Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cadmium may exacerbate pulmonary infections. In a previous study, however, cadmium appeared to enhance mouse resistance to influenza pneumonia. We report herein on the influence of cadmium intoxication in mice on different factors of anti-influenza immunity, e.g., antibody response, local production of interferon, pulmonary cellular response, and the interaction between pulmonary alveolar macrophages and the influenza virus. Cadmium inhalation did not affect production of antibodies or interferon. The protective effect appeared to be related to an enhanced supply to phagocytic cells into the lung.
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PMID:Influence of inhaled cadmium on the immune response to influenza virus. 170 3

Nine consecutive patients with HCL seen over a period of five years were reviewed. Male: Female ratio was 8:1. Median age at diagnosis was 49 years. Weakness and fatigue (66%) were the commonest presenting symptoms and splenomegaly (66%) was the commonest physical findings. Varying degrees of pancytopenia was the consistent feature in majority of cases. Diagnosis was made on the basis of bone marrow biopsy and characteristic EM picture. Forty-four percent of cases developed serious infection during their clinical course. Gram negative bacilli and fungi were the most frequently isolated organisms. Major sites of infections were pneumonia and septicemia. Splenectomy was carried out in four cases. Rapid recovery of haematological parameters without any significant complication was observed in all these cases. Two patients were treated with alfa-interferon. In both the cases recovery of haematological parameters was slow compared to those under going splenectomy. One patient treated with alfa-interferon died due to infection related complications while the other went into remission.
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PMID:Hairy cell leukaemia. A review of nine cases. 178 82

A study of 30 patients suffering of acute pneumonia indicates that the development of acute pneumonia occurs against the background of disorders of the functional activity of monocytes with prevalent reduction of the functional activity of phagocytosis and inhibition of the unspecific cellular antiviral resistance. Leucocytic interferon sharply activates phagocytosis. The number of phagocytic cells and activity of phagocytosis reduced and the number of virus-involved immunocompetent cells increased under the effect of antibiotics.
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PMID:[Pharmacological action on antiviral resistance in patients with acute pneumonia]. 180 50

Symptomatic pulmonary toxoplasmosis is a relatively rare disease process, although the lung is frequently infected with the causative agent Toxoplasma gondii. Acute infection resulting in diffuse pneumonia is most likely in the immunosuppressed transplant recipient, and reinfection pneumonia occurs in this patient population as well as in patients with acquired immunodeficiency syndrome. The authors discuss the methods this protozoan uses to invade cells, to evade host defenses, and to cause tissue necrosis. The epidemiology of the disease relates directly to an inability to mount the effective cell-mediated immunity needed to keep the tissue cysts from undergoing effective replication into destructive tachyzoites. Alveolar macrophages and gamma interferon have been shown to be two important effector mechanisms in this control. Outcome is directly related to the ability to make an early diagnosis, which requires increased awareness of this disease in the patient populations at risk.
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PMID:Pulmonary toxoplasmosis. 188 67

To evaluate the significance of bronchoalveolar lavage fluid, levels of tumor necrosis factor-alpha (TNF), gamma-interferon, interleukin 2, and soluble IL-2 receptor in early detection of canine lung allograft rejection, bronchoalveolar lavages were performed serially in mongrel dogs before and after single lung transplantation. The dogs were divided into three groups. Group 1 (control group) consisted of one in which neither donor nor recipient dogs were treated with cyclosporine. In group 2 (CsA-pretreated group) only donors were treated with CsA orally at a single dose of 20 mg/kg/day for 3 days prior to single lung transplantation. In group 3 only recipients were treated with CsA orally at a single dose of 20 mg/kg/day for a short period of 9 days after single-lung transplantation. Marked elevation was found of TNF, IFN-gamma, IL-2, and IL-2R in BALF obtained from the grafted lungs in group 1 and group 2 dogs. The levels of these markers were significantly higher than those obtained from the normal, native lungs (P less than 0.05). Two of three recipients in group 2 had pneumonia in the native lungs on day 10 after single-lung transplantation. All markers except IFN-gamma in BALF obtained from the infected native lungs were also increased, but the titers were less than those obtained from the grafted lungs at the same time. There were significantly higher levels of TNF, IL-2, and IL-2R present in the BALF of grafted lungs of dogs in group 1 than group 2 (P less than 0.05). In group 3, BALF levels of these markers from the grafted lungs were not significantly different from those of the normal and native lungs during the period of CsA treatment after single-lung transplantation. On various days after discontinuation of CsA treatment, BALF levels of all markers began to rise. Abnormal levels of BALF markers obtained from the grafted lungs heralded the appearance of abnormalities detected by chest x-ray films. Our study suggests that serially measuring BALF levels of TNF, IFN-gamma, IL-2, and IL-2R may serve as a useful means in monitoring the immunologic status of canine lung allografts and in the early detection of lung allograft rejection. The role of BALF IFN-gamma in distinguishing lung allograft rejection from pulmonary infection needs further studies.
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PMID:Significance of biochemical markers in early detection of canine lung allograft rejection. 190 Sep 61

