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)

The prevalence of gamma delta T cells in bronchoalveolar lavage (BAL) populations recovered from the respiratory tract of young, adult C57BL/6J mice infected intranasally (i.n.) with Sendai virus has been assessed by FACS-phenotyping, and by probing cytocentrifuge preparations for expression of TCR gamma mRNA. The surface gamma delta TCR+ set comprised from 5 to 20% of the inflammatory lymphocytes in sequential samples taken throughout the course of this nonfatal viral pneumonia. The BAL population also contained numerous cells expressing mRNA for C gamma 1/2 and C gamma 4; the C-regions were utilized for productive TCR gene rearrangement. Sorting the lymphocytes from the BAL established that greater than 90% of both the TCR gamma and TCR beta mRNA partitioned to cells with the appropriate surface TCR phenotype, while less than 7% of the TCR mRNA+ cells in the total inflammatory exudate were phagocytes that engulfed latex particles. Both the frequency and the total numbers of the gamma delta TCR+ and TCR gamma mRNA+ cells were increased in mice depleted of alpha beta T cells by in vivo treatment with mAbs to CD4 and CD8, indicating that the CD4+ and CD8+ alpha beta and CD4-8- gamma delta T cell subsets may operate independently in this virus disease. The C gamma 1/2 mRNA phenotype predominated throughout the course of the active infection, with a transition to maximal prevalence of the C gamma 4 mRNA+ set occurring very late (Day 20) in the resolving inflammatory process. Large numbers of macrophages expressing mRNA (greater than 50%) for a mammalian 65-kDa heat shock protein (hsp65), a possible target for some of the gamma delta T cells, were present early (Days 5-7) and remained at lower levels (less than 20%) thereafter. These hsp65 mRNA+ macrophages were much less apparent in BAL populations from mice depleted concurrently of the CD4+ and CD8+ T cell subsets, indicating that exposure to Sendai virus alone is not the major factor inducing the transcription of this endogenous gene. These experiments thus establish that gamma delta T cells are a minority of the infiltrating lymphocytes in Sendai virus pneumonia and provide new insights into the spectrum of hsp65 mRNA and TCR gamma mRNA expression during an inflammatory process.
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PMID:Extent of gamma delta T cell involvement in the pneumonia caused by Sendai virus. 132 Apr 65

To determine the role that the host response to the chlamydial 60 kDa heat shock protein (hsp) plays in the pathogenesis of infertility, C3H/HeN (H-2k) and C57BL/6 (H-2b) mice were inoculated in the left ovarian bursa with 1 x 10(5) inclusion forming units of the Chlamydia trachomatis mouse pneumonitis (MoPn) biovar, and in the right ovarian bursa with mock-infected HeLa-229 cell extracts. Control mice were inoculated with mock-infected HeLa-229 cell extracts. These two strains of mice were chosen because the C3H mice mount a strong immune response to the 60 kDa hsp, whereas the C57BL/6 mice respond only weakly. Vaginal cultures obtained after inoculation were positive for 4 weeks in both strains of mice. Histological sections showed a marked acute inflammatory infiltrate that permeated all the layers of the oviduct and lasted for approximately 2 weeks in both strains. By the third week, mononuclear inflammatory cells were also observed and from 4 weeks after inoculation, hydrosalpinx formation was observed, particularly in the C3H mice. An inclusion immunofluorescence assay detected antibodies specific for chlamydia in the serum and the vaginal washes of the C3H and C57BL/6 mice. Western blot analysis of the serum samples showed an immune response to lipopolysaccharide, and the 30, 40 (major outer membrane protein) and 60 kDa cysteine-rich protein in both strains of mice. In addition, in the C3H mice a strong immune reaction was mounted against a 50 kDa component and the 60 kDa hsp. Six weeks after inoculation, the female mice were mated with male mice of proven fertility and the outcome of the pregnancies evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of infertility by the Chlamydia trachomatis mouse pneumonitis biovar in strains of mice that differ in their response to the 60 kDa heat shock protein. 793 61

