Detection of cytokines in bovine colostrum

Colostrum contains factors that are protective for the neonate and may be a source of immunomodulary molecules that positively influence the immune status of the neonate. To confirm that colostrum contains a variety of cytokines with immunomodulatory properties, we established a bovine cytokine specific ELISA and five cytokines (IL-1 beta, IL-6, TNF-alpha, INF-gamma or IL-1 receptor antagonist, IL-1ra) in the whey samples from cows at different stages of lactation were monitored. The expression of cytokine mRNAs (IL-1 beta, IL-6, TNF-alpha and INF-gamma) in the colostral cells was detected by RT-PCR. The concentrations of cytokines in colostrum were significantly higher concentrations than those in the mature milk. A positive correlation was observed between the concentrations of IL-1ra and IL-1 beta in the colostrum samples. In conclusion, colostrum contains high levels of cytokines that could be produced and secreted in the mammary gland and that may have an immunomodulatory activity and influence neonatal immunity.     

Differential cytokine gene expression in CD4+ and CD8+ T cell subsets of calves

The distinct patterns of cytokine expression in CD4+ and CD8+ T cells are well understood in mice and humans. However, little information is available about cytokine expression in bovine CD4+ and CD8+ T cells. In this study, mRNA expression of 19 different cytokines was analyzed in CD4+ and CD8+ T cells of calves with or without Concanavalin A (Con A) stimulation. CD4+ and CD8+ T cell populations were enriched to 98% purity by positive selection using magnetic cell sorting (MACS). CD4+ T cells spontaneously expressed the mRNAs of interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-6, IL-7, IL-8, IL-10, IL-18, IFN-gamma, TNF-alpha, TNF-beta and TGF-beta, and augmented the mRNA expression of IL-10, IFN-gamma and TNF-beta after Con A stimulation. The mRNAs of IL-3, IL-4, IL-5, IL-13 and GM-CSF were newly expressed in Con A-stimulated CD4+ T cells. CD8+ T cells displayed spontaneous mRNA expression of IL-6, IL-18, TNF-alpha, TNF-beta and TGF-beta, and newly expressed the mRNA of IL-2, IL-7, interferon-gamma (IFN-gamma) and GM-CSF after Con A stimulation. It was found that CD4+ T cells expressed the mRNA of 17 cytokines except for IL-12 and IL-15, while CD8+ T cells expressed only the mRNA of 9 cytokines after Con A stimulation. The profile of cytokine mRNA expression was substantially different in the CD4+ and CD8+ T cells of calves, indicating that CD4+ T cells can be distinguished from CD8+ T cells by the cytokine gene expression of IL-1alpha, IL-1beta, IL-3, IL-4, IL-5, IL-8, IL-10 and IL-13. Differential cytokine expression between CD4+ and CD8+ T cells serve to interpret an individual function of T cell subsets in the immune system of calves.     

Immune and endocrine regulation of food intake in sick animals

To understand why sick animals do not eat, investigators have studied how the immune system interacts with the central nervous system (CNS), where motivation to eat is ultimately controlled. The focus has been on the cytokines secreted by activated mononuclear myeloid cells, which include interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Either central or peripheral injection of recombinant IL-1β, IL-6, and TNF-α reduce food-motivated behavior and food intake in rodents. Moreover, these cytokines and their receptors are present in the endocrine system and brain, and antagonism of this system (i.e., the cytokine network) has been shown to block or abrogate anorexia induced by inflammatory stimuli. Recent studies indicate that the same cytokines act on adipocytes and induce secretion of leptin, a protein whose activity has been neuroanatomically mapped to brain areas involved in regulating food intake and energy expenditure. Therefore, many findings converge to suggest that the reduction of food intake in sick animals is mediated by inflammatory cytokines, which convey a message from the immune system to the endocrine system and CNS. The nature of this interaction is the focus of this short review.     

