人主动脉硫酸乙酰肝素蛋白聚糖对培养人的脐静脉内皮细胞生长的影响

为探讨硫酸乙酰肝素蛋白聚糖（ＨＳＰＧ）对内皮细胞生长的作用,用解聚提取及离子交换柱层析法分离出人主动脉ＨＳＰＧ,用倒置显微镜、细胞计数、及￣３Ｎ－ＴｄＲ参入观察其对培养的第一代人脐静脉内皮细胞（ｈＵＶＦＣ）生长的影响。结果发现：（１）倒置显微镜下观察,加入ＨＳＰＧ（１．７０μｇ已糖醛酸／ｍｌ）的ｈＵＶＥＣ生长密度高于对照组（未加ＨＳＰＧ）．（２）随着培养时间增加（２４,４８及７２ｈ）．根据细胞计数计算出同一剂量的ＨＳＰＧ（１７．０μｇ已糖醛酸／ｍｌ）对ｈＵＶＥＣ的促增殖％增高（分别为１４％,３０％及３７％）。（３）随着加入ＨＳＰＧ浓度的升高（４．３,８．５及１７．０μｇ已糖醛酸／ｍｌ．培养７２ｈ）．根据￣３Ｈ－ＴｄＲ参入计算出ＨＳＰＧ对ｈＵＶＥＣ的促增殖％亦增高（分别为４９％,７１％及９８％）。故人主动脉ＨＳＰＧ对培养的人脐静脉内皮细胞有促增殖作用。     

缺氧—再给氧刺激培养的脑微血管内皮细胞表达细胞间粘附分子—1

在缺氧－再给氧条件下,观察了体外分离培养的大鼠脑微血管内皮细胞表面粘附分子ＩＣＡＭ－１的表达及中性粒细胞与内皮细胞粘附作用的改变。结果表明,单纯缺氧１０ｈ不引起内皮细胞ＩＣＡＭ－１的上调,再给氧６ｈＩ－ＣＡＭ－１的表达升高（Ｐ＜０．０１）,再给氧１２ｈ表达量增加了１００％（Ｐ＜０．０１）,此时中性粒细胞与内皮细胞的粘附作用也明显增强（Ｐ＜０．０１）。缺氧前用盐酸川芎嗪（２ｍｇ／ｍｌ）预处理内皮细胞可阻断ＩＣＡＭ－１的表达（Ｐ＜０．０１）,同时也可降低ＰＭＮ与内皮细胞的粘附（Ｐ＜０．０５）。结果提示,脑微血管内皮细胞在缺氧－再给氧刺激下可自身调节Ｉ－ＣＡＭ－１的表达,为中性粒细胞与内皮细胞的粘附提供特异的结合位点。     

鼻咽癌细胞对HA的粘附作用及微丝的共聚焦显微镜观察

本文研究了人鼻咽癌上皮细胞系ＣＮＥ－２Ｚ对透明质酸（ＨＡ）的粘附作用及其粘附后微丝的改变,结果表明,鼻咽癌细胞粘附的ＯＤ值随ＨＡ浓度的升高而升高,３００μｇ／ｍｌ、１２５０μｇ／ｍｌ组与对照组比较有极显著性意义,Ｐ＜０．０１;癌细胞粘附的ＯＤ值随培养时间延长而升高,２４０ｍｉｎ组及１２０ｍｉｎ组与６０ｍｉｎ组比较有极显著性意义,Ｐ＜０．０１。ＬＳＭ观察ＨＡ浓度为３００μｇ／ｍｌ时培养４ｈ和２４ｈ的癌细胞微丝的分布明显不同,培养４ｈ的癌细胞呈圆形,微丝均匀地分布于胞浆内;培养２４ｈ的癌细胞呈不规则形,微丝主要分布于与ＨＡ的粘附面上。上述结果提示ＨＡ可促进鼻咽癌细胞粘附,癌细胞与ＨＡ结合后可诱导ＭＦ重组     

