Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role(s) of novel chemotactic cytokines as mediators in the pathogenesis of many acute and chronic disease states is becoming increasingly apparent. One of these cytokines, interleukin 8, is a product of both immune and non-immune cells. In this manuscript, we describe the suppression of IL-8 gene expression from stimulated monocytes by IL-4, while IL-4 had no suppressive effects on IL-8 gene expression from stimulated fibroblasts and endothelial cells. Our data suggest that IL-4 may function as an endogenous regulator of monocyte cytokine expression, including the chemotactic cytokine IL-8.
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PMID:Disparate regulation of interleukin 8 gene expression from blood monocytes, endothelial cells, and fibroblasts by interleukin 4. 220 28

Mycoplasma arthritidis is an arthritogenic organism for rodents, producing a superantigen (MAS). It has been postulated that mycoplasmas or superantigens thereof might play a role in human rheumatoid arthritis. Since M. arthritidis fulfills both, the present study was performed to investigate MAS-specific cytokine induction. Human or murine leukocytes were stimulated with MAS, staphylococcal enterotoxin E (SEE), or lipopolysaccharide (LPS). Cytokines were measured by ELISA, Bioassay, and RT-PCR. The response to MAS in humans was individually restricted, in contrast to the response to SEE or LPS. Furthermore, MAS showed the same capacity for inducing proinflammatory cytokines as interleukin (IL)-1 IL-6, and IL-8 as SEE and LPS. However, MAS showed a significantly decreased capacity to induce the anti-inflammatory cytokine IL-10 and IL-1RA. In mice, the reactivity to MAS was strictly MHC-II restricted, in contrast to that of SEE or LPS. The individual response to MAS in humans might be explained by the difference of the HLA-DR haplotype because H-2-differing mouse strains showed the same discrepancies. MAS induced an overproduction of proinflammatory cytokines, when its ability to induce proinflammatory and anti-inflammatory cytokines was compared with those of SEE and LPS. The individual response may explain an MHC linkage, and the failure to induce anti-inflammatory cytokines may be the reason for a chronic disease in contrast to acute inflammation.
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PMID:Induction of a proinflammatory cytokine network by Mycoplasma arthritidis-derived superantigen (MAS). 891 Jul 72

Interleukin-1 beta (IL-1 beta), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) induce acute anorexia by direct action in the central nervous system (CNS) at estimated pathophysiological concentrations reported in the cerebrospinal fluid (CSF). Cytokine-induced anorexia may also participate in the long-term anorexia observed during disease. Here, we studied the effects of chronic intracerebroventricular (ICV) microinfusion (through osmotic minipumps) of various cytokines on feeding and drinking in rats. The results show: IL-1 beta decreased nighttime feeding dose-dependently (with 0.5, 1.0, 2.0 and 8.0 ng/24 h, n > or = 8/group). The decrease of feeding and corresponding decrease of body weight persisted during the 7-day infusion. Total daily food intake decrease was less prominent relative to the nighttime decrease because daytime food intake slightly increased. Feeding and body weight increased toward baseline following the end of the IL-1 beta infusion. ICV microinfusion of heat-inactivated IL-1 beta or IL-1 beta plus IL-1 receptor antagonist had no effect, suggesting specificity of action of IL-1 beta. Water intake did not decrease in any IL-1 beta-treated group, suggesting specificity on feeding. Chronic ICV administration of TNF-alpha (20, 100, or 300 ng/24 h), IL-6 (100 ng/24 h), or IL-8 (20 ng/24 h) was significantly less effective than IL-1 beta in inducing behavioral modifications. The results suggest that IL-1 beta, at doses that yield estimated pathophysiological concentrations in the CSF, is capable of inducing long-term anorexia and this effect may participate in the anorexia observed during chronic disease.
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PMID:Anorexia induced by chronic central administration of cytokines at estimated pathophysiological concentrations. 911 Sep 49

Helicobacter pylori has been widely recognized as an important human pathogen responsible for chronic gastritis, peptic ulcers, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma. Little is known about the natural history of this infection since patients are usually recognized as having the infection only after years or decades of chronic disease. Several animal models of H. pylori infection, including those with different species of rodents, nonhuman primates, and germ-free animals, have been developed. Here we describe a new animal model in which the clinical, pathological, microbiological, and immunological aspects of human acute and chronic infection are mimicked and which allows us to monitor these aspects of infection within the same individuals. Conventional Beagle dogs were infected orally with a mouse-adapted strain of H. pylori and monitored for up to 24 weeks. Acute infection caused vomiting and diarrhea. The acute phase was followed by polymorphonuclear cell infiltration, interleukin 8 induction, mononuclear cell recruitment, and the appearance of a specific antibody response against H. pylori. The chronic phase was characterized by gastritis, epithelial alterations, superficial erosions, and the appearance of the typical macroscopic follicles that in humans are considered possible precursors of MALT lymphoma. In conclusion, infection in this model mimics closely human infection and allows us to study those phases that cannot be studied in humans. This new model can be a unique tool for learning more about the disease and for developing strategies for treatment and prevention.
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PMID:A conventional beagle dog model for acute and chronic infection with Helicobacter pylori. 1033 28

