Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the effect of heat stress on histopathology of acute lung injury (ALI) caused by administration of lipopolysaccharide (LPS), and to determine the roles of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, interferon (IFN)-gamma, IL-10 and surfactants in heat-induced tolerance to ALI, we administered either saline or LPS (3 mg/kg of body weight) intravenously to male Sprague-Dawley rats without and with heat pretreatment. Five hours after LPS or saline treatment (23 h after heat-pretreatment), samples were obtained. We found that the histopathologic features of LPS-induced ALI were attenuated by heat-pretreatment. Heat-pretreatment did not decrease the elevated plasma or BAL fluid levels of TNF-alpha, IL-1beta, and IFN-gamma by LPS. The plasma level of IL-10 in LPS-treated rats with heat-pretreatment, however, was increased compared to that of LPS-treated rats without heat-pretreatment (P = 0.001). There were no differences in the BAL fluid concentrations of light or heavy density pulmonary surfactant phospholipids depending on heat-pretreatment in LPS-treated rats. These observations suggest that IL-10 might play a role in decreasing LPS-induced acute lung injury after heat-pretreatment.
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PMID:Effects of heat pretreatment on histopathology, cytokine production, and surfactant in endotoxin-induced acute lung injury. 1140 10

It is widely known that fungal airways infections may deteriorate the course of bronchial asthma. The mechanism of the phenomenon is still unclear. The aim of our study was to assess the effect of fungal infections on the secretion of selected cytokines by bronchoalveolar leukocytes. Five patients (group FA) with bronchial asthma and Candida albicans or Aspergillus fumigatus airways infections (confirmed by bronchoscopy and culture) were included in the study. All of them were on the chronic treatment with corticosteroids (10-20 mg of prednisone per day) and underwent several courses of therapy with antibiotics. The control groups comprised 5 previously untreated asthmatics without bronchial colonization with fungi (group A) as well as 5 healthy volunteers (group H). Leukocytes were isolated from bronchoalveolar lavage fluid (BALF) and cultured in the presence or absence of cytokine inducers such as phytohemagglutin L (PHA), lipo-polysaccharide (LPS) from E. coli. The activity of TNF-alpha, IL-6 and IFN-gamma were measured in the BAL cell culture supernatants by using specific bioassays. In comparison with healthy controls the spontaneous or induced secretion of cytokines were significantly augmented in patients from group A. In contrast the asthmatics who represented group FA demonstrated normal levels of spontaneous cytokine secretion. However, the tendency to increase LPS and PHA-induced production was observed in BAL leukocytes from the patients. The above results support the view that beneficial effect of corticosteroid treatment in bronchial asthma may act, at least in part, by inhibition of the high spontaneous secretion of proinflammatory cytokines. Nevertheless, fungal airways infections may lead to increase of LPS- or PHA-induced production of TNF-alpha, IL-6 or IFN-gamma (despite prednisone therapy) by prestimulation of the BAL cells with fungi.
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PMID:TNF-alpha, IL-6 and IFN-gamma secreted by bronchoalveolar leukocytes isolated from patients with bronchial asthma, complicated by fungal airways infections. 1171 87

We have compared the role of IgM antibodies with the role of B cells in control of primary influenza virus infection. Mice deficient in IgM (IgM(-/-)), but capable of producing other Igisotypes, exhibited increased pulmonary virus titers compared to wild-type mice. However, IgM(-/-) mice were less susceptible compared to B cell-deficient micro MT) mice. CD4(+) T cells from spleen and lung draining lymph nodes of infected micro MT mice showed reduced proliferation upon virus re-stimulation in vitro. Furthermore, numbers of IFN-gamma-producing CD4(+) effector T cells were reduced in the alveolar lavage (BAL) of micro MT mice but not IgM(-/-) mice. In contrast, total number of virus-specific CTL was almost comparable in BAL of micro MT and wild-type mice. Pulmonary recruitment of inflammatory macrophages and neutrophils occurred normally in both micro MT and IgM(-/-) mice. Interestingly, virus-specific IgG2a and IgG2b antibody responses were affected locally in the BAL and in the serum of IgM(-/-) mice, while IgG1 responses remained largely normal. Taken together, our data suggest a role for B cells to promote effector T cell responses and a role of both IgM and IgG antibodies in the defense against acute influenza virus infection.
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PMID:Role of IgM antibodies versus B cells in influenza virus-specific immunity. 1220 35