剪夏罗鲜汁及黄酮组分对体外Ⅰ型单纯疱疹病毒的抑制作用

在人胚肺纤维母细胞体外培养系统中,以微量单层细胞病变法观察剪夏罗（ＬｙｃｈｎｉｓｃｏｒｏｎａｔａＴｈｕｎｂ．）鲜汁液及其黄酮组分对体外Ⅰ型单纯疱疹病毒增殖性感染的抑制作用。剪夏罗高浓度鲜汁液（１∶５０、１∶２０及１∶１０稀释液）及其高浓度黄酮组分Ⅰ、Ⅱ（＞１００μｇ／ｍｌ）对细胞有明显的毒性作用;剪夏罗鲜汁液１∶１００～１∶４００稀释液,可明显抑制病毒复制,使病毒诱导的细胞病变明显减轻,培养液中子代病毒感染滴度明显下降,且培养上清液中病毒感染滴度与鲜汁液和黄酮组分的浓度呈直线负相关;剪夏罗鲜汁液的黄酮组分Ⅰ、Ⅱ在１０μｇ／ｍｌ～０１μｇ／ｍｌ浓度范围内对病毒诱导的细胞病变有明显的抑制作用。     

人主动脉硫酸乙酰肝系蛋白聚糖对培养人的脐静脉内皮细胞生长…

为探讨硫酸乙酰肝素蛋白聚糖（ＨＳＰＧ）对内皮细胞生长的作用,用解聚提取及墩子交换柱层析法分离出人主动脉ＨＳＰＧ,用倒置显微镜,细胞计数,及＾３Ｈ－ＴｄＲ参入观察其对培养的第一代人脐静脉内皮细胞（ｈＵＶＥＣ）生长的影响,结果表明,（１）倒置显微镜下观察,加入ＨＳＰＧ（１．７０μｇ己糖醛酸／ｍｌ）的ｈＵＶＥＣ生长密度高于对照组（未加ＨＳＰＧ）（２）随着培养时间增加（２４,４８及７２ｈ）根据细胞计数计算     

产胡萝卜素酵母的筛选

从被油污染的土样和植物的落花中分离筛选出几株产胡萝卜素的酵母菌,其中从椰子油污染的土样中分离获得的菌株ＣＯＳ－５的胡萝卜素产量最高。ＣＯＳ－５菌株经鉴定为红酵母（Ｒｈｏｄｏｔｏｒｕｌａ ｓｐ．）ＣＯＳ－５。该菌株以蔗糖为碳源,添加桔子皮和盐酸硫胺素的培养基２８℃振荡培养９６ｈ,细胞生物量为２７．５ｍｇ干重／ｍｌ发酵液,胡萝卜素产量为１３．５５μｇ／ｍｌ发酵液。菌体胡萝卜素含量达４９２．７μｇ／ｇ干     

纯化眼镜蛇毒蛋白对乙酰胆碱受体通道的阻断作用

在培养的抓蟾胚胎神经和肌肉细胞上用膜片箝技术研究了从中国华南产眼镜蛇毒分离出的神经毒组分对乙酰胆碱受体（ＡＣｈ－Ｒ）通道的影响,发现它在微终板电位和单通道水平上都有明显的阻断作用。完全阻断神经肌肉接点传递的剂量约为２．０μｇ／ｍｌ,对乙酰胆碱受体通道的半阻断量约为０．２３μｇ／ｍｌ。这表明它与α－银环蛇毒有相似功效。     

灵芝菌丝体深层培养及多糖提取工艺研究

灵芝ＳＤ－２２菌株培养条件,培养基组分、ｐＨ、通气量、培养时间等对该菌的生物量和多糖含量均有影响。初步确定了灵芝多糖提取工艺。在优化条件下,生物量为１．８６ｇ／１００ｍｌ培养基,灵芝多糖产量为５１ｍｇ／１００ｍｌ培养基     