In an earlier study in Indonesia we reported on adverse reactions to diethylcarbamazine (DEC) in brugian filariasis patients identified as microfilaraemics (n = 26), endemic normals (n = 11) and elephantiasis patients (n = 17). To assess the link between adverse reactions and cytokines we have now analysed an array of inflammatory mediators in plasma samples collected during the same study. Pre-treatment levels of interleukin (IL)-6 and soluble tumour necrosis factor receptor 75 (sTNF-R75) were higher in elephantiasis patients compared to microfilaraemics and endemic normals, indicating the presence of an ongoing inflammation in patients with chronic disease. After initiation of treatment, the levels of IL-6 and LPS-binding protein (LBP) were consistently and significantly higher in microfilaraemics who suffered most from adverse reactions compared with endemic normals and elephantiasis patients. In microfilaraemics the levels of sTNF-R75 increased after treatment to reach levels recorded in elephantiasis patients. IL-6 increased early, concurrent with the development of adverse reactions and peaked by 24 h post treatment. The levels of LBP and sTNF-R75 in microfilaraemics also increased to peak, later than IL-6, at 32 h post DEC therapy. Although changes were recorded in IL-8 and IL-10 levels in some individuals, no significant differences were found between the 3 clinical groups. These results demonstrate that intake of DEC leads to an increase in a selected number of inflammatory mediators in the group of filarial patients who suffer most from adverse systemic reactions.
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PMID:Inflammatory cytokines following diethylcarbamazine (DEC) treatment of different clinical groups in lymphatic filariasis. 1071 62

Acute viral respiratory tract infections are well known to precipitate asthma attacks and acute exacerbations of chronic obstructive pulmonary disease, but their role in the pathogenesis of chronic disease is poorly defined. Double-stranded DNA viruses have the ability to persist in airway epithelial cells long after the acute infection has cleared. During these latent infections, viral genes are expressed at the protein level without replication of a complete virus. The expression of the adenoviral trans-activating protein has been demonstrated in the airway epithelium of both human and animal lungs and is associated with an amplification of the cigarette smoke-induced inflammatory response. Studies of cultured human airway epithelial cells have also shown that transfection with this viral gene upregulates the expression of intercellular adhesion molecule 1 and interleukin 8 by these cells when they are challenged with endotoxin. In guinea pigs, cigarette smoke-induced emphysema is amplified by latent adenoviral infection. Furthermore, this infection independently increased the number of CD-8 cells, whereas the cigarette smoke independently increased the number of CD-4 cells in the inflammatory infiltrate. On the other hand, allergen-induced lung inflammation was uninfluenced by latent adenoviral infection in the guinea pig, but the latent infection caused the eosinophilic component of this response to become steroid resistant. These studies suggest that latent adenoviral infections may have a role in the pathogenesis of obstructive airway disease by amplifying the response to cigarette smoke and inducing steroid resistance.
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PMID:Role of latent viral infections in chronic obstructive pulmonary disease and asthma. 1173 71

