UMLS:C0032285 - FACTA Search

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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the pathogenesis of pulmonary Cryptococcus neoformans infection and passive Ab efficacy in mice deficient in inducible NO synthase (NOS2(-/-)) and the parental strain. Parental mice lived significantly longer than NOS2(-/-) mice after intratracheal infection, despite having a higher lung fungal burden. Administration of Ab reduced lung CFU in both NOS2(-/-) and parental mice, but prolonged survival and increased the inflammatory response only in parental mice. Ab administration was associated with increased serum nitrite and reduced polysaccharide levels in parental mice. Eosinophils were present in greater numbers in the lung of infected NOS2(-/-) mice than parental mice, irrespective of Ab administration. C. neoformans infection in NOS2(-/-) mice resulted in significantly higher levels of IFN-gamma, monocyte chemoattractant protein-1, and macrophage-inflammatory protein-1alpha than parental mice. Ab administration had different effects on infected NOS2(-/-) and parental mice with respect to IFN-gamma, monocoyte chemoattractant protein-1, and macrophage-inflammatory protein-1alpha levels. Ab administration increased lung levels of IFN-gamma in parental mice and reduced levels in NOS2(-/-) mice. The results indicate that NO is involved in the regulation of cytokine expression in response to cryptococcal pneumonia and is necessary for Ab efficacy against C. neoformans in mice. Our findings indicate a complex relationship between Ab efficacy against C. neoformans and cytokine expression, underscoring the interdependency of cellular and humoral defense mechanisms.
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PMID:Antibody efficacy in murine pulmonary Cryptococcus neoformans infection: a role for nitric oxide. 1190

Mycoplasma infection is a leading cause of pneumonia worldwide and can lead to other respiratory complications. A component of mycoplasma respiratory diseases is immunopathologic, suggesting that lymphocyte activation is a key event in the progression of these chronic inflammatory diseases. The present study delineates the changes in T cell populations and their activation after mycoplasma infection and determines their association with the pathogenesis of murine Mycoplasma respiratory disease, due to Mycoplasma pulmonis infection. Increases in T cell population numbers in lungs and lower respiratory lymph nodes were associated with the development of mycoplasma respiratory disease. Although both pulmonary Th and CD8(+) T cells increased after mycoplasma infection, there was a preferential expansion of Th cells. Mycoplasma-specific Th2 responses were dominant in lower respiratory lymph nodes, while Th1 responses predominated in spleen. However, both mycoplasma-specific Th1 and Th2 cytokine (IL-4 and IFN-gamma) responses were present in the lungs, with Th1 cell activation as a major component of the pulmonary Th cell response. Although a smaller component of the T cell response, mycoplasma-specific CD8(+) T cells were also a significant component of pulmonary lymphoid responses. In vivo depletion of CD8(+) T cells resulted in dramatically more severe pulmonary disease, while depletion of CD4(+) T cells reduced its severity, but there was no change in mycoplasma numbers in lungs after cell depletion. Thus, mycoplasma-specific Th1 and CD8(+) T cell activation in the lung plays a critical regulatory role in development of immunopathologic reactions in Mycoplasma respiratory disease.
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PMID:Depletion of CD8+ T cells exacerbates CD4+ Th cell-associated inflammatory lesions during murine mycoplasma respiratory disease. 1190 10

The effect of gamma interferon (IFN-gamma) on apoptosis due to infection by Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis) was studied in epithelial cells in culture and in the genital tracts of mice. IFN-gamma concentrations that induce the formation of aberrant, persistent chlamydiae inhibit apoptosis due to C. muridarum infection. In cells treated with an IFN-gamma concentration that leads to the development of a heterogenous population of normal and aberrant Chlamydia vacuoles, apoptosis was inhibited preferentially in cells that contained the aberrant vacuoles. The inhibitory effect of IFN-gamma appears to be due in part to expression of host cell indoleamine 2,3-dioxygenase activity, since inhibition of apoptosis could be partially reversed through coincubation with exogenous tryptophan. Apoptotic cells were observed in the genital tracts of wild-type mice infected with C. muridarum, and a significantly larger number of apoptotic cells was detected in infected IFN-gamma-deficient mice. These results suggest that IFN-gamma may contribute to pathogenesis of persistent Chlamydia infections in vivo by preventing apoptosis of infected cells.
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PMID:Inhibition of apoptosis by gamma interferon in cells and mice infected with Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis). 1195 96

Chlamydia are intracellular bacteria which infect many vertebrates, including humans. They cause a myriad of severe diseases, ranging from asymptomatic infection to pneumonia, blindness or infertility. IFN-gamma plays an important role in defense against acute infection and in the establishment of persistence. Chlamydia have evolved mechanisms to escape IFN-gamma functions. IFN-gamma-mediated effector mechanisms may involve effects on the metabolism of tryptophan or iron, on the inducible NO synthase (iNOS), on the secretion of chemokines and adhesion molecules or on the regulation of T-cell activities. IFN-gamma is secreted by the innate and the adaptive arms of the immune system. Within the former, Chlamydia-infected macrophages express IFN-gamma that in turn mediates resistance to infection. IFN-alpha/beta are pivotal for both IFN-gamma- and iNOS-mediated resistance to chlamydial infection in macrophages.
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PMID:The role of IFN-gamma in the outcome of chlamydial infection. 1208 78