喹诺酮类药物抗乙型肝炎病毒体外实验研究

本文以２．２．１５细胞株为模型,以ＨＢｓＡｇ、ＨＢｅＡｇ、ＨＢＶＤＮＡ、细胞存活率为观察指标,综合评价了喹诺酮类药物吡哌酸（ＰｉｐｅｍｉｄｉｃＡｃｉｄ）、氟哌酸（Ｎｏｒｆｌｏｘａｃｉｎ）、环丙氟哌酸（Ｃｉｐｒｏｆｌｏｓｘａｃｉｎ）、氟嗪酸（Ｏｆｌｏｘａｃｉｎ）体外抗ＨＢＶ效果。结果表明：吡哌酸、氟哌酸、环丙氟哌酸、氟嗪酸对ＨＢｓＡｇ、ＨＢｅＡｇ５０％抑制浓度（ＩＤ＿（５０））分别为１１μｇ／ｍｌ、６４μｇ／ｍｌ、９３μｇ／ｍｌ、１０５μｇ／ｍｌ和１９９μｇ／ｍｌ、１１１μｇ／ｍｌ、２４μｇ／ｍｌ、２１７μｇ／ｍｌ,细胞存活率为５０％时的药物浓度（ＣＤ＿（５０））分别为２１９μｇ／ｍｌ、９０μｇ／ｍｌ、１８１μｇ／ｍｌ、１６９μｇ／ｍｌ,在所选定的用药浓度范围内不同程度抑制培养上清液及细胞内ＨＢＶＤＮＡ及其复制中间体的产生。尤其对超螺旋结构ＤＮＡ（ｓｃＤＮＡ）有不完全抑制作用。     

黄芪多糖和白细胞介素2对LAK细胞毒活性的调节作用

采用扶正中药黄芪的有效成分黄芪多糖（ＡＰＳ）和不同来源的白细胞介素２的伍用,探讨其对ＬＡＫ细胞毒性的调节作用,乳酸脱氢酶释放法（ＬＤＨ）测定ＬＡＫ细胞毒性的实验结果表明：ＡＰＳ自身具有增强ＬＡＫ细胞毒性的作用,有效剂量范围为１μｇ／ｍｌ￣１００μｇ／ｍｌ;ＬＡＫ细胞发挥细胞毒活性伍用一定剂量的白细胞介素２;ＡＰＳ（１０μｇ／ｍｌ）和ＩＬ－２（５００μ／ｍｌ）对ＬＡＫ细胞毒性具有非常显著的协同增强作     

Inhibition of heterochromatin condensation of human Y chromosome by distamycin-A

Distamycin-A, an oligopeptide antibiotic with a N-methylpyrrole ring system and propionamide side chain, preferentially forms stable bonds with AT rich double stranded DNA. When introduced to cell cultures, it inhibits condensation of the heterochromatic region of the Y chromosome. The frequency of metaphases showing inhibition of heterochromatin condensation of the Y chromosome was found to be dependent on the treatment time and concentration of distamycin-A in the culture medium. When distamycin-A was added to a concentration of 100 micrograms/ml at the start of the culture (72 hours), the frequency of Y heterochromatin decondensation was found to be 48%, 30% and 6% in amniotic fluid, lymphocyte and fibroblast cultures respectively. The highest frequency of metaphases with decondensed Y heterochromatin were observed when distamycin-A treatment was carried out for the last 24 hours prior to harvest, the frequencies being 94%, 72% and 59% in amniotic fluid, lymphocyte and fibroblast cultures respectively. Increase in the concentration of distamycin-A from 25 micrograms/ml to 50 micrograms/ml during the last 24 hours of culture increased the incidence of metaphases with Y heterochromatin decondensation from 51% to 69% in amniotic fluid, 40 to 49% in lymphocyte and 29% to 31% in fibroblast cultures. Highest frequency of metaphases with Y heterochromatin decondensation were observed when the cultures were exposed to distamycin-A at a concentration of 100 micrograms/ml for the last 24 hours of culture.     

Elastin synthesis by ligamentum nuchae fibroblasts: effects of culture conditions and extracellular matrix on elastin production

Fetal bovine ligamentum nuchae fibroblasts maintained in culture synthesized soluble elastin but were unable to form the insoluble elastic fiber. Secreted elastin precursors accumulated in culture medium and were measured using a radioimmunoassay for elastin. When elastin production was examined in ligament tissue from fetal calves of various gestational ages, cells from tissue taken during the last trimester of development produced significantly more elastin than did cells from younger fetal tissue, with maximal elastin synthesis occurring shortly before birth. Soluble elastin was detected in ligament cells plated at low density until proliferation began to be density inhibited and the cells became quiescent. Also, soluble elastin production per cell declined with increasing population doubling or with age in culture. Cells grown in the presence of 5% fetal calf serum produced approximately four times as much soluble elastin as cells grown in serum-free medium. The addition of dexamethasone (0.1 microM) and bleomycin (1 microgram/ml) increased soluble elastin production by cultured cells 180% and 50%, respectively, whereas theophylline (5 micrograms/ml) depressed production 50% and antagonized stimulation by dexamethasone. Ascorbate (50 micrograms/ml), soybean trypsin inhibitor (1 mg/ml), insulin (100 microunits/ml), and aminoacetonitrile (50 micrograms/ml) had no effect, but cycloheximide at 10(-4) M completely inhibited soluble elastin production. In contrast to cells in culture, ligament tissue minces (ligament cells surrounded by in vivo extracellular matrix) efficiently incorporated soluble elastin precursors into insoluble, cross-linked elastin. In addition, soluble elastin production per cell (per microgram of DNA) was higher in tissue minces than elastin production by cells maintained on plastic. These results suggest a role for extracellular matrix in formation of the elastic fiber and in stabilizing elastin phenotypic expression by ligament fibroblasts. Fibroblasts from the bovine ligamentum nuchae present an excellent model for in vitro studies of elastin biosynthesis.     