Pathogens have developed different strategies to survive and multiply within their host. Among them is the ability to control phagocyte apoptosis while another is to affect the expression of cytokines which is necessary for a normal protective function of the immune response. To establish themselves and cause chronic disease in humans and animals, Brucella spp. invade and proliferate within monocytic phagocytes. We have established that in humans, Brucella suis impairs the apoptosis of monocytes and macrophages, thus preventing its host cell elimination. In mice, which are not naturally colonized by the bacteria, Brucella infection results in Type1 (Th1) cellular immune response which promotes a clearance of the bacterial organism. The development of this response is under the control of major cytokines like TNF-alpha, IFN-gamma and IL-12 produced at the onset of infection. We have observed that in humans, B. suis-infected macrophages which produce IL-1, IL-6, IL-10 and several chemokines including IL-8, do not secrete TNF-alpha. By constructing null mutants, we demonstrated that this inhibition involves the outer membrane protein Omp25 of Brucella, however the mechanism regulating the inhibition has not yet been clearly defined. It is likely that the Omp25-induced effect on TNF-alpha production assists bacterial evasion of antimicrobial defences at different levels. Firstly, by preventing the autocrine activation of macrophages thus inhibiting innate immunity and secondly by impairing the production of IL-12 and the development of a Th1 type specific immunity. In addition to the central role of the macrophage in Brucella infection, others cells of the innate immune response are recruited and influenced by the interactions between bacteria and host. For instance, human Vgamma9Vdelta2 T-cells play an important role in the early response to infection with intracellular pathogens. Evidence has been presented that their number dramatically increased in the peripheral blood of patients with acute brucellosis. We have shown that human Vgamma9Vdelta2 T-cells can be specifically activated by non-peptidic low molecular weight compound(s) from B. suis lysate or by soluble factors produced by B. suis-infected macrophages. Under these conditions, they produce TNF-alpha and IFN-gamma and reduce the bacterial multiplication inside infected autologous macrophages. This impairment of B. suis multiplication is due to both soluble factors released from activated gammadeltaT-cells (including TNF-alpha and IFN-gamma) and to a contact-dependent cytotoxicity directed against the infected cells. The interactions between the bacteria and these cells can counteract the intramacrophagic development of the bacteria and finally influence the further development of the host defense. We hypothesize that the chronicity or the elimination of the infection will depend on the balance between contradictory effects induced by the bacteria which favor either the host or the pathogen. Moreover, the interrelationship between the different cells must be taken into account in the analysis of the virulence of the bacteria and in the development of in vitro models of human macrophage infection.
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PMID:The innate immune response against Brucella in humans. 1241 58

Chlamydia/Chlamydophila are a family of intracellular gram-negative bacteria that infect their hosts primarily via mucosal epithelia. Chronic disease associated with bacterial persistence, inflammation and tissue damage are common sequelae of infection with these organisms. Human epithelial cell lines respond to infection by releasing pro-inflammatory cytokines and chemokines such as interleukin (IL)-6 and IL-8, and upregulating the expression of mRNA encoding Ikappa-Balpha, the endogenous inhibitor of NF-kappaB. However, Ikappa-Balpha is not upregulated in response to bacterial lipopolysaccharide (LPS). The failure of epithelial cells to respond to LPS is associated with the absence of surface expression of CD14. Identification of the components of Chlamydia/Chlamydophila that can induce pro-inflammatory mediators coupled with the mechanisms by which epithelial cells detect infection and respond accordingly will advance the development of preventative strategies.
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PMID:Induction of inflammatory host immune responses by organisms belonging to the genera Chlamydia/Chlamydophila. 1520 55

Induction of host cytokines plays a critical role in infection as well as disease in human filariasis. Measurements of such molecules in plasma could be used as windows of markers both for understanding the pathogenesis of the disease and for identifying markers of morbidity. Eight inflammatory and non-inflammatory host molecules in circulation were quantified in 207 subjects in filariasis endemic area of Orissa, India. IL-6, IL-8, IL-10, TNF-alpha, TNFR-I, TNFR-II, LBP and sICAM-1 were quantified by immunoassays and were analyzed by multivariate exploratory data analysis methods followed by multivariate analysis of variance. Raised levels of IL-6 and IL-8 emerged as markers of acute as well as chronic disease, while increased TNF-alpha was a feature found only in acute filariasis. Decreased sICAM-1 was a feature found only in asymptomatic subjects with filarial infection. There was a dichotomy in plasma levels of two TNF receptors between infected subjects and patients with filarial disease. Since plasma levels of these cytokines are often determined by host genetics, studies on cytokine genetic polymorphisms could offer new insights into the relationship between infection and disease in human lymphatic filariasis.
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PMID:Human bancroftian filariasis: immunological markers of morbidity and infection. 1683 94

Serum levels of interleukin(IL)-8, IL-6, and (TNF)-alpha were measured in 25 patients during active uveitis and uveitis in remission and compared to age-matched controls. Levels of IL-8 and IL-6 were significantly elevated in patients with active disease and were decreased during remission. IL-8 levels were highest in patients with anterior uveitis, with greatest difference between active disease and remission. No consistent pattern was observed for TNF-alpha. In conclusion, serum cytokine levels are elevated in active noninfectious uveitis. The rise in IL-8 may suggest innate immune mechanisms in the acute disease, while IL-6 participates in modulation of inflammation in the chronic disease.
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PMID:Serum cytokine levels in active uveitis and remission. 1785 91


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