) in end-stage renal disease (ESRD) patients, we evaluated these parameters during an AFB session and 24 hr after it ended. In second time we verified the existence of eventual correlations among serum levels of all these cytokines at different times. We investigated 48 subjects: 24 healthy volunteers (controls) (12 females, 12 males, mean age 55 +/- 9 yrs) and 24 ESRD patients (12 females, 12 males, mean age 58 +/- 6.7 yrs, mean dialytic age 2.7 +/- 1.6 yrs, residual glomerular filtration rate (GFR) 2.3 +/- 0.6 ml/min). All dialyzed patients received regular AFB with polyacrilonitrile filters for 4 hr thrice-weekly. Statistical analysis showed significant increase in basal serum OPG, IL-6 and TNF-alpha concentrations in dialyzed patients compared to controls, while it did not show significant variations for the other cytokines. During the dialytic session, OPG and TGF-beta concentrations did not show significant variations, while serum TNF-alpha, IL-6 and IL-1 levels significantly decreased from the 1st hour of AFB. None of the cytokines showed significant differences between basal and interdialytic values. We did not find correlations between OPG, IL-1, IL-6, TNF-alpha and TGF-beta concentrations during hemodialytic sessions and during the interdialytic interval. It is our opinion that the lack of correlation between serum concentrations, observed in our study, could not exclude the presence of local interferences between OPG and the other cytokines.     

雷米芬太尼对腹腔镜胆囊切除术患者IL-6、IL-8和IL-10的影响

目的观察全麻下雷米芬太尼与芬太尼对腹腔镜胆囊切除术(LC)患者白细胞介素(IL)-6、IL-8和IL-10的影响。方法20例LC患者,随机分为两组,每组10例。雷米芬太尼组(Ⅰ组)和芬太尼组(Ⅱ组),分别测定麻醉诱导前、气腹手术前、气腹手术后0.5h、术毕0.5h、术后24h的血清IL-6、IL-8和IL-10的水平。结果IL-6、IL-8和IL-10在创伤后1~1.5h开始升高,IL-6的变化最早,IL-8、IL-10在手术结束时逐渐升高,IL-6、IL-8在术后24h仍在继续上升(P<0.05),而IL-10则有不升或缓升趋势。IL-10对IL-6和IL-8的升高有一定的平衡作用。组间比较,术后24hⅠ组IL-6、IL-8较Ⅱ组都有明显升高(P<0.01)。结论与芬太尼相比,雷米芬太尼可更为有效地减轻创伤刺激后IL-6、IL-8和IL-10的释放。     

血清IL-6、IL-10、IL-12在消化道肿瘤中的表达及其意义

目的探讨消化道肿瘤患者血清IL-6、IL-10、IL-12的变化及其意义.方法应用酶联免疫法测定了胃癌、结肠癌及健康者血清IL-6、IL-10、IL-12含量,比较其相互间的关系.结果胃癌和结肠癌组IL-10、IL-12含量低于对照组;IL-6含量则高于对照组,且随着肿瘤临床病理分期的进展而不断升高;胃癌血清IL-6、IL-10、IL-12含量与结肠癌接近.结论消化道肿瘤患者血清细胞因子IL-6、IL-10、IL-12的变化可能与肿瘤的生长及机体抗肿瘤免疫功能的受损有关.     

