Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to cope with the worldwide increase in the prevalence of multidrug-resistant tuberculosis and Mycobacterium avium complex (MAC) infections, a number of new antimycobacterial drugs have been or are being synthesized and developed. Development of new protocols for chemotherapy of refractory mycobacterioses is also sharing promise. In this context, one promising strategy is to devise regimens to treat patients with refractory mycobacterioses using ordinary antimycobacterial agents in combination with appropriate immunomodulators. This article deals with the following matters: an outline of the host immune response to mycobacterial pathogens, particularly in terms of mobilization of the cytokine network in response to mycobacterial infection, and adjunctive immunotherapy using (1) recombinant immunomodulating cytokines, (especially Th-1 and Th-1-like cytokines such as IFN-gamma, IL-2, IL-12, IL-18 and GM-CSF), (2) inhibitors of immunosuppressive cytokines (TGF-beta) and some proinflammatory tissue-damaging cytokines (TNF-alpha), and (3) immunomodulatory agents such as ATP and its analogs, imidazoquinoline, diethyldithiocarbamate, poloxamer, dibenzopyran, galactosylceramide, nonsteroidal anti-inflammatory drugs, Chinese traditional medicines, levamisole, synthesized mycobacterial oligoDNA, DNA vaccine expressing mycobacterial HSP65 or IL-12, and heat-killed Mycobacterium vaccae. Although adjunctive immunotherapy is fairly efficacious in treating intractable mycobacterioses, it still features serious problems and dilemmas, such as high cost, occasionally severe side effects, and, in many cases, only modest efficacy in potentiating host defense mechanisms against mycobacterial infections, primarily because of the induction of macrophage-deactivating cytokines during the course of long-term administration of adjunctive agents.
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PMID:Adjunctive immunotherapy of mycobacterial infections. 1554 17

Immune system dysfunction in the perioperative period, with its combined pro-inflammatory and immuno-suppressive effects, can influence long term disease progression, morbidity, and mortality. Literature on postoperative immune response in schistosomiasis patients is scarce. The aim of this study was to assess the impact of isoflurane anesthesia on pro- and anti-inflammatory cytokine balance in schistosomal patients undergoing minor procedures. The study was conducted on 24 patients (ASA class I-II) scheduled for elective urologic endoscopic procedures. Patients were divided into two groups 12 patients each: control group (n=12) and patient group (n=12). Anaesthesia was induced by a bolus dose of sufentanil 0.2 microg x kg(-1), thiopentone sodium 5 mg x kg(-1), vecuronium 0.1 mg x kg(-1) and maintained by isoflurane 1-1.5 MAC with additional sufentanil bolus of 0.15 microg x kg(-1) when indicated. Venous blood samples were obtained from each patient: before induction, fifteen minutes, one hr after induction and 24 hrs after surgery. Plasma levels of IL-1beta, TNF-alpha, IL-8, IFN-gamma, IL-1ra and TNF-BP1, as well as stress hormones (cortisol and prolactin) were measured. As for pro- and anti-inflammatory cytokine balance, the overall end-result was a rise at 24 hr postoperatively, in the level of TNF-alpha (a key pro-inflammatory cytokine) and IFN-gamma, as well as both anti-inflammatory cytokines (IL-Ira & sTNF-R1). The anti-inflammatory response was more conspicuous in the patients than controls.
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PMID:Does isoflurane anesthesia alter immuno-modulatory response in schistosomal patients? Assessment of serum pro- and anti-inflammatory cytokine balance. 1692 76

We sought to determine whether prolactin (PRL) could influence the neutrophilic inflammation that characterizes chronic mastitis. Most of the genes encoding inflammatory proteins depend on the nuclear factor kappaB (NF-kappaB) for their expression. We addressed the hypothesis that immunomodulatory activities of PRL might arise from an increase in NF-kappaB activity. MAC-T cells, a bovine mammary epithelial cell line, were stimulated with increasing concentrations of bovine PRL (1, 5, 25, 125, and 1,000 ng/mL). Level of NF-kappaB binding activity was measured and mRNA was evaluated for IL-1beta, IL-6, IL-8, granulocyte-macrophage colony-stimulating factor (GMCSF), IFN-gamma, and tumor necrosis factor (TNF)-alpha, cytokines known to require NF-kappaB for their maximal transcription. Prolactin activated NF-kappaB; maximal NF-kappaB activation was weaker with PRL than with TNF-alpha at 30 or 180 min poststimulation. In addition, PRL significantly amplified, in a dose-dependent manner, mRNA expression of IL-1beta, IL-6, IL-8, GMCSF, and TNF-alpha. We measured PRL concentrations in blood and milk from healthy and chronic mastitis-infected cows, and studied the relationship between the PRL concentration and the degree of inflammation in the mammary gland as indirectly assessed by somatic cell counts (SCC). Plasma PRL did not differ significantly between healthy and chronic mastitis-affected cows (63.7 and 67.5 ng/mL, respectively). Milk PRL concentration was significantly increased in chronic mastitis-affected quarters with the highest SCC, and had a positive significant correlation between SCC, as well as between the number of neutrophils present in milk samples. The present findings show that PRL promotes an inflammatory response in bovine mammary epithelial cells via NF-kappaB activation, and suggest a role for PRL in the pathogenesis of chronic mastitis.
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PMID:Prolactin-induced activation of nuclear factor kappaB in bovine mammary epithelial cells: role in chronic mastitis. 1718 84

Nontuberculous mycobacteria (NTM) are intracellular pathogens that elicit a specific T-cell response characterized by the production of proinflammatory cytokines, including interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-12. However, little information exists regarding the levels of specific cytokines in patients with NTM lung disease. Therefore, we compared cytokine production in peripheral blood mononuclear cells (PBMCs) from patients with NTM lung disease with that in PBMCs from healthy controls. Pro- and anti-inflammatory cytokine production was measured by enzyme-linked immunosorbent assay in the PBMCs of 29 patients with NTM lung disease and 15 healthy controls. Phytohemagglutinin (PHA)-induced IFN-gamma production and lipopolysaccharide (LPS)-induced production of TNF-alpha and IL-12p40 were significantly lower in the PBMCs of patients with NTM lung disease than in those of the healthy controls. The production of these cytokines did not differ significantly between patients infected with Mycobacterium avium complex (MAC) and those infected with Mycobacterium abscessus; however, IL-10 production was lower in patients infected with M. abscessus than in those infected with MAC. Decreased IFN-gamma, TNF-alpha, and IL-12 production may be associated with host susceptibility to the development of MAC and M. abscessus lung disease.
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PMID:Decreased cytokine production in patients with nontuberculous mycobacterial lung disease. 1792 95


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