Escherichia coli inoculation of porcine mammary glands affects local mRNA expression of Toll-like receptors and regulatory cytokines

The expression of mRNAs for the Toll-like receptors (TLRs) TLR2 and TLR4, pro- and anti inflammatory cytokines and their receptors was evaluated in mammary gland biopsy material collected from sows intramammarily inoculated with Escherichia coli strain O127 at parturition. Quantitative real-time RT-PCR analysis showed increased mRNA levels for TLR2, the proinflammatory cytokines interleukin IL-1beta and tumor necrosis factor-alpha TNF-alpha, and the anti-inflammatory cytokine IL-10 in the inoculated mammary glands 24h after inoculation. Increased mRNA levels of the proinflammatory cytokine IL-6 were only observed in the inoculated mammary glands of sows that developed clinical signs of mastitis. In contrast, the expression of the anti-inflammatory cytokine, transforming growth factor-beta 1 (TGF-beta1) mRNA was unaltered, as was mRNA expression for the IL-1 receptor type I (IL-1R1). Furthermore, IL-1beta and IL-10 mRNA expression was higher in the inoculated mammary glands of sows that developed clinical signs of mastitis compared with sows that remained clinically healthy. Notably, sows that developed clinical signs of mastitis had significantly lower pre-inoculation levels of IL-1beta mRNA than sows that remained clinically healthy. These findings suggest that development of coliform mastitis is associated with the level of local expression of regulatory cytokines in response to intramammary E. coli inoculation and infection.     

Alteration of helper T-cell related cytokine production in splenocytes during Trichinella spiralis infection

Infection by Trichinella spiralis takes place in two distinct phases: one is the intestinal phase and the other is the muscle phase. To evaluate alterations in cytokine production during a T. spiralis infection, we periodically assessed the cytokine production of splenocytes in mice after infection (AI). The levels of Th2-related cytokines immediately increased after the initiation of T. spiralis larval intestinal invasion (1 week AI). These early elevations in the Th2 response might be associated with the innate immune responses of intestine epithelial cells against T. spiralis larval invasion. IL-4 and IL-13 levels reached a peak prior to the initiation of nurse cell formation (2 weeks AI). Additionally, all Th17-related cytokines, except for IL-17, increased slightly until 2 weeks AI. However, expression levels for all of the Th2 and Th17-related cytokines began to decrease after the initiation of nurse cell formation and reached basal levels at 4 weeks AI, except for IL-5. At the same time, the CD4(+)CD25(+)Foxp3(+) T (regulatory T, T(reg)) cell population increased significantly in the spleen. Additionally, the number of cells in the peripheral lymph nodes increased. In conclusion, T. spiralis larva intestinal invasion induced the production of Th2 and Th17 cell-related cytokines, and the cytokines decreased with T(reg) cell-related cytokine.     

白细胞介素21及其免疫调节研究进展

白细胞介素21(IL-21)是新近发现的一种细胞因子,主要由激活的CD4+T细胞产生。IL-21通过其受体IL-21R发挥多种生物作用。IL-21R属于I型细胞因子受体家族,与IL-2、IL-4、IL-7、IL-9和IL-15受体共同享有γ链(γc)。许多研究表明IL-21独自或与其他细胞因子协同影响多种免疫细胞的增殖、生存、分化和功能,参与对免疫反应稳态平衡的调节。为了更全面了解IL-21研究进展,论文对IL-21与IR-21R的发现、结构特征、表达分布、信号通路以及IL-21对免疫细胞的调节作用进行综述。     

Th1 and Th2 indices of the immune response in pigs vaccinated against Taenia solium cysticercosis suggest various host immune strategies against the parasite

Kinetics of the production of serum antibody levels and Th1 (IL-2, IFN-gamma) and Th2 (IL-4, IL-10) cytokines was studied in five pigs vaccinated with a synthetic tri-peptide vaccine (S3Pvac) against Taenia solium, a vaccine that has been shown protects pigs against naturally acquired infection. Healthy pigs of mixed genetic background, similar to those bred in rural villages of Mexico, were vaccinated with S3Pvac or with adjuvant alone, kept in sanitary conditions and bled at different times after vaccination to study the development of their specific immune response. Peripheral blood mononuclear cells (PBMCs) of vaccinated pigs showed a significant increment in the production of Th1 cytokines (IL-2 and IFN-gamma) but not of Th2 cytokines (IL-4 and IL-10) after specific PBLs stimulation with all the individual peptides. A Th1-inclined cytokine profile leading to an exacerbated local inflammation at the early installation stage of the cysticercus may possibly interfere with their successful establishment in the serum antibodies against total cysticercus antigens and against each of the three different peptides comprising S3Pvac were detected 7-51 days after vaccination. Antibodies against GK-1 interfered with the cysticerci development into intestinal tapeworms in prednisolone-treated hamsters. The sub-lethal crippling effect of anti-GK-1 antibodies upon cysticerci indicates to a therapeutic application of S3Pvac in infected pigs having potential epidemiological consequences, as it could aid in decreasing the number of tapeworms expected to develop from the few cysticerci that survive in the vaccinated pigs.     