RNA synthesis inhibitors on young rat adrenal in primary culture. An ultrastructural study

Adrenal cells of newborn rat adrenals in primary tissue culture were treated with actinomycin D (2, 10 and 25 micrograms/ml), alpha-amanitin (5 and 50 micrograms/ml) and cordycepin (100 micrograms/ml) and studied with the electron microscope. The most striking changes observed with the three drugs were localized on the nucleoli, and consisted, respectively, of segregation (actinomycin D), fragmentation (alpha-amanitin) and microsegregation (cordycepin). These results are consistent with the molecular sites of action of the drugs and are comparable to previous in vivo findings.     

Minoxidil-induced changes in the contraction of collagen lattices by human skin fibroblasts.

This investigation has studied the effect of minoxidil on the contraction of hydrated collagen lattices by human dermal fibroblasts. Type I collagen was mixed with a fibroblast suspension and polymerized, and minoxidil 10 to 800 micrograms/ml (0.05 to 4 mM) was added at the time the lattices were released. Minoxidil at concentrations from 100 to 600 micrograms/ml inhibited contraction in a dose-dependent manner, whereas 800 micrograms/ml prevented contraction completely, most cells remaining rounded. Considerable inhibition was already evident within 24 hours. Visualization of living cells with MTT and cell counts showed that inhibition in the first 48 hours was not due to fibroblast death. Exchange of minoxidil to normal medium led to a resumption of contraction and a return to an elongate morphology. Minoxidil at 10 micrograms/ml had no significant effect on lattice contraction, whereas at 100 micrograms/ml it slowed contraction without affecting proliferation or morphology, as observed under the light microscope. The inhibitory effect of minoxidil should be investigated further in relation to the control of contraction of wounds in vivo.     

锌诱导的蛋白合成增加可抵抗链佐霉素所致的胰岛细胞损伤

本工作在离体细胞水平观察ZnGl_2对链佐霉素(STZ)诱发的胰岛β细胞损伤的保护作用,并分析其可能的作用机制。结果如下:向培养的胰岛细胞中加入生理盐水和STZ(3mmol/L),孵育12h后,活细胞数由实验前的70万个/ml降至43.93±1.16万个/ml;将ZnCl_2(0.25、0.5、1.0mmol/L)和相同剂量的STZ一同加入细胞,可不同程度地缓解STZ对胰岛的破坏作用,在含不同浓度ZnCl_2的培养液中活细胞数分别恢复至47.39±0.88,58.06±2.29,67.72±1.48万个/ml,与STZ破坏组相比,分别具有显著差异,并呈量效关系。在给予ZnCl_2(1.0mmol/L)的同时,向细胞中加入蛋白合成抑制剂亚胺环已酮(100μg/ml),可翻转ZnCl_2的作用,活细胞数由63.17±2.15万个/ml,又重新减至45.77±0.76万个/ml。单独加亚胺环己酮对活细胞数目无明显影响。用~3H-亮氨酸掺入实验观察ZnCl_2对胰岛细胞蛋白合成的影响发现,单独给予ZnCl_2(1.0mmol/L)仅使蛋白合成轻微增加,与盐水对照组无显著差异;在给ZnCl_2的同时加入STZ,则蛋白合成明显增多,保护组与STZ破坏组比较,差异显著。上述结果表明,增加细胞内蛋白合成,以加强细胞自身对外来损伤的修复力,可能是ZnCl_2保护胰岛细胞的机制之一。     

The response of small vessel endothelial cells from fetal rat lung to growth factors