痔组织中肥大细胞及白细胞介素-6和白细胞介素-10的表达

目的研究痔组织中肥大细胞的变化并探讨其在痔发病机制中的可能作用。方法混合痔行痔上黏膜环切钉合术(PPH)切除标本100例,将突出的母痔组织作为病变组织,将相对正常的肛垫组织作为对照组。以肥大细胞类胰蛋白酶(MCT)标记的肥大细胞,免疫组化SP法检测病变组织及对照组织MCT,白细胞介素-6(IL-6)和IL-10表达。结果 MCT阳性的肥大细胞主要位于痔黏膜固有层腺体之间。IL-6和IL-10阳性区域主要位于腺体之间或血管旁组织。痔组织中肥大细胞细胞计数显著高于对照组织中肥大细胞计数[(18±3.14)vs(6±1.53),P0.05]。痔组织IL-6评分显著高于对照组织,而痔组织IL-10评分显著低于对照组织。肥大细胞计数与IL-6评分呈正相关(r=-0.31,P0.05),与IL-10呈负相关(r=0.28,P0.05)。结论痔组织中肥大细胞数目及释放的IL-6、IL-10显著增加,而IL-10水平显著降低,肥大细胞可能在痔发生发展中起一定作用。     

盆腔手术病人围术期血清TNF-α、IL-6、IL-8、IL-10水平的变化

目的：观察盆腔手术病人围术期血清肿瘤坏死因子－α（TNF－α）、白细胞介素－6（IL－6）、白细胞介素－8（IL－8）、白细胞介素－10（IL－10）水平的动态变化，分析手术麻醉对患者免疫力的影响。方法：选择30例子宫手术病人，用0．25％丁卡因＋1％利多卡因理解外阻滞。于手术前、手术开台后30分钟，术结、术后1天和2天分别检测外周血清中TNF－α、IL－6、IL－8、IL－10水平。结果：与术前比较，TNF－α没有明显变化；IL－6在手术开始后30分钟及术结明显升高（P＜0．05）；IL－8在术后1天达高峰，至术后2天仍高于正常；IL－10在术后1天、2天水平较术前明显下降（P＜0．05）。结论：手术创伤要引起促炎性细胞因子释放增加，抗炎性细胞因子分泌的不足可能是重要的原因。     

Upregulated interleukins (IL-6, IL-10, and IL-13) in immunoglobulin G4-related aortic aneurysm patients

Objective

Immunoglobulin (Ig) G4-related aortic aneurysms (IgG4-AAs) are a special aortic aneurysm among IgG4-related diseases (IgG4-RDs), which are inflammatory and fibrous conditions characterized by tumorous swelling of affected organs and high serum IgG4 concentrations. Recently, IgG4-RD pathogenesis was shown to be associated with T-helper-2 (Th2) and regulatory T (Treg) dominant cytokine production, such as interleukin (IL)-4, IL-10, and IL-13. IL-6 is a key proinflammatory cytokine contributing to lymphocyte and plasmacyte maturation and to atherosclerosis and aneurysm development. We serologically and histopathologically evaluated the cytokine profile in IgG4-AA patients.

IL-18、IL-6、IL-10在糖尿病大鼠肾脏的表达

目的检测IL-18、IL-6、IL-10在糖尿病大鼠肾脏的表达,探讨其在糖尿病肾脏病变过程中的作用。方法将40只雄性Wistar大鼠随机分为正常对照4周组（NC1组）、8周组（NC2组）、糖尿病4周组（DMI组）、8周组（DM2组）,每组10只。DM组给予一次性腹腔内注射60mg／kg链脲佐菌素建立糖尿病大鼠模型。检测各组大鼠体重、肾重、尿微量白蛋白排泄率（UAER）。用免疫组化方法检测肾组织IL-18、IL-6、IL-10的表达,利用计算机图像分析系统进行定量分析。结果DM组大鼠的肾重指数（KWI）、UAER较NC组显著增高;DM2组较DM1组明显增高;IL-18、IL-6在NC组肾组织中仅少量表达,而在DM1组表达明显增多,在DM2组表达增高则更为显著。IL-10在NC组丰富表达,而在DM1组表达明显减弱,在DM2组几乎无表达。肾脏局部IL-18、IL-6与IL-10的表达呈显著负相关。结论糖尿病大鼠肾脏局部IL-18、IL-6表达明显升高、IL-10水平显著降低,IL-18、IL-6与IL-10之间平衡的紊乱在糖尿病肾脏损害病程中发挥重要的作用。     