Female BALB/c mice were immunized intranasally with the mouse pneumonitis biovar of Chlamydia trachomatis and subsequently challenged in the ovarian bursa (C. trachomatis immunized, C. trachomatis challenged). Two groups of mice served as controls. One group was sham immunized intranasally with mock-infected HeLa 229 cell extracts and was challenged in the ovarian bursa with C. trachomatis MoPn (sham immunized, C. trachomatis challenged). The second control group was sham immunized and not challenged (sham immunized, nonchallenged). Before challenge, the C. trachomatis-immunized, C. trachomatis-challenged animals mounted a significant humoral response as shown by high immunoglobulin G (IgG), IgM, and IgA levels and high levels of neutralizing antibodies in serum and moderate IgG and IgA titers in vaginal secretions. Reactivity by Western blot (immunoblot) to the lipopolysaccharide, 30-, 40- (major outer membrane protein), and 60-kDa cysteine-rich proteins and 75- and 100-kDa chlamydial components could be demonstrated. However, reactivity to the 60-kDa heat shock protein was only observed 22 days after challenge. In addition, this group of animals mounted a significant immune response to chlamydial antigens, as shown by a lymphocyte proliferation assay, compared with the sham-immunized nonchallenged mice. After intrabursal challenge, there was no C. trachomatis shedding from the vagina in the C. trachomatis-immunized, C. trachomatis-challenged animals, while 63% of the sham-immunized, C. trachomatis-challenged mice had a positive C. trachomatis culture. In addition, histological sections from the genital tract showed, at 2 weeks postchallenge, a marked acute inflammatory reaction in the sham-immunized, C. trachomatis-challenged animals while in the C. trachomatis-immunized, C. trachomatis-challenged mice there was minimal inflammatory reaction. When the animals were mated, only 12% of the mice from the sham-immunized, C. trachomatis-challenged mice were fertile. In contrast, 94 and 80% of the sham-immunized, nonchallenged and C. trachomatis-immunized, C. trachomatis-challenged mice, respectively, were fertile.
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PMID:Protection against infertility in a BALB/c mouse salpingitis model by intranasal immunization with the mouse pneumonitis biovar of Chlamydia trachomatis. 803 6

The effects of depleting CD4+ and CD8+ T cells on macrophage recruitment have been analyzed for bronchoalveolar lavage (BAL) populations from mice with primary or secondary influenza pneumonia. Macrophages were characterized by both the capacity to engulf latex particles and the expression of mRNA for a 65 kD heat shock protein (hsp65). The localization of hsp65 mRNA+ cells to the pneumonic lung was greatly enhanced in the secondary response. Eliminating the CD4+ and CD8+ T cells decreased the prevalence of hsp65 mRNA+latex+ macrophages as much as seven-fold, though the frequency of latex+ cells was higher in the residual inflammatory process. The CD4-8- gamma delta T cells were also relatively enriched in the BAL from the depleted mice. However, the localization of gamma delta T cells to the pneumonic lung does not compensate either quantitatively or qualitatively for the lack of the CD4+ and CD8+ alpha beta T-cell subsets, which are responsible for activating a substantial proportion of the phagocytic cells to express transcripts of an endogenous hsp65 gene.
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PMID:hsp65 mRNA+ macrophages and gamma delta T cells in influenza virus-infected mice depleted of the CD4+ and CD8+ lymphocyte subsets. 810 Jun 10

A Swiss Webster white mouse model of salpingitis was used to characterize the immune response following an intrauterine infection with the Chlamydia trachomatis mouse pneumonitis biovar. Western blot (immunoblot) analyses of the serum samples showed that the immunodominant bands corresponded to molecular masses of 72, 60, 42, and 28 kDa and to the lipopolysaccharide. Antibodies to the 60-kDa heat shock protein and to the 60-kDa cysteine-rich protein were detected at 2 and 3 weeks postinfection, respectively. Neutralization was observed in an in vitro assay with serum samples as early as the 3rd day postinfection and remained high for the 7 weeks of observation. The mice were mated in the 7th week following infection. Of the infected experimental mice, 71.4% were found to be either unilaterally or bilaterally infertile, whereas only 27.4% of the noninfected control mice were found to be infertile.
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PMID:Analysis of the immune response in mice following intrauterine infection with the Chlamydia trachomatis mouse pneumonitis biovar. 842 4