The guinea pig has been utilized as a model for studying infectious diseases because its reactions closely resemble those of humans biologically and immunologically. However, the cytokine responses in this animal remain to be studied. Initially, we established a quantitative assay using a real-time reverse transcription-PCR (RT-PCR) to measure guinea pig gamma interferon (IFN-gamma), interleukin-12 (IL-12), IL-10, and transforming growth factor beta (TGF-beta) mRNA. By preparing primer-fluorogenic probe sets for these cytokines and standard RNA templates corresponding to the target sequence of each cytokine, we obtained linear standard curves essential for quantitative determination. In guinea pigs immunized by intradermal (i.d.) vaccination with the Tokyo strain of Mycobacterium bovis BCG (0.1 mg) or else hyperimmunized with the same vaccine (10 mg) given intravenously (i.v.), peripheral blood mononuclear cells (PBMCs) at 4 weeks showed an increase in IFN-gamma mRNA expression in the latter but not the former animals. However, at week 10, IFN-gamma mRNA expression was markedly elevated in PBMCs, spleen cells, and cells in bronchoalveolar lavage fluid in both the i.d.- and the i.v.-immunized animals, the level of expression being 10 times higher in the latter. In contrast, the expression levels of IL-12 mRNA in PBMCs, spleen cells, and BAL cells were not enhanced in either group at 10 weeks postimmunization. The expression of IL-10 and TGF-beta increased slightly only in PBMCs. Regardless of differences in the levels of cytokine responses, the magnitudes of the purified protein derivative of tuberculin-specific delayed-type hypersensitivity (DTH) skin reactions for the two groups did not differ significantly at 8 weeks postvaccination. In this study, we quantitatively measured IL-10, IL-12, TGF-beta, and IFN-gamma mRNA in BCG-immunized guinea pigs and showed that the level of IFN-gamma mRNA expression does not necessarily reflect the magnitude of the DTH response, suggesting that there may be an intricate relationship between protective immunity, the level of IFN-gamma, and the DTH response. Thus, our quantitative assay would be of use for the development of vaccines using guinea pig models.
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PMID:Dynamics of gamma interferon, interleukin-12 (IL-12), IL-10, and transforming growth factor beta mRNA expression in primary Mycobacterium bovis BCG infection in guinea pigs measured by a real-time fluorogenic reverse transcription-PCR assay. 1243 33

The pulmonary granulomatous diseases may be staged using clinical examination, pulmonary function tests, ⁶⁷Ga scans, chest X-rays, BAL and serum ACE levels; furthermore, these disorders are clearly associated to changes in lymphocyte subpopulations, CD4+/CD8+ ratio and surface receptors; in particular, T cell activation characterizes early alveolitis phase, while activated macrophages and related cytokines prevail in granulomata and fibrosis development. In this study, we dosed the serum and blood concentrations of IL-6 (a well-known pro-inflammatory cytokine), sIL-2R (marker of T-cell activation), TNF-alpha and IFN-gamma (associated with the granuloma development), in patients affected by active or inactive sarcoidosis, primary tuberculosis, idiopathic pulmonary fibrosis and healthy control subjects, using the ELISA method. Cytokines assay showed significant changes only in subjects with primary tuberculosis and active sarcoidosis; infact, primary tuberculosis was characterized by high values of IL-6 and IFN-gamma both in peripheral blood and in BAL, with high values of sIL-2R in BAL; patients with active sarcoidosis showed high levels of IFN-gamma and TNF-alpha both in BAL and in peripheral blood, associated to an increase of serum sIL-2R levels. Our data confirm that the compared assay of these cytokines in peripheral blood and BAL specimens, may be useful to diagnose and to assess the disease activity in pulmonary granulomatous diseases; in particular, the levels of sIL-2R are a marker of the alveolitis phase, while TNF-alpha and IL-6 levels discriminate patients with sarcoidosis or tuberculosis granulomata, respectively.
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PMID:Cytokines assay in peripheral blood and bronchoalveolar lavage in the diagnosis and staging of pulmonary granulomatous diseases. 1265 92