骨髓源肥大细胞通过甘露糖受体识别FMDV-VLPs的细胞因子应答

为了研究骨髓源肥大细胞（BMMCs）通过甘露糖受体对口蹄疫病毒样颗粒（FMDV-VLPs）的细胞因子应答效应，本研究构建了重组pCMV-HA-HBcAg-VP1-VP4质粒，并转染CHO-K1细胞以制备FMDV-VLPs。用FMDV-VLPs负载经甘露糖受体（MR）抑制剂Mannan处理的BMMCs （iMR-VLP组），并设置只负载FMDV-VLPs组（VLP组）和单纯细胞组（Control组）作为对照，收集细胞上清液，用细胞因子芯片检测不同处理组BMMCs细胞上清中细胞因子的含量。结果显示：与Control组相比，VLPs组BMMCs表达IL-1α、IL-2、IL-4、IL-15、IL-17A、IL-21、TNF-α、IFN-γ、CC17和CCL21均显著上调（P<0.05），而IL-10没有显著变化，iMR-VLP组BMMCs表达IL-1α、IL-2、IL-4、IL-15、IL-17A、TNF-α、IFN-γ、CCL-17和L-Selectin显著下调（P<0.05），而IL-9、IL-10、CCL19和CCL21的表达则呈上调变化。综上所述，FMDV-VLPs可以促进BMMCs一系列细胞因子的分泌，而抑制MR后，BMMCs分泌细胞因子能力受到了一定程度的抑制，表明FMDV-VLPs可能通过BMMCs的甘露糖受体增强Th1型细胞因子分泌、有效抑制能引起免疫抑制的IL-10的分泌，并降低介导T细胞的再循环的CCL19和CCL21的形成。研究结果为基于肥大细胞甘露糖受体应答效应的口蹄疫新型疫苗的研发提供了理论依据和新思路。     

Cell adhesion molecules, leukocyte trafficking, and strategies to reduce leukocyte infiltration

Leukocyte-endothelial cell interactions are mediated by various cell adhesion molecules. These interactions are important for leukocyte extravasation and trafficking in all domestic animal species. An initial slowing of leukocytes on the vascular endothelium is mediated by selectins. This event is followed by (1) activation of beta2 integrins after leukocyte exposure to cytokines and pro-inflammatory mediators, (2) adherence of leukocyte beta2 integrins to vascular endothelial ligands (eg, intercellular adhesion molecule-1 [ICAM-1]), (3) extravasation of leukocytes into tissues through tight junctions of endothelial cells mediated by platelet and endothelial cell adhesion molecule-1 (PECAM-1), and (4) perivascular migration through the extracellular matrix via beta1 integrins. Inhibiting excessive leukocyte egress and subsequent free radical-mediated damage caused by leukocyte components may attenuate or eliminate tissue damage. Several methods have been used to modify leukocyte infiltration in various animal models. These methods include nonspecific inhibition of pro-inflammatory mediators and adhesion molecules by nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, inhibition of cytokines and cytokine receptors, and inhibition of specific types of cell adhesion molecules, with inhibitors such as peptides and antibodies to beta2 integrins, and inhibitors of selectins, ICAMs, and vascular cell adhesion molecule-1 (VCAM-1). By understanding the cellular and molecular events in leukocyte-endothelial cell interactions, therapeutic strategies are being developed in several animal models and diseases in domestic animal species. Such therapies may have clinical benefit in the future to overcome tissue damage induced by excessive leukocyte infiltration.     

Impact of heparin and short term anesthesia on the quantification of cytokines in laboratory mouse plasma

Background

Studies have reported that heparin may be unsuitable as an anticoagulant in human plasma samples when quantifying cytokines using multiplex bead array assays. For mouse samples, multiplex assays have been validated for serum and EDTA-plasma, but it remains to be elucidated whether heparin influences the quantification of cytokines, and if so – to what extent. Furthermore, laboratory mice are often anesthetized for blood sampling, which causes acute stress that may influence circulating cytokine concentrations and thus bias experimental results. The objectives of the present study were to identify whether specific cytokine concentrations varied between heparin-plasma, serum, and EDTA-plasma, and whether short isoflurane anesthesia would influence the concentrations of these cytokines in the circulation. Twenty-three acute phase and pro-inflammatory cytokines were quantified in matched serum, EDTA-plasma, and heparin-plasma samples from anesthetized and unanesthetized male NMRI mice using a multiplex assay. In addition, samples from unanesthetized mice were spiked with three levels of heparin.