Sputum and serum from patients with active pulmonary tuberculosis (TB), healthy purified protein derivative-positive adults, and patients with bacterial pneumonia were collected to simultaneously assess local immunity in the lungs and peripheral blood. To determine whether cytokine profiles in sputum from TB patients and control subjects were a reflection of its cellular composition, cytospin slides were prepared in parallel and assessed for the presence of relative proportions of epithelial cells, neutrophils, macrophages, and T cells. Gamma interferon (IFN-gamma) in sputum from TB patients was markedly elevated over levels for both control groups. With anti-TB therapy, IFN-gamma levels in sputum from TB patients decreased rapidly and by week 4 of treatment were comparable to those in sputum from controls. Further, IFN-gamma levels in sputum closely followed mycobacterial clearance. Although detected at fourfold-lower levels, IFN-gamma immunoreactivities in serum followed kinetics in sputum. TNF-alpha, interleukin 8 (IL-8) and IL-6 also were readily detected in sputum from TB patients at baseline and responded to anti-TB therapy. In contrast to IFN-gamma, however, TNF-alpha and IL-8 levels also were elevated in sputum from pneumonia controls. These data indicate that sputum cytokines correlate with disease activity during active TB of the lung and may serve as potential early markers for sputum conversion and response to anti-TB therapy.
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PMID:Sputum cytokine levels in patients with pulmonary tuberculosis as early markers of mycobacterial clearance. 1209 79

Although a clear relationship between alphabeta T-cell receptor-positive (alphabeta-TCR(+)) CD4(+) T cells and susceptibility to Pneumocystis carinii infection exists, the role of other T-cell subsets is less clearly defined. Previous studies have shown that gammadelta-TCR(+) T cells infiltrate into the lung during P. carinii pneumonia. Therefore, the present study examined the role of gammadelta-TCR(+) T cells in host defense against P. carinii pneumonia. C57BL/6 (control) and B6.129P2-Tcrd(tm1Mom) (gammadelta-TCR(+) T-cell-deficient) mice were inoculated intratracheally with P. carinii. At specific time points, mice were sacrificed and analyzed for P. carinii burden, T-cell subsets, and cytokine levels in lung tissue. Analysis of P. carinii burden showed a more rapid and complete resolution of infection in gammadelta-TCR(+) T-cell-deficient mice than in C57BL/6 controls. This augmented resolution was associated with elevated gamma interferon (IFN-gamma) levels in bronchoalveolar lavage fluid predominantly produced by CD8(+) T cells, as well as an increased recruitment of CD8(+) T cells in general. In separate experiments, neutralization of IFN-gamma or depletion of CD8(+) T cells early during infection abolished the augmented resolution previously observed in gammadelta-TCR(+) T-cell-deficient mice. These results show that the presence of gammadelta-TCR(+) T cells modulates host susceptibility to P. carinii pneumonia through interactions with pulmonary CD8(+) T cells and tissue production of IFN-gamma.
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PMID:Increased host resistance against Pneumocystis carinii pneumonia in gammadelta T-cell-deficient mice: protective role of gamma interferon and CD8(+) T cells. 1218 72

Host responses to Pneumocystis carinii infection mediate impairment of pulmonary function and contribute to the pathogenesis of pneumonia. IL-10 is known to inhibit inflammation and reduce the severity of pathology caused by a number of infectious organisms. In the present studies, IL-10-deficient (IL-10 knockout (KO)) mice were infected with P. carinii to determine whether the severity of pathogenesis and the efficiency of clearance of the organisms could be altered in the absence of IL-10. The clearance kinetics of P. carinii from IL-10 KO mice was significantly enhanced compared with that of wild-type (WT) mice. This corresponded to a more intense CD4(+) and CD8(+) T cell response as well as an earlier neutrophil response in the lungs of IL-10 KO mice. Furthermore, IL-12, IL-18, and IFN-gamma were found in the bronchoalveolar lavage fluids at earlier time points in IL-10 KO mice suggesting that alveolar macrophages were activated earlier than in WT mice. However, when CD4(+) cells were depleted from P. carinii-infected IL-10 KO mice, the ability to enhance clearance was lost. Furthermore, CD4-depleted IL-10 KO mice had significantly more lung injury than CD4-depleted WT mice even though the intensity of the inflammatory responses was similar. This was characterized by increased vascular leakage, decreased oxygenation, and decreased arterial pH. These data indicate that IL-10 down-regulates the immune response to P. carinii in WT mice; however, in the absence of CD4(+) T cells, IL-10 plays a critical role in controlling lung damage independent of modulating the inflammatory response.
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PMID:IL-10 modulates host responses and lung damage induced by Pneumocystis carinii infection. 1251 67