In this study, the hsp60 and hsp70 heat shock protein antigens of Mycobacterium tuberculosis were tested as potential vaccine candidates, using purified recombinant protein antigens or antigens encoded in the form of a DNA plasmid vaccine. Guinea pigs vaccinated with a mixture of the two proteins showed no evidence of resistance to low-dose aerosol challenge infection and quickly developed severe lung damage characterized by necrotizing bronchointerstitial pneumonia and bronchiolitis. As a result, we turned instead to a DNA vaccination approach using a plasmid encoding the hsp60 antigen of M. tuberculosis. Although immunogenic in mice, vaccination with plasmid DNA encoding hsp60 was not protective in that model or in the guinea pig model and again gave rise to similar severe lung damage. This study seriously questions the safety of vaccines against tuberculosis that target highly conserved heat shock proteins.
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PMID:Lack of protection in mice and necrotizing bronchointerstitial pneumonia with bronchiolitis in guinea pigs immunized with vaccines directed against the hsp60 molecule of Mycobacterium tuberculosis. 1081 27

The most common pathologic form of idiopathic pulmonary fibrosis is usual interstitial pneumonia, which is characterized by patchy fibrotic areas, marked increase in the number of fibroblasts and type II pneumocytes, and excessive deposition of extracellular matrix proteins, especially collagen. Heat shock protein 47 is a collagen-binding stress protein and has a specific role in intracellular processing of procollagen molecules as a collagen-specific molecular chaperone. However, its role in the causation of fibrosis in usual interstitial pneumonia is unknown. In this study, we examined the expression of heat shock protein 47 and type I procollagen in 12 patients with usual interstitial pneumonia by immunohistochemistry on sequential sections. Heat shock protein 47 was localized predominantly in alpha-smooth muscle actin-positive myofibroblasts and surfactant protein-A-positive type II pneumocytes in active fibrotic areas of usual interstitial pneumonia. Type I procollagen was also expressed in those cells. In contrast, heat shock protein 47 and type I procollagen were weakly or not at all expressed in myofibroblasts and type II pneumocytes in bronchiolitis obliterans organizing pneumonia and normal lung tissue samples obtained from excised lung cancer tissues. The numbers of heat shock protein 47- and type I procollagen-positive cells to type II pneumocytes or myofibroblasts were significantly higher in usual interstitial pneumonia than in bronchiolitis obliterans organizing pneumonia and normal lung tissue specimens. Our results suggest that myofibroblasts and type II pneumocytes play an important role in the progression of fibrosis through the induction of heat shock protein 47, which regulates the synthesis/assembly of type I procollagen in usual interstitial pneumonia. HUM PATHOL 31:1498-1505.
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PMID:Involvement of collagen-binding heat shock protein 47 and procollagen type I synthesis in idiopathic pulmonary fibrosis: contribution of type II pneumocytes to fibrosis. 1115 Mar 75