Immunohistochemical analysis was performed in a case of pulmonary cryptococcosis that showed granulomatous pneumonia. The patient had no immunologic defects or other diseases. To cryostat sections, the immunocytes in granulomatous lesion were examined by application of monoclonal antibodies for T-lymphocytes, B-lymphocyte, macrophage series cells, lymphokines containing gamma interferon (gamma IFN), interleukin 1 (IL-1) and interleukin 2 (IL-2), and interleukin 2 receptor (IL-2R). CD2+ cells, CD3+ cells and CD4+ cells were in and around the granulomas. On the other hand, CD8+ cells were around the granulomas. In granulomatous lesions, the CD4/CD8 ratio was 2.0. Some T-lymphocytes were considered as activated lymphocytes showing OKDR+, IL-2+, gamma IFN+ or IL-2R+. The lymphoid cells that aggregated near the granulomas were B-lymphocytes showing CD21+, CD24+, s-IgD+, s-IgM+, OKDR+. According to these results they were mature B lymphocytes. Alveolar macrophages (AMs) were CD11+, CD36+, IL-1+, OKDR+. Epithelioid cells were CD4+, CD11+, CD36+, OKDR+, IL-1+, IL-2R+. CD1+ cells showing dendritic forms were scattered in granulomas. They were recognized to be Langerhans giant cells. These results suggest that in pulmonary cryptococcosis the formation of epithelioid cell granulomas is mainly induced by CD4+ cells (helper/inducer T-lymphocytes). Additionally, Langerhans giant cells and mature B lymphocytes may be related to humoral immunity in pulmonary cryptococcosis.
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PMID:[Immunohistochemical analysis of granulomatous lung lesion in primary pulmonary cryptococcosis]. 190 96

From 1986 to 1989, 5 desert bighorn sheep (3 Ovis canadensis mexicana and 2 O c nelsoni), ranging in age from 2 to 3 years, were exposed to a flock of exotic wild and domestic sheep to potentially achieve naturally acquired pneumonia. Pasteurella multocida was isolated from nasal samples from 4 of 6 sheep randomly sampled from the flock. Bighorn sheep were exposed individually and each exposure period was a trial. Treatment before and after exposure varied and included combinations of alpha interferon, antibiotics, anti-inflammatory drugs, and vaccines. Treatments were chosen on the basis of recommendations of others for treating pneumonia in desert bighorn sheep as well as our own experience in sheep and cattle. Regardless of treatment used, bighorn sheep in trials 1 to 4 developed signs of pneumonia within 10 to 14 days of exposure. Bighorn sheep in trials 1 to 3 died within 11 to 17 days of initial exposure. In trial 4, the bighorn sheep was isolated from the carrier sheep for treatment of pneumonia on day 14 and died on day 30. Pasteurella multocida was isolated from lung tissue in 3 of the 4 bighorn sheep. On the basis of results of trials 1 to 4, a more in depth clinical study was conducted in trial 5. Nasal and blood specimens were collected prior to and during trial 5 for bacteriologic culturing and serologic testing for bovine viral diarrhea virus, infectious bovine rhinotracheitis, parainfluenza-3 virus, and respiratory syncytial virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of pneumonia in desert bighorn sheep after exposure to a flock of exotic wild and domestic sheep. 203 14