Influence of pro-inflammatory (IL-1 alpha,IL-6, TNF-alpha,IFN-gamma) and anti-inflammatory (IL-4) cytokines on chondrocyte function

OBJECTIVE: Cytokines produced by inflammatory cells play a pivotal role in synovial inflammation and joint destruction in rheumatoid arthritis. To investigate the influence of pro-inflammatory cytokines (IL-1 alpha, IL-6, TNF-alpha, IFN-gamma) and subsequently the possible beneficial role of an anti-inflammatory cytokine (IL-4) on chondrocyte viability (necrosis/apoptosis), proliferation and nitric oxide (NO) production. METHODS: Primary bovine chondrocytes were cultured until monolayers were obtained. Cells were incubated with cytokines (IL-1 alpha, IFN-gamma, TNF-alpha, IL-4, IL-6) at 0.1, 1, 10 and 100 ng/mL. After 48 h, the viability of the chondrocytes was measured flow cytometrically with propidium iodide. Proliferation was determined by the incorporation of tritiated thymidine. The morphology of the chondrocytes, including presence of apoptotic nuclei, was evaluated by a May-Grünwald-Giemsa staining. In addition, the number of apoptotic chondrocytes was detected flow cytometrically with a TUNEL technique and annexin-V/propidium iodide staining. NO production was evaluated using a spectrophotometric assay, based upon the Griess reaction. RESULTS: The viability and proliferation of bovine chondrocytes decreased after incubation with 100 ng/mL IL-1 alpha, TNF-alpha or IFN-gamma. In contrast, incubation of chondrocytes with IL-4 or IL-6 had no influence on the viability or the proliferation of cells. IL-1 alpha was able to enhance NO production in a dose dependent manner. IFN-gamma and TNF-alpha induced NO production only at the highest concentration (100 ng/mL), whereas IL-4 and IL-6 did not. There was a dose dependent increase in apoptosis of bovine chondrocytes cultured in the presence of IL-1 alpha and TNF-alpha. This effect could not be prevented by preincubation with IL-4. Preincubation with IL-4 diminished IL-1 alpha and TNF-alpha induced NO production and increased proliferation of chondrocytes. In an additional experiment, incubation of human chondrocytes with anti-Fas did not induce apoptosis as measured by annexin-V/propidium iodide staining. CONCLUSIONS: Pro-inflammatory cytokines are able to induce apoptosis, whereas IL-4 as an anti-inflammatory cytokine can inhibit the effect of IL-1 alpha and TNF-alpha on NO production and proliferation of bovine chondrocytes.     

IL-1 beta induces COX2, MMP-1, -3 and -13, ADAMTS-4, IL-1 beta and IL-6 in human tendon cells.

Overuse injuries and trauma in tendon often involve acute or chronic pain and eventual matrix destruction. Anti-inflammatory drugs have been used as a treatment, however, the cellular and molecular mechanisms of the destructive processes in tendon are not clearly understood. It is thought that an inflammatory event may be involved as an initiating factor. Mediators of the inflammatory response include cytokines released from macrophages and monocytes. Interleukin-1 beta (IL-1 beta) is a candidate proinflammatory cytokine that is active in connective tissues such as bone and cartilage. We hypothesized that tendon cells would express receptors and respond to IL-1 beta in an initial "molecular inflammation" cascade, that is, connective tissue cell expression of cytokines that induce matrix destructive enzymes. This cascade results in expression of matrix metalloproteinases (MMPs) and aggrecanases that may lead to matrix destruction. Normal human tendon cells from six patients were isolated, grown to quiescence and treated with human recombinant IL-1 beta in serum-free medium for 16 h. Total RNA was isolated and mRNA expression assessed by semiquantitative RT-PCR. IL-1 beta (1 nM) induced mRNAs for cyclooxygenase 2 (COX2), MMP-1, -3, -13 and aggrecanase-1 as well as IL-1 beta and IL-6, whereas mRNAs for COX1 and MMP-2 were expressed constitutively. The IL-1 beta-treated tendon cells released prostaglandin E(2) (PGE(2)) in the medium, suggesting that the inducible COX2 catalyzed this synthesis. Induction of PGE(2) was detectable at 10 pM IL-1 beta. IL-1 beta also stimulated MMP-1 and -3 protein secretion. Induction of MMP-1 and -3 was detectable at 10 pM IL-1 beta. Post-injury or after some other inciting events, exogenous IL-1 beta released upon bleeding or as leakage of local capillaries may drive a proinflammatory response at the connective tissue cell level. The resulting induction of COX2, MMP-1 and -3 may underscore a potential for nonlymphocyte-mediated cytokine production of MMPs that causes matrix destruction and a loss of tendon biomechanical properties. Endogenous IL-1 beta might contribute to the process through a positive feedback loop by stimulating expression and accumulation of MMPs in the tendon matrix.     