Group B streptococci (GBS) are an important cause of neonatal sepsis, pneumonia and meningitis. In some newborns, GBS sepsis may have a severe course, including septic shock with high mortality rate, whereas other newborns are colonized with GBS on their surfaces without any clinical signs of bacterial infections. Interferon (IFN)-gamma is produced in neonatal GBS sepsis, and transforming growth factor (TGF)-beta is also found in the uterus. The involvement of IFN-gamma and TGF-beta in the earliest phase of infection might be a determinant of susceptibility and/or progression of infection in vivo. The aim of this study was to assess the effect of IFN-gamma and TGF-beta on adherence and intracellular viability in ECV304 cells of GBS serotype III isolated from cerebrospinal fluid (CSF) and vagina (strains 90356 and 80340, respectively). Interaction of GBS-ECV304 cells showed that the CSF isolate exhibited a more efficient adherence mechanism than the vagina isolate (P<0.001). Intracellular viability was observed for the CSF 90356 isolate within 2 h incubation. Results suggest the expression of additional bacterial virulence factors that favor some GBS type III strains to cause invasive disease. Detection of genotypic virulence marker (162-kb) in the CSF 90356 isolate by PFGE emphasizes the high risk of invasive infection by some GBS-III strains. Treatment of ECV304 cells with IFN-gamma and/or TGF-beta increased adherence of both GBS strains (P<0.001). Intracellular survival of the CSF 90356 isolate was observed after 24 h incubation following treatment of ECV304 cells with IFN-gamma and TGF-beta. Our data suggest that both IFN-gamma and TGF-beta may favor virulence of GBS strains. Variation of IFN-gamma and TGF-beta producing capacity of host cells of different individuals may influence development of invasive disease by GBS-III.
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PMID:The effects of interferon-gamma and transforming growth factor-beta on adherence and survival of group B Streptococcus type III strains in ECV304 cells. 1257 48

Illness severity and frequency of complications in infants with respiratory syncytial virus (RSV) infection may be influenced by the local elaboration of cytokines. Cytokine gene polymorphisms moderate severity of illness in various inflammatory and infectious diseases. We performed cytokine genotyping on 77 infants hospitalized with confirmed RSV infection to determine whether specific cytokine gene polymorphisms are associated with illness severity or complications. DNA was extracted from buccal brushings and assayed for tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-6 and IL-10, and transforming growth factor (TGF)-beta1 genotypes using polymerase chain reaction-sequence-specific primer technology. Clinical outcomes consisted of severity scores of lower respiratory illness, blood oxygen saturation, lengths of oxygen supplementation, and intensive care unit (ICU) and hospital stays, and the presence or absence of pneumonia and otitis media. IFN-gamma genotype was related to severity of lower respiratory illness, duration of ICU stay, and frequency of otitis media. Additionally, IL-6 genotype was related to the length of oxygen (O(2)) supplementation and hospital stay, IL-10 genotype to the frequency of pneumonia, and TGF-beta1 genotype to O(2) saturations at presentation. There were no associations between TNF-alpha genotype and any of the outcome parameters. These results demonstrate that certain cytokine gene polymorphisms contribute to illness severity and complications during RSV infection in infants. If future prospective studies confirm these observations, cytokine genotyping may be a useful tool for identifying "at risk" infants who may benefit from the selective use of preventive or early intervention treatments for RSV.
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PMID:Cytokine gene polymorphisms moderate illness severity in infants with respiratory syncytial virus infection. 1259 Sep 78

Rhodococcus equi is a gram-positive bacterium that infects alveolar macrophages and causes rhodococcal pneumonia in horses and humans. The virulence plasmid of R. equi appears to be required for both pathogenicity in the horse and the induction of protective immunity. An understanding of the mechanisms by which virulent R. equi circumvents protective host responses and by which bacteria are ultimately cleared is important for development of an effective vaccine. Six adult horses were challenged with either virulent R. equi or an avirulent, plasmid-cured derivative. By using a flow cytometric method for intracytoplasmic detection of gamma interferon (IFN-gamma) in equine bronchoalveolar lavage fluid (BALF) cells, clearance of the virulent strain was shown to be associated with increased numbers of pulmonary CD4(+) and CD8(+) T lymphocytes producing IFN-gamma. There was no change in IFN-gamma-positive cells in peripheral blood, suggesting that a type 1 recall response at the site of challenge was protective. The plasmid-cured strain of R. equi was cleared in horses without a significant increase in IFN-gamma-producing T lymphocytes in BALF. In contrast to these data, a previous report in foals suggested an immunomodulating role for R. equi virulence plasmid-encoded products in downregulating IFN-gamma expression by equine CD4(+) T lymphocytes. Intracytoplasmic detection of IFN-gamma provides a method to better determine whether modulation of macrophage-activating cytokines by virulent strains occurs uniquely in neonates and contributes to their susceptibility to rhodococcal pneumonia.
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PMID:Clearance of virulent but not avirulent Rhodococcus equi from the lungs of adult horses is associated with intracytoplasmic gamma interferon production by CD4+ and CD8+ T lymphocytes. 1262 44

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