Pulmonary A2 strain respiratory syncytial virus infection of BALB/c laboratory mice persisted for up to 7 days after initial infection with peak virus titres being recovered on day 4. Virus antigen within the lungs was found to be restricted essentially to the alveolar regions. Similarly, pulmonary histopathological changes remained confined to the peri-alveolar regions being consistent with mild pneumonia. Infection was found to elicit a pulmonary major histocompatibility complex-restricted cytotoxic T lymphocyte (CTL) response which was first detectable 6 days after infection and optimal 7 to 9 days after infection. This local CTL response was preceded by a rapid transient virus-specific lymphocyte transformation response which was detectable only 3 days after intranasal infection. In addition, infection induced rapid interferon production within the lungs which was accompanied by an equally rapid rise in pulmonary natural killer (NK) cell cytotoxic activity. Enhanced NK cell cytotoxicity could be detected after only 1 day post-infection and continued to rise to maximum levels on day 3. This response like the acute CTL response was found to be restricted to the lower respiratory tract. IgG was the first class of virus-specific immunoglobulin to be detected in the lungs of infected animals after experimental infection. However, IgG was not detected until day 10 post-infection, 5 days after the initial decline of virus shedding. Virus-specific IgA although detectable did not appear in the lung until day 24.
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PMID:Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection. 219 71

A 59 years old woman, born in Fukuoka Prefecture, was admitted to our hospital in Aug, 1988 because of diarrhea, fever and skin eruption. Physical examination revealed systemic lymphadenopathy and hepatosplenomegaly. The white blood cell count was 11,200/microliters with 28% atypical lymphocytes with convoluted nuclei. Mild anemia, thrombocytopenia and hypercalcemia were also observed. Antibody against the adult T-cell leukemia (ATL) associated antigen in serum was positive. OKT 4/8 ratio was high. A diagnosis of ATL was made. Because of the complications of pneumonia and herpes simplex, systemic chemotherapy was not given, and interferon (IFN)-alpha-2b was intramuscularly injected daily from Oct, 1988, resulting in the disappearance of atypical lymphocytes and improvement of skin lesions. The effect of IFN therapy lasted for three months, followed by increase of atypical lymphocytes. Although the patient became refractory to systemic IFN therapy, local injection of IFN into a buccal tumor infiltrated with atypical lymphocytes resulted in its regression of size. In spite of continued administration of IFN, the patient died of pneumonia in Jan, 1989.
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PMID:[Successful treatment of adult T-cell leukemia with interferon-alpha-2b by systemic and local administration]. 224 35

Table III summarizes clinical applications of antiviral agents in respiratory viral infections. (table: see text) For influenza A virus infections, both oral amantadine and rimantadine are effective when used for seasonal prophylaxis and for prophylaxis in institutional populations. Both of these drugs, as well as aerosolized ribavirin, have antiviral and therapeutic effects in uncomplicated influenza. It remains to be determined whether any of these modalities or possibly their combined use [44] will be useful in treating severe influenza hospitalized patients or whether they can prevent the development of complications in high risk patients. Unfortunately, there is no parenteral formulation of amantadine or rimantadine for use in critically ill patients. Aerosolized ribavirin has also been shown to have modest therapeutic effects in influenza B virus infection. However, a major need exists for an antiviral which is active against influenza B virus and which can be used on an outpatient basis. Controlled clinical trials have shown that aerosolized ribavirin therapy improves arterial oxygenation and modifies the severity of respiratory syncytial virus bronchiolitis and pneumonia [3,5]. Its role in treating life-threatening disease or in modifying the long-term sequelae of RSV infections are unknown at the present time. Again, a specific antiviral agent is needed for outpatient use in preventing or treating RSV infections. Finally, after over a decade of work since the original observation that intranasal interferon could prevent experimental rhinovirus infection [11], recent studies have established that intranasal rIFN-a2 is effective in the postexposure prophylaxis of rhinovirus colds in families [42]. This strategy needs to be studied with regard to the prevention of infection and its complications in high risk patients and it remains to be determined whether intranasal interferon will have therapeutic activity in established colds.
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PMID:Clinical applications of antiviral agents for chemophrophylaxis and therapy of respiratory viral infections. 241 51


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