Small vessel pulmonary endothelial cells were obtained from rat fetal lung at day 20 of gestation, and were maintained in culture to passage three for study. Endothelial cells grown on a collagen matrix with Dulbecco's minimal essential medium: Ham's F12 medium (1:1, v/v) supplemented with 20 ml/l fetal bovine serum, bovine pituitary extract (50 mg/l), endothelial cell growth supplement (100 mg/l), hydrocortisone (1 mg/l) and an increased (10 mmol/l) magnesium concentration retained the characteristic endothelial cell marker factor VIII antigen during the third passage in culture. The factors responsible for small vessel growth in the developing fetal lung are unknown. To test the hypothesis that small vessel pulmonary endothelial cells would respond to autocrine or paracrine growth factors the effects of conditioned media from fetal lung endothelial cells, fibroblasts and pneumocytes from lungs of the same gestational age were studied in vitro. None of the tested conditioned media had any effect on endothelial cell DNA synthesis in the presence of 20 ml/l fetal bovine serum. Since no paracrine or autocrine effects of conditioned media were observed, the effect of other growth factors that could be derived from the circulation, or from storage sites in subcellular matrix, were studied for effect. When endothelial cells were studied in the presence of 20 ml/l fetal bovine serum and 100 mg/l endothelial cell growth supplement they had enhanced DNA synthesis in response to the progression-type growth factors insulin (5 mg/l), insulin-like growth factor-I and insulin-like growth factor-II (20 micrograms/l) and epidermal growth factor (10 micrograms/l). In the absence of serum or endothelial growth supplement endothelial cell DNA synthesis was enhanced by the competence-type growth factors acidic and basic fibroblastic growth factors at 100 micrograms/l and platelet derived growth factor at 10 micrograms/l. In the absence of exogenous competence-type growth factors neutralizing antibodies to basic fibroblast growth factor reduce DNA synthesis. Of various cytokines tested only interleukin-1 (1 x 10(3) U/l) and tumor necrosis factor (25 x 10(4) U/l) had an effect on endothelial cell DNA synthesis. Endothelial cell division during fetal lung development may be controlled by progression growth factors present in serum, and by either autocrine release of the competence factor basic fibroblast growth factor or paracrine release of platelet-derived growth factor by other cell types.     

In vitro development of rat embryos undergoing organogenesis in heparin-plasma.

This study examines the use of heparin-plasma as a culture medium for mammalian postimplantation whole-embryo culture. The growth and differentiation of head-fold rat embryo explants over 48 hours in a standard serum medium was compared with development of same stage explants over 48 hours in a plasma medium prepared using sodium heparin. Heparin disrupted the morphological differentiation of embryos, in a concentration-dependent manner, from 25 micrograms sodium heparin/ml media (i.e., 5 IU/ml media), with overall embryo growth being adversely affected from a concentration of 200 micrograms sodium heparin/ml media (i.e., 40 IU/ml media). Defects of cranial neural tube development were the first apparent structural anomalies resulting from culture in heparin media. Forebrain development was grossly abnormal and associated with failure of eye development. As the heparin concentration in media increased, the cephalic neural folds remained widely open and the edges became increasingly everted, although differentiation of the heart, otic primordia, and pharyngeal arch persisted. Similar concentration-dependent dysmorphogenic effects were seen when embryos were cultured in the standard serum media with added heparin. A minimum heparin concentration of 100 micrograms sodium heparin/ml media (i.e., 20 IU/ml media) was required to effectively inhibit coagulation of the plasma medium over the 48 hour culture period. Although embryonic growth was not adversely affected at this heparin concentration, morphological differentiation was severely disrupted. Therefore, heparin is not a suitable anticoagulant for the preparation of plasma for use in postimplantation whole-embryo culture.     

