Cytokines ; immunology ; Embolism ; immunology ; metabolism ; pathology ; Endometriosis ; immunology ; metabolism ; pathology ; Female ; Hormones ; metabolism ; Humans

With the imminent and widespread ban of the use of antibiotic feed additives and chemical antimicrobials in food production animals, alternative measures need to be sought to ensure that the livestock industry will not be adversely affected. Cytokines are proteins that control the type and extent of an immune response following infection or vaccination. They therefore represent excellent naturally occurring therapeutics. The identification, cloning and characterisation of cytokine genes in chickens have lagged somewhat behind similar work in mammals. Progress in isolating chicken homologues of mammalian cytokines has also been slowed by the generally low level of sequence similarity. Chicken cytokine genes that have been cloned to date include ChIFN-gamma, ChIL-1beta, ChIFN-alpha, ChIL-15, ChIL-18, ChIL-8, ChIL-2, ChIL-6, ChIL-16, SCF, MGF, TGFbeta, Lymphotactin, MIP-1beta, CXC and CC chemokines, so the use of cytokines in poultry has become more feasible with the discovery of a number of avian cytokine genes. The delivery methods for chicken cytokine are of prime importance and are required to be safe, easy to administer and cost-effective. Live viral vectors such as fowl adenovirus (FAV) expressing cytokine genes can be delivered via drinking water or aerosol sprays, making it very easy to administer. Since the immune system of chickens is similar to that of mammals, they offer an attractive model system to study the effectiveness of cytokine therapy in the control of disease in livestock. This review focus on the recent advances made in avian cytokines, with a particular focus on their assessment as therapeutic agents and vaccine adjuvants.
Adjuvants, Immunologic ; metabolism ; Animals ; Cytokines ; genetics ; immunology ; metabolism ; Immunotherapy ; methods

OBJECTIVETo evaluate immunologic mechanisms underlying Aspergillus fumigatus pulmonary infections in immunocompetent Dark Agouti (DA) and Albino Oxford (AO) rats recognized as being susceptible to some inflammatory diseases in different manners.

METHODSLung fungal burden (quantitative colony forming units, CFU, assay), leukocyte infiltration (histology, cell composition) and their function (phagocytosis, oxidative activity, CD11b adhesion molecule expression) and cytokine interferon-γ (IFN-γ) and interleukin-17 and -4 (IL-17 and IL-4) lung content were evaluated following infection (intratracheally, 1x10(7) conidia).

RESULTSSlower reduction of fungal burden was observed in AO rats in comparison with that in DA rats, which was coincided with less intense histologically evident lung cell infiltration and leukocyte recovery as well as lower level of most of the their activities including intracellular myeloperoxidase activity, the capacity of nitroblue tetrazolium salt reduction and CD11b adhesion molecule expression (except for phagocytosis of conidia) in these rats. Differential patterns of changes in proinflammatory cytokine levels (unchanged levels of IFN-γ and transient increase of IL-17 in AO rats vs continuous increase of both cytokines in DA rats) and unchanged levels of IL-4 were observed.

CONCLUSIONGenetically-based differences in the pattern of antifungal lung leukocyte activities and cytokine milieu, associated with differential efficiency of fungal elimination might be useful in the future use of rat models in studies of pulmonary aspergillosis.

Animals ; Aspergillus fumigatus ; immunology ; Cytokines ; metabolism ; Lung ; immunology ; metabolism ; microbiology ; pathology ; Male ; Pulmonary Aspergillosis ; immunology ; Rats

Cytokines ; metabolism ; Humans ; Leukocytes, Mononuclear ; immunology ; secretion ; Ubiquitin ; blood

Animals ; Antigens, CD ; immunology ; Cytokines ; metabolism ; Hepacivirus ; immunology ; Hepatitis C ; immunology ; prevention & control ; virology ; Hepatitis C Antibodies ; biosynthesis ; immunology ; Hepatitis C Antigens ; immunology ; Humans ; Killer Cells, Natural ; immunology ; T-Lymphocytes ; immunology ; metabolism ; T-Lymphocytes, Regulatory ; immunology ; metabolism ; Viral Proteins ; immunology

Aplastic anemia(AA) is mostly considered as an immune-mediated bone marrow failure syndrome, characterized by pancytopenia and bone marrow hypoplasia. The pathogenesis of AA is complicated, until now it is not fully understood. Further study on the pathological mechanism will be helpful for the diagnosis and treatment of AA. CD8(+) T cells and their secreted cytokines play important roles in the abnormal immunity during the process of AA. Thus, this review focuses on the role of CD8(+) T cells and their secreted cytokines in the pathogenesis of AA.
Anemia, Aplastic ; immunology ; metabolism ; pathology ; CD8-Positive T-Lymphocytes ; immunology ; metabolism ; secretion ; Cytokines ; metabolism ; Humans ; Immunity, Cellular

OBJECTIVEA general review was made of studies involving: (1) the concept and mechanism of the cholinergic anti-inflammatory pathway (CAP), (2) the important role of inflammatory response in myocardial ischemia reperfusion (I/R) injury and (3) the evidence and mechanisms by which CAP may provide protection against myocardial I/R injury.