Results

The concentrations of five out of 23 cytokines were significantly different between sample types, but only one cytokine (IL-17A) differed between heparin-plasma and serum. When further spiking the heparin-plasma with increasing concentrations of heparin, there was a significant effect on 11 cytokines, where the cytokine recovery could be correlated to the heparin concentration for ten of these cytokines. Anesthesia resulted in lower concentrations of G-CSF, but had no significant impact on the concentrations of the other 22 cytokines.

Conclusion

In mice, heparin seems like a suitable anticoagulant for obtaining plasma for multiplex assays for the cytokines IL-1α, IL-1β, IL-2, IL-6, IL-9, IL-12p40, IL-12p70, IL-13, G-CSF, GM-CSF, IFN-γ, KC, MCP-1, MIP-1α, MIP-1β, RANTES and TNFα, but an effect of heparin in high concentrations should be considered for the cytokines IL-9, IL-12p40, IL-12p70, KC, MCP-1, MIP-1β and RANTES. Short isoflurane anesthesia had significant impact on G-CSF, but none of the other cytokines.     

Semi-quantitative analysis of cytokine expression in asymptomatic canine leishmaniasis

The dog is the main reservoir of Leishmania infantum, the parasite responsible for visceral leishmaniasis in Mediterranean countries. The infection in dogs shows different clinical presentations, from subclinical/asymptomatic to a fully developed disease, depending on the host's immune responses. The Th1/Th2 dichotomy is not clear in the different forms of canine leishmaniasis, since the data available from studies of immunity response in canine leishmaniasis are scarce and fragmented. The present work describes the cytokine expression in peripheral blood mononuclear cells (PBMC) obtained from asymptomatic dogs experimentally infected with L. infantum that present a cellular protective immune response. The results obtained from freshly isolated PBMC showed expressions of TNF-alpha, IL-2, IFN-gamma, IL-10 and IL-18 mRNA, similar to those from non-infected dogs. However, there was almost no expression of IL-4 mRNA detected in the asymptomatic infected dogs compared to the control dogs. Unspecific stimulation with ConA promoted the expression in a greater or lower degree of all the cytokines studied. In vitro stimulation of PBMC with soluble leishmanial antigen (SLA) promoted the expression of IL-2, IFN-gamma, TNF-alpha, IL-18, IL-4, IL-6 and IL-10 mRNA, with the two first being specifically induced. Although both Th1 and Th2 cytokines are produced, cell mediated immunity observed in these L. infantum-infected asymptomatic dogs depended on the preferential expression of Th1 cytokines.     

Interleukin-1beta reduces galactose transport in intestinal epithelial cells in a NF-kB and protein kinase C-dependent manner

Interleukins (IL), aside from their role in the regulation of the immune cascade, they have also been shown to modulate intestinal transport function. IL-1β is a potent inflammatory cytokine involved in many important cellular functions. The aim of this work was to study the in vitro effect of IL-1β on d-galactose transport across intestinal epithelia in rabbit jejunum and Caco-2 cells. The results showed that d-galactose intestinal absorption was diminished in IL-1β treated jejunum rabbits without affecting the Na⁺, K⁺-ATPase activity. The presence of IL-1 cell-surface receptors was confirmed by addition to tissue of a specific IL-1 receptor antagonist (IL-1ra). The cytokine did not inhibit either the uptake of d-galactose nor modified the sodium-glucose transport (SGLT1) protein levels in the brush border membrane vesicles, suggesting an indirect IL effect. The IL-inhibition was significantly reversed in the presence of inhibitors of protein kinase C (PKC) and mitogen-activated protein kinases (MAPKs). The proteasome selective inhibitor completely abolished the IL-effect. Furthermore, the cytokine inhibition on galactose transport related to NF-kB activation was also confirmed in Caco-2 cells. In summary, the direct addition of IL-1β to intestinal epithelia inhibits d-galactose transport by a possible reduction in the SGLT1 activity. This event may be mediated by several transduction pathways activated during the inflammatory processes related to several protein kinases and nuclear factor, NF-kB. The IL-effect is independent of hormonal milieu and nervous stimuli.     