Reaction of the cell center to exposure to the calcium ionophore A-23187

Calcium ionophore A23187, taken at a concentration of 0.1 microgram/ml, quickly uncouples mitochondria in PE culture cells in medium 199. The cell ultrastructure undergoes reversible changes (especially that of mitochondria): maximum changes occur 2 hours after the start of the treatment; in 8 hours they become less pronounced. The adaptation of cells does not involve the ionophore inactivation in the medium. 10 micrograms/ml of A23187 induces gradual but irreversible alterations. Microtubules in PE cells are not destroyed when incubated in medium 199 containing 10 micrograms/ml of A23187 and 11 mM Ca2+. The addition of 10 micrograms/ml ionophore to the normal 199 medium (1.26 mM Ca2+) results in the formation of electron dense bodies in the cell center 30 minutes after the start of incubation. These bodies disappear in the course of a subsequent incubation. The number of cells with primary cilia decreases. The percentage of centrioles located perpendicularly to the substrate increases 30 minutes following treatment with 0.1 microgram/ml A23187 in medium 199. 2 hours after the start of treatment with 0.1 microgram/ml ionophore no such changes are detected; an electron dense halo appears around the centriolar cylinders. 8 hours after the start of treatment the structure of the cell center does not differ from the normal one.     

Proteoglycans and glycosaminoglycans induce gap junction synthesis and function in primary liver cultures

Intercellular communication via gap junctions, as measured by dye and electrical coupling, disappears within 12 h in primary rat hepatocytes cultured in serum-supplemented media or within 24 h in cells in a serum-free, hormonally defined medium (HDM) designed for hepatocytes. Glucagon and linoleic acid/BSA were the primary factors in the HDM responsible for the extended life span of the electrical coupling. After 24 h of culture, no hormone or growth factor tested could restore the expression of gap junctions. After 4-5 d of culture, the incidence of coupling was undetectable in a serum-supplemented medium and was only 4-5% in HDM alone. However, treatment with glycosaminoglycans or proteoglycans of 24-h cultures, having no detectable gap junction protein, resulted in synthesis of gap junction protein and of reexpression of electrical and dye coupling within 48 h. Most glycosaminoglycans were inactive (heparan sulfates, chondroitin-6 sulfates) or only weakly active (dermatan sulfates, chondroitin 4-sulfates, hyaluronates), the weakly active group increasing the incidence of coupling to 10-30% with the addition of 50-100 micrograms/ml of the factor. Treatment of the cells with 50-100 micrograms/ml of heparins derived from lung or intestine resulted in cells with intermediate levels of coupling (30-50%). By contrast, 10-20 micrograms/ml of chondroitin sulfate proteoglycan, dermatan sulfate proteoglycan, or liver-derived heparin resulted in dye coupling in 80-100% of the cells, with numerous cells showing dye spread from a single injected cell. Sulfated polysaccharides of glucose (dextran sulfates) or of galactose (carrageenans) were inactive or only weakly active except for lambda-carrageenan, which induced up to 70% coupling (albeit no multiple coupling in the cultures). The abundance of mRNA (Northern blots) encoding gap junction protein and the amounts of the 27-kD gap junction polypeptide (Western blots) correlated with the degree of electrical and dye coupling indicating that the active glycosaminoglycans and proteoglycans are inducing synthesis and expression of gap junctions. Thus, proteoglycans and glycosaminoglycans, especially those found in abundance in the extracellular matrix of liver cells, are important in the regulation of expression of gap junctions and, thereby, in the regulation of intercellular communication in the liver. The relative potencies of heparins from different tissue sources at inducing gap junction expression are suggestive of functional tissue specificity for these glycosaminoglycans.     

Induction of inflammatory cytokine release from cultured human monocytes by C-reactive protein.

The human acute phase protein, C-reactive protein (CRP), is capable of specifically binding to and modulating the function of mononuclear phagocytes. To investigate whether CRP can also affect the capacity of these cells to produce inflammatory cytokines, enzyme immunoassays and Western blot techniques were used to quantitate interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) produced by freshly-isolated normal human monocytes. CRP induced the rapid release of each cytokine, with significantly elevated levels in culture supernatants at 4 hours and maximal levels of TNF-alpha at 8 hours, and of IL-1 beta and IL-6 at 16 hours of culture. The effects of CRP were dose-dependent; greater than 10-fold increases of each cytokine were observed following culture with greater than or equal to 50 micrograms/ml CRP, concentrations which are often found in the presence of moderate to severe inflammation or tissue injury. The induction of cytokine release by CRP was unaffected by inclusion of 25 micrograms/ml polymyxin-B in culture media, but was completely abrogated by prior boiling of the CRP, a procedure which had no effect on induction of monocyte cytokine release by lipopolysaccharide. The dose-dependent induction of inflammatory cytokines by CRP provides further support for the hypothesis that interaction with mononuclear phagocytes constitutes an important biological role for this acute phase protein.