IL-23, not IL-12, Directs Autoimmunity to the Goodpasture Antigen

The autoantigen in Goodpasture disease is the noncollagenous domain of α3 type IV collagen [α3(IV)NC1]. We previously demonstrated that IL-12p40^−/− mice are protected from experimental autoimmune anti–glomerular basement membrane (anti-GBM) glomerulonephritis, seemingly defining a role for IL-12 in this disease; however, the recent identification of IL-23, a heterodimer composed of IL-12p40 and IL-23p19 subunits, raises the possibility that IL-23, rather than IL-12, may modulate this disease instead. We immunized wild-type, IL-12p35^−/− (IL-12 deficient, IL-23 intact), IL-12p40^−/− (deficient in both IL-12 and IL-23), and IL-23p19^−/− (IL-12 intact, IL-23 deficient) mice with recombinant mouse α3(IV)NC1. Wild-type mice developed autoreactivity to α3(IV)NC1: Humoral responses, cellular responses, renal histologic abnormalities, leukocyte accumulation, autoantibody deposition, and IL-17A mRNA expression (a cytokine produced by the IL-23–maintained Th17 subset). IL-23 but not IL-12 was detected in the immune system. Regardless of the presence of IL-12, mice deficient in IL-23 were protected, but mice with IL-23 were not. Both IL-23–deficient strains exhibited lower autoantibody titers, reduced cellular reactivity, diminished cytokine production (IFN-γ [Th1], IL-17A [Th17], TNF, and monocyte chemoattractant protein 1), and less renal disease and glomerular IgG deposition. The deficient responses in the absence of IL-23 were not due to increased regulatory T cells; IL-12p40^−/− and IL-23p19^−/− mice did not show increased proportions of CD4⁺CD25⁺FoxP3⁺ cells or IL-10 levels early in the immune response. In conclusion, autoreactivity to the Goodpasture antigen is directed primarily by IL-23, absence of which results in hyporeactivity including but extending beyond a deficient Th17 response.Some forms of glomerulonephritis are caused by immune responses against autoantigens that are dependent on a CD4⁺ autoimmune response. Arguably the best characterized antigen involved in glomerulonephritis is the Goodpasture antigen, the noncollagenous domain of the α3 chain of type IV collagen [α3(IV)NC1].¹ Loss of tolerance in humans to α3(IV)NC1 results in anti–glomerular basement membrane (anti-GBM) glomerulonephritis.² Substantial evidence exists for the involvement of both cellular^3,4 and humoral^5,6 effectors directed against α3(IV)NC1. The detection of anti-GBM antibodies is required for diagnosis.⁷ Antibodies binding to the GBM can activate complement and recruit macrophages and neutrophils. Passive transfer of anti-GBM antibodies can induce disease in monkeys,⁵ rats,⁸ and mice.⁹ Patients with anti-GBM also exhibit the effectors of delayed-type hypersensitivity (DTH), infiltrating CD4⁺ cells and macrophages in glomeruli¹⁰ together with prominent fibrin deposition.¹¹ Effector T cells can induce injury in experimental autoimmune anti-GBM glomerulonephritis.