Heme oxygenase-1 (HO-1) is an inducible heat shock protein that regulates heme metabolism to form bilirubin, ferritin and carbon monoxide. Based on recent evidence that HO-1 is involved in the resolution of inflammation by modulating apoptotic cell death or cytokine expression, the present study examined whether overexpression of exogenous HO-1 gene transfer provides a therapeutic effect on a murine model of acute lung injury caused by the type A influenza virus. We demonstrate herein that the transfer of HO-1 cDNA resulted in (1) suppression of both pathological changes and intrapulmonary hemorrhage; (2) enhanced survival of animals; and (3) a decrease of inflammatory cells in the lung. TUNEL analysis revealed that HO-1 gene transfer reduced the number of respiratory epithelial cells with DNA damage, and caspase assay suggested that HO-1 suppressed lung injury via a caspase-8-mediated pathway. These findings suggest the feasibility of HO-1 gene transfer to treat lung injury induced by a pathogen commonly seen in the clinical setting. Since oxidative stress and lung injury are involved in many lung disorders, such as pneumonia induced by a variety of microorganisms and pulmonary fibrosis, HO-1 may be useful for wider clinical applications in gene therapy targeting lung disorders including acute pneumonia and pulmonary fibrosis.
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PMID:Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice. 1159 63

We researched the application of immunohistochemistry for the purpose of establishing forensic pathological diagnoses. In the present study, we examined the induction and expression of heat shock protein (HSP), oxygen regulated protein (ORP), inducible nitric oxide synthase (iNOS), excitatory amino acid transporter 2 (EAAT2) and apolipoprotein E (apo E) in the human brain using forensic autopsy cases as our subjects. Hypoxic/ischemic brain damage. In cases of longer survival and with a history of hypoxic attacks, the proteins HSP and ORP were found in the parieto-occipital lobe and hippocampus. And we are able to observe a weak stain for EAAT2 in almost all asphyxia deaths. Traumatic brain injury (TBI). In traumatic brain injury (TBI), the prolonged induction of iNOS was demonstrated in the neutrophils, microglia/macrophage, and vascular smooth muscle cells in the traumatized brain. Apo E was identified with neurons in the traumatized cortical hemisphere from only a two-hour survival case to long survival cases. To the contrary, there was no positive apo E staining in the contralateral cortical hemisphere at all. In one one-hour survival case, a weak stain for EAAT2 was observed, but intensive expression of EAAT2 was observed from brief to one-day survival cases. Sudden infant death (SID). Numerous ferritin-positive cells were observed in the brain in the cases of pneumonia or myocarditis that we examined. To the contrary, the numbers of ferritin-positive cells were obviously decreased in the cases of sudden infant death syndrome (SIDS). The transferrin-positive cells were in an inverse proportion to the ferritin positive cells in each SIDS case. Also, numerous ORP-150 positive cells were observed in the brain in cases of pneumonia and the SIDS group. In forensic practice, immunohistochemical investigation of these proteins can be a great value for diagnosing not only the cause of death but also the pathophysiological changes and the victims past history.
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PMID:[Application of immunohistochemistry for forensic pathological diagnosis: finding of human brain in forensic autopsy]. 1190 39

Mycoplasma hyopneumoniae is the etiological agent of swine enzootic pneumonia, a chronic nonfatal disease affecting pigs of all ages. The goal of this study was to design DNA vaccines by constructing plasmid pcDNA3/P42, carrying the heat shock protein gene P42 of M. hyopneumoniae, and to evaluate the immune responses elicited in BALB/c mice. The expression of P42 was first examined in transfected NIH 3T3 cells by reverse transcription-PCR to ensure that the construct was functional. The humoral and cell-mediated immune responses induced by the plasmid were further evaluated in BALB/c mice through intramuscular injection. Both immunoglobulin G1 (IgG1) and IgG2a levels were 64 times those of the control groups during the first 8 weeks. The levels of interleukin-2 (IL-2), IL-4, and gamma interferon mRNAs in the immunized animals were elevated, and the proliferation of spleen cells was also enhanced in the immunized animals. The results indicate that pcDNA3/P42 DNA immunization induces both Th1 and Th2 immune responses. In addition, antiserum from the immunized animals was found to inhibit the growth of M. hyopneumoniae. The present study reveals that DNA vaccination could be a new strategy against infection by M. hyopneumoniae and may have potential for developing vaccines for other infectious diseases as well.
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PMID:Expression and immunogenicity of Mycoplasma hyopneumoniae heat shock protein antigen P42 by DNA vaccination. 1259 27


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