Interleukin-4 increases cortisol release and decreases adrenal androgen release from bovine adrenal cells

ACTH is the primary regulator of adrenal function during acute stress. However, during chronic inflammatory stress additional factors play a major role in the regulation of adrenal secretion. Many cytokines circulate in the blood and are synthesized and released from adrenal tissue. Furthermore, these peptides modify adrenal function. Recently, interleukin-4 (IL-4) was demonstrated to be released from a human adrenal tumor cell line. Therefore, we hypothesized that normal bovine adrenocortical cells could express IL-4 and that this cytokine may modify adrenal function. We determined that IL-4 and IL-4 receptors (IL-4R) are expressed in the bovine adrenal cortex whereas the expression of IL-4 and IL-4R in the adrenal medulla was not apparent. Exposure of dispersed bovine adrenocortical cells isolated from the zona fasciculate to IL-4 did not modify basal release of cortisol. However, the ACTH-stimulated release of cortisol from the bovine adrenal cells was augmented by IL-4. IL-4 exposure had no affect on adrenal androgen release from bovine zona reticularis cells, but IL-4 inhibited the ACTH-stimulated release of adrenal androgens from these cells. The effects of IL-4 on ACTH-stimulated cortisol and adrenal androgen release were dependent upon the IL-4 incubation interval and the IL-4 concentration. Because communication between the immune and endocrine systems is important in inflammatory conditions, IL-4 may play a role in coordinating the adrenal response to inflammatory stress.     

The anti-gonadotropic effects of cytokines: the role of neuropeptides

The inhibitory effect of inflammation and endotoxins on the secretion of reproductive hormones from the hypothalamo-pituitary axis is well documented. A comparison of the luteinizing hormone (LH) suppressing effects of several pro-inflammatory cytokines revealed that centrally administered IL-1β was the most potent inhibitor of pituitary LH secretion; interleukin (IL)-1α and tumor necrosis factor (TNF)α were relatively less effective, whereas IL-6 was ineffective. This order of potency suggested that the anti-gonadotropic effects of an immune challenge are most likely attributable to the action of centrally released IL-1β, and this was supported by the demonstration that IL-1β suppressed hypothalamic luteinizing hormone releasing hormone (LHRH) release. We used a multifaceted approach to identify the afferent signals in the brain that convey immune messages to hypothalamic LHRH neurons. Pharmacological studies with specific antagonists of opioid receptor subtypes demonstrated that activation of the μ1 receptor subtype was required to transmit the cytokine signal. Furthermore, icv IL-1β upregulated hypothalamic POMC mRNA and increased the concentration and release of β-endorphin, the primary ligand of μ1 receptors. We have obtained evidence that IL-1β also enhanced the gene expression and concentration of tachykinins, a family of nociceptive neuropeptides in the hypothalamus. Blockade of tachykinergic NK2 receptors attenuated IL-1β induced inhibition of LH secretion. Collectively, these results demonstrate that IL-1β, generated centrally in response to inflammation, upregulates the opioid and tachykinin peptides in the hypothalamus. These two groups of neuropeptides are critically involved in relaying the cytokine signal to neuroendocrine neurons and causing the suppression of hypothalamic LHRH and pituitary LH release.     

Ketamine inhibits LPS-induced tumour necrosis factor-alpha and interleukin-6 in an equine macrophage cell line

Ketamine is widely used in equine anaesthesia. Beside its anaesthetic and analgesic properties, ketamine possesses a cytokine-modulating activity. However, to date, no data are available regarding the inhibitory effect of ketamine on the cytokine response in horses. In horses, cytokines such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) play a pivotal role in the pathogenesis of equine endotoxaemia following gastrointestinal disorders. Hence, the objective of this study was to assess the influence of ketamine on LPS-induced TNF-alpha and IL-6 formation in an equine macrophage cell line (eCAS cells). The results demonstrate a cytokine-modulating activity of ketamine in an equine cell line, suggesting a beneficial role for ketamine in the treatment of equine endotoxaemia.     

Does cortisol bias cytokine production in cultured porcine splenocytes to a Th2 phenotype?