Heaves is a common condition of horses of cold climate that is characterized by small airway inflammation and obstruction following exposure of susceptible horses to moldy hay and straw. It has been shown that helper T lymphocytes (Th) orchestrate the inflammatory response in asthma and in various animal models of allergic lung diseases by the release of Th2-type cytokines. Results of previous studies indicate that a predominant expression of Th2-type response by airway cells may also be present in heaves. To evaluate the temporal mRNA expression of Th1 (IFN-gamma) and Th2 (IL-4, IL-5) type cytokines in heaves and their relationship to clinical disease, we studied the pulmonary mechanics and cytokine mRNA expression (IL-4, IL-5 and IFN-gamma) in bronchoalveolar lavage lymphocytes of horses with heaves (n=6) and control (n=6) before and after 24h and 9 days of continuous natural inhalation challenge. Starting 24h after challenge horses with heaves, but not control horses, had a significant increase in pulmonary elastance and the number of lymphocytes expressing mRNA for IL-4 and IL-5. These changes were further increased at 9 days, at which time the number of cells positive for IFN-gamma mRNA was decreased. In this study we have shown that BAL lymphocytes of horses with heaves during clinical exacerbation have a predominant Th2-type cytokine response and that this response coincides in time with the presence of airway obstruction.
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PMID:IL-4, IL-5 and IFN-gamma mRNA expression in pulmonary lymphocytes in equine heaves. 1470 May 40

Idiopathic Pulmonary Fibrosis/ Usual Interstitial Pneumonia (IPF/UIP) represents the most important interstitial pneumonia. ATh2 cytokine pathway predominance, favoring collagen deposition, associated to a deficit in (IFN- gamma) network, seems to be involved in the pathogenesis of this disease. Nonetheless, few data are available about the potentially involved cells. Natural killer cells (NK), are one of the most important subsets implicated in the IFN-gamma network. The aim of this study was to assess NK cells, both in BAL and peripheral blood of 11 patients suffering from IPF (group A) with respect to 11 patients with other interstitial pneumonia (Group B). Our results did not show any statistically significant difference in NK percentage in BAL between group A and B. On the contrary, patients with IPF showed a higher percentage of NK cells (t = 2.41; p < 0.05) and absolute number of cells (t = 2.32; p < 0.05) in peripheral blood, as well as a strong positive correlation between circulating and BAL NK cells (r = 0.69; p < 0.05). This finding shows, for the first time, a relationship between peripheral and lung resident cell environments in humans suggesting a possible systemic involvement in the natural history of IPF.
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PMID:Natural killer cells in Bal and peripheral blood of patients with idiopathic pulmonary fibrosis (IPF). 1616 35

RANTES (CC chemokine ligand 5) contributes to airway inflammation through accumulation of eosinophils, but the exact role of RANTES (CCL5) is not defined. C57BL/6 mice, sensitized by injection of ovalbumin (OVA) on Days 1 and 14, were challenged with OVA on Days 28, 29, and 30 (3 challenges, short-term-challenge model) or on Days 28, 29, 30, 36, 40, 44, and 48 (7 challenges, repeated-challenge model) and evaluated 48 h later. Anti-mouse RANTES was given intravenously, and recombinant mouse RANTES or PBS was given intratracheally. These reagents were given on Days 28, 29, and 30 in the short-term-challenge study and on Days 44 and 48 in the repeated-challenge study. After short-term challenge, there were no effects after administration of anti-RANTES or RANTES. In the repeated-challenge study, although control mice showed a decrease in airway hyperresponsiveness, administration of anti-RANTES sustained and enhanced airway hyperresponsiveness and increased goblet cell numbers. In contrast, administration of RANTES normalized airway function but reduced goblet cell numbers. IL-12 and IFN-gamma levels in BAL decreased in the anti-RANTES group and increased in the RANTES group. IFN-gamma-producing CD4 T cells in lung, and IFN-gamma production from lung T cells in response to OVA in the anti-RANTES group, were significantly decreased but were increased in the RANTES group. Anti-IFN-gamma, administered with RANTES, decreased the effects of RANTES on AHR after repeated challenge. These data indicate that RANTES plays a role in the regulation of airway function after repeated allergen challenge, in part through modulation of levels of IFN-gamma and IL-12.
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PMID:RANTES (CCL5) regulates airway responsiveness after repeated allergen challenge. 1684 5