^9,12,13CD4⁺ T helper (Th) cells tend to be polarized into subsets characterized by the cytokines that they produce. IFN-γ is the signature cytokine of Th1 cells, IL-4 is the signature cytokine of Th2 cells, and IL-17A is the signature cytokine of Th17 cells. Th cells help determine patterns of the effector immune responses, patterns that aid in host defense but also play a key role in inflammatory tissue damage. Th1 responses classically result in CD4⁺ T cell/macrophage mediated cellular responses and drive IgG subclass switching toward complement-fixing and macrophage-recruiting subclasses. Th2 responses promote IgE-mediated humoral responses. A more recently described subset, Th17, acts against extracellular pathogens, and there is increasing evidence that it drives organ-specific autoimmunity.^14–16A number of factors underpin the differentiation and maintenance of Th cell subsets, but the cytokine milieu during differentiation and effector CD4⁺ cell expansion is particularly important. IL-12, a heterodimer composed of IL-12p40 and IL-12p35 subunits, is the key cytokine in Th1 differentiation. Studies using neutralizing antibodies and IL-12p40^−/− mice, including studies in experimental glomerulonephritis, seemed to define an important role for IL-12 in both autoimmune¹⁷ and nonautoimmune^18,19 glomerulonephritis; however, the subsequent discovery of IL-23, a newer IL-12 family member that is also a heterodimer (composed of IL-12p40 and IL-23p19 subunits), prompted a reevaluation of studies that used IL-12p40^−/− mice and anti–IL-12p40 antibodies. Other lines of evidence have defined IL-23 as important for the maintenance of the Th17 subset and implicated Th17 in the pathogenesis of organ-specific autoimmune disease.¹⁴We previously showed that in experimental autoimmune anti-GBM glomerulonephritis, IL-12p40^−/− mice are protected from disease but IFN-γ^−/− mice develop worse injury.¹⁷ With the knowledge of the structure of IL-12 and IL-23, together with the recent delineation of the Th17 subset, we sought to define definitively the individual and collective roles of the IL-12 family members IL-12 and IL-23 in the genesis, maintenance, and pattern of autoimmune responses to the Goodpasture antigen. C57BL/6 mice were immunized with recombinant mouse (rm) α3(IV)NC1. Our hypothesis was that IL-23 would drive pathogenetic Th17 responses and mice that were deficient in IL-23, by virtue of lacking either IL-23p19 or IL-12p40, would develop a selective defect in Th17 responses and less glomerulonephritis.     

全髋关节置换术后血清炎性因子表达特点及临床意义

目的：研究血清炎性因子白介素1（IL1）、白介素2（IL2）、白介素6（IL6）及白介素10（IL10）在人工全髋关节置换术后变化特点及意义。方法：自2010年2月至6月,选择初次行单侧人工全髋关节置换术的30例股骨头无菌性坏死患者,男18例,女12例;年龄52～70岁,平均（58.4±6.6）岁;FicatⅡ型20例,Ⅲ型10例。分别在术前第1天及术后第1、3天用放射免疫方法检测IL1、IL2、IL6及IL10,同时检测C反应蛋白,对结果进行统计学分析。结果：人工全髋关节置换术后第1天患者血清中IL1、IL6和IL10值均较术前升高（t=2.62,3.51,2.21,P〈0.05）,在术后1～3d达到高峰,3d后开始降低。患者血清IL2水平术后降低（t=2.16,P〈0.05）,后逐渐升高。结论：全髋关节置换术后3d是抗炎治疗的关键,术后及时监测IL1、IL2、IL6及IL10的变化,同时观察临床症状,可更敏感地掌握患者的治疗效果,预测病情发展。