Glucocorticoids are reported to bias the production of cytokines from a type 1 to a type 2 phenotype. However, this dogma has been advanced largely from studies utilizing potent glucocorticoid analogs, particularly dexamethasone (DEX). Although studies utilizing DEX certainly have clinical and pharmacological relevance, DEX is probably not the best glucocorticoid for studies designed to evaluate the interaction and regulation of endogenous corticosteroids with immune cells in vivo in the domestic pig. Functional measures of immune suppression suggest that the pig is relatively resistant to DEX. Furthermore, type II corticosteroid receptors exclusively bind DEX with high affinity, whereas type I receptors, the so-called mineralocorticoid receptors, have a higher affinity for cortisol. In addition, DEX is not bound by serum binding proteins as are endogenous corticosteroids.These issues prompted us to revisit glucocorticoid regulation of type 1 and type 2 cytokines in cultured pig splenocytes and to test the broad hypothesis that cortisol biases cytokine production in favor of a Th2 response. We evaluated interferon gamma (IFNgamma) (also interleukin 2 (IL-2) in one experiment) and interleukin 10 (IL-10) as representative Th1 and Th2 cytokines, respectively. Furthermore, we evaluated macrophage migration inhibitory factor (MIF) because it is reported to be an essential factor in T cell activation; it is also upregulated by glucocorticoids and reported to be a product of Th2 lymphocytes. In general, both IFNgamma and IL-10 were sensitive to cortisol inhibition early in culture. However, IFNgamma ultimately escaped cortisol inhibition, whereas IL-10 continued to be substantially suppressed by high physiological concentrations of cortisol. Similarly, MIF mRNA could be suppressed by cortisol, but only when cortisol was added to cultures after ConA (concanavalin A) stimulation of splenocytes. So, taken together, our studies do not support the hypothesis that cortisol favors a Th2 cytokine profile in cultured pig splenocytes.     

DNA vaccination in the avian

The skin has long been recognized as a major producer of cytokines, but the keratinocyte as principal epidermal cell has received less attention as potential source and target of cytokines. Nevertheless, keratinocytes produce a plethora of cytokines including interleukin (IL)-1, -6, -7, -8, -10, -12, -15, -18, and -20, and tumor necrosis factor alpha (TNF). The production by keratinocytes of pro-inflammatory (IL)-1, -6, -8, and TNF was recognized early and is well studied. Keratinocyte-derived IL-7 and -15 are considered to be significant in T-cell trafficking, possibly even in the pathogenesis of cutaneous T-cell lymphoma. Immunomodulatory IL-10 and -12 originating from keratinocytes are considered to be responsible for systemic effects, and IL-18 perhaps has a similar action. Keratinocytes were fairly recently recognized as being source or target of other IL-10 family members like IL-20 and IL-24 and the role of these cytokines in specific diseases is under investigation. In addition, a variety of cytokine receptors are present on keratinocytes like those for IL-4, -13, and -17 and to lesser degree IL-2. The ability to study the expression of cytokines by keratinocytes in vivo and in vitro using primary cells, immortalized cells or even organotypic culture systems offers many possibilities to further investigate the role of cytokine production in keratinocyte biology and disease.     

Cytokines as markers for infections and their effect on growth performance and well-being in the pig

Exposure to micro-organisms commonly elicit the production of cytokines. These soluble factors enhance several innate immune functions that aim to limit the spread of infection. Further, many of the pro-inflammatory cytokines regulate the ensuing specific immune response. In addition to their effects on cells of the immune system, cytokines also are important regulators in the so called immune-neuroendocrine network. The microbial structures that are necessary for induction of cytokine production are not conclusively determined but in general, bacteria preferentially induce the production of IL-1, TNF-α, IL-6, and IL-8, whereas virus induce the production of Type 1 interferons (IFN-α/β). The onset of production of these cytokines is rapid, and several of them may reach systemic levels during a short period after infection. Thus, cytokines can serve as markers for ongoing infections and be used for discrimination between infections of bacterial or viral origin. Results from experimental and field studies show that serum IFN-α and IL-6 seem to be useful markers for ongoing (subclinical) viral and bacterial infections, respectively, in the pig. Consequently, demonstration of these cytokines can be valuable tools in heard health monitoring programs.     

头孢喹肟的体外抗炎作用

通过构建的细菌脂多糖(LPS)诱导小鼠巨噬细胞(RAW264.7)的体外炎症模型,研究了不同浓度头孢喹肟对肿瘤坏死因子(TNF-α),IL-1β,IL-6,IL-10和一氧化氮(NO)合成的影响,以及对NF-κB活性的影响.结果显示,1、5、10 mg/L的头孢喹肟能显著抑制RAW264.7合成的TNF-α、IL-1β、IL-6和NO,但是对IL-10无显著调节作用.头孢喹肟以剂量依赖的方式显著抑制了LPS对NF-κB的激活作用.结果表明,头孢喹肟可能通过NF-κB这条通路发挥抗芡作用.