DATA SOURCESThe data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1987 to 2009. The search terms were "vagal nerve stimulation", "myocardial ischemia reperfusion injury", "nicotine acetylcholine receptor" and "inflammation".

STUDY SELECTION(1) Clinical and experimental evidence that the inflammatory response induced by reperfusion enhances myocardial I/R injury. (2) Clinical and laboratory evidence that the CAP inhibits the inflammation and provides protection against myocardial I/R injury.

RESULTSThe myocardial I/R injury is really an inflammatory process characterized by recruitment of neutrophils into the ischemic myocardium and excessive production of pro-inflammatory cytokines. Because the CAP can modulate the inflammatory response by decreasing the production and release of pro-inflammatory cytokines, it can provide protection against myocardial I/R injury.

CONCLUSIONSThe CAP can inhibit the inflammatory response induced by reperfusion and protect against myocardial I/R injury. It represents an exciting opportunity to develop new and novel therapeutics to attenuate the myocardial I/R injury.

Animals ; Cytokines ; metabolism ; Humans ; Inflammation ; immunology ; Models, Biological ; Myocardial Reperfusion Injury ; immunology ; metabolism ; prevention & control ; Vagus Nerve Stimulation

OBJECTIVE: To explore the relationship of the expression of thymic stromal lymphopoietin (TSLP) in nasal polyps tissues and the Th2 inflammatory response. METHOD: Sixty patients with nasal polyps were collect ed. The immunohistochemical staining method was used to detect the expression of TSLP in nasal polyps tissues and ELISA method to the expression of IL-4, IL-5, IFN-gamma, IL-13 and analyzed the correlation between them. RESULT: The expression of TSLP in nasal polyp tissues was higher than that in normal inferior turbinate mucosa (P < 0.05). The expression level of IL-4, IL-5, IFN-gamma and IL-13 in nasal polyps tissues were significantly higher than those in control group (P < 0.05). TSLP staining was a statistically significant positive correlation with IL-4, IL5 and IL-13 (r = 0.475, 0.594 and 0.582, respectively, P < 0.01), while inverse correlation with IFN-gamma (r = -0.614, P < 0.01). CONCLUSION The high expression of TSLP might promote T cell differentiation towards Th2, and participated in the occurrence/development of nasal polyps, aggravated the nose Th2 inflammatory response.
Adult ; Cytokines ; metabolism ; Female ; Humans ; Interferon-gamma ; metabolism ; Interleukin-13 ; metabolism ; Interleukin-4 ; metabolism ; Interleukin-5 ; metabolism ; Male ; Nasal Polyps ; immunology ; metabolism ; Th2 Cells ; immunology ; Young Adult

Animals ; Cytokines ; metabolism ; Fatty Liver ; immunology ; metabolism ; Humans ; Immune Tolerance ; Killer Cells, Natural ; immunology ; Liver ; immunology ; Liver Diseases ; immunology ; metabolism ; Liver Failure ; immunology ; metabolism ; T-Lymphocytes ; immunology ; United States

Reactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and deveolpment of pancreatitis. A hallmark of the inflammatory response is the induction of cytokine gene expression, which may be regulated by oxidant-sensitive transcription factor, nuclear factor-kappaB (NF-KB). Present study aims to investigate whether neutrophils primed by 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA) affect the productions of H2O2 and lipid peroxide (LPO), NF-kappaB activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by N-acetylcysteine (NAC) and superoxide dismutase (SOD). ROS generation in neutrophils increased by PMA, which was inhibited by NAC and SOD. The productions of H2O2, LPO and TNF-alpha were increased with the amounts of PMA-primed neutrophils added to acinar cells while the productions of H2O2, LPO and cytokines increased with time. PMA-primed neutrophils resulted in the activation of two species of NF-kappaB dimers (a p50/p65 heterodimer and a p50 homodimer). Both NAC and SOD inhibited neutrophil-induced alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates NF-kappaB, resulting in upregulation of inflammatory cytokines in acinar cells. Antioxidants such as NAC might be clinically useful antiinflammatory agents by inhibiting oxidant-mediated activation of NF-KB and decreasing cytokine production.
Acute Disease ; Chronic Disease ; Cytokines/immunology* ; Human ; NF-kappa B/metabolism* ; Pancreas/metabolism* ; Pancreas/immunology* ; Pancreas/cytology ; Pancreatitis/metabolism ; Pancreatitis/immunology ; Support, U.S. Gov't, Non-P.H.S.