Respiratory Mycoplasma pneumoniae (Mp) infection is involved in several acute and chronic lung diseases including community-acquired pneumonia, asthma and chronic obstructive pulmonary disease. In the chronic disease process, recurrent respiratory bacterial infections could occur, which may result in varying degrees of symptoms and lung inflammation among patients. However, the lung immunologic differences of host responses to repeated bacterial (i.e., Mp) infections remain to be determined. In the present study, we examined cellular and humoral responses to multiple (up to 3) Mp infections in two genetically different strains of mice (BALB/c and C57BL/6). Mice were intranasally inoculated with one Mp infection, two or three Mp infections (4 weeks apart), and sacrificed on days 3, 7 and 14 after the last Mp infection. Overall, compared to C57BL/6 mice, BALB/c mice demonstrated a significantly higher degree of lung tissue inflammatory cell infiltrate, BAL cellularity, and release of pro-inflammatory cytokines (TNF-alpha, keratinocyte-derived chemokine (KC, a mouse homolog of human chemokine Gro-alpha [CXCL1], and IFN-gamma). In addition, BALB/c mice presented higher levels of serum Mp-specific IgG and IgM, but not IgA. Consistently with lung and serum data, Mp load in BAL and lung specimens was significantly higher in BALB/c mice than C57BL/6 mice. Moreover, repeated Mp infections in BALB/c, but not C57BL/6 mice, produced a greater inflammatory response than did a single Mp infection. Our results suggest that hosts with different genetic background may have different susceptibility to repeated respiratory Mp infections along with inflammatory responses.
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PMID:Repeated respiratory Mycoplasma pneumoniae infections in mice: effect of host genetic background. 1671 27

Integracions among T cells, B cells and macrophages is central to the immune response. These cells produce a number of biologically active proteins, which form complex network of cell-to-cell interaction, and regulate proliferation and function of the immune systems. Cytokines act on variety of cells type in a non-antigen specific manner. Only helper cells receive antigen specific signal and convert them via lymphokines secretion into antigen-nonspecific mediators of immune response. The followings cytokines have been found in asthamic airways: IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, TNF-alfa, GM-CSH. CD+4 cells are major source of cytokines in astmatic airway. It has been identified that two subsets of helper cells (TH-1 and TH-2) exist, which secret different cytokines profils. Both produce IL-1, IL-3, GM-CSF and TNF-alfa. TH-1 produce IL-2, IFN-gamma and TNF-beta (LT). TH-2 cells produce IL-4, IL-5 and IL-10. IL-4 produced by activited TH-2 subset, mast cells, and basophils is enhanced in asthma and responsible for IgE synthesis and expresion of IgE Fc-R-II. TH-1 specific IFN-gamma inhibits IL-4 induced IgE synthesis whereas TH-2 specific IL-10 supresses IFN-gamma secretion. IL-3, IL-4 and IL-5 stimulate the growth of mucosal mast cells and eosinophils. The presence of activated T cells and eosinophils in BAL-fluid as well as increased amount of IFN-gamma and slL-2R in circulation correlate with severity of disease. Interplay between T cells and inflammatory cells through the cytokines is crucial in regulating of inflammatory processes in allergic asthma.
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PMID:[Cytokines in bronchial asthma]. 1817 9


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