Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026936 (Mycoplasma)
 14,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction between chronic infection and chronic asthma is receiving increased investigation as a factor in the pathophysiology of asthma. To further understand this interaction, we used an animal model (BALB/c mice) with a Mycoplasma pneumoniae respiratory infection. Mice were studied 3, 7, 14, and 21 d after infection. Bronchial hyperresponsiveness (BHR) was assessed by methacholine challenge and was significantly heightened in the infected mice compared with saline controls at Days 3, 7, and 14. The associated inflammatory response was mainly neutrophils. The tissue inflammatory score significantly correlated to BHR (r = 0.78, P < 0.0001). Additionally, tissue interferon (IFN)-gamma was significantly suppressed at Days 3 and 7 in the infected group compared with controls; and at Days 3, 7, and 14 compared with Day 21 in the infected group. There was a significant negative correlation between lung tissue messenger RNA levels of IFN-gamma corrected for beta-actin and BHR (r = -0.50, P = 0.022). Thus, M. pneumoniae respiratory infection is associated with BHR in this murine model. It appears that acute mycoplasma infection suppresses IFN-gamma, which may be a pivotal factor in the control of BHR.
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PMID:Airway inflammation and bronchial hyperresponsiveness after Mycoplasma pneumoniae infection in a murine model. 1135 Aug 27

Mycoplasma infection affects the host's immune system in different ways. In this work, a kinetic approach was used to try to determine the mechanisms by which Mycoplasma cause these effects. Experiments were performed using Balb/c mice infected with Mycoplasma pulmonis and several immunological parameters were determined. It was found that at days 10 and 15 post-infection, there were significant changes in the percentages of CD4+ and CD8 + cells, in both peripheral blood and the thymus. Significant sequential increases in concentrations of both IFN-gamma and IL-4 were detected in sera, such that at day 15, there was a peak in IFN-gamma, concentration and at day 38, IL-4 concentration also peaked. By day 46, both IFN-gamma and IL-4 fell to control levels despite continued infection. Delayed hypersensitivity (DTH) was reduced in infected animals compared to non-infected controls. A small recovery in DTH was observed at day 30, which was reduced again by day 40. Altogether, the results show features of a transitional shift from Th1 to Th2 in animals that are ultimately immunologically incompetent (in both cellular and humoral immunity). It appears to be this state of incompetence that allows the microorganism to survive and thus provides an explanation for the chronic state of the disease, which is a characteristic of Mycoplasma infection.
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PMID:Immunomodulatory properties of Mycoplasma pulmonis. II. Studies on the mechanisms of immunomodulation. 1156 61

Experiments are presented that were performed in order to understand the mechanisms causing these effects on the immune system. Mitogenic effects of Mycoplasma membranes on mouse spleen cells were shown using M. capricolum. The observed mitogenic activity is proportional to the amount of membranes used, as measured by protein content. Separation of T and B cells was performed by two techniques, the anti-Thyl.2 plus complement method and the Dynabead technique. Using the former technique, it was shown that removal of T cells markedly reduced effects of stimulation by mycoplasma membranes, but did not abolish it. The separated cells were still stimulated by PHA, indicating that the preparation still contained T cells. Furthermore, removal of T cells preferentially reduced the PHA response over that of mycoplasma membranes, indicating that mycoplasma membranes stimulate both B and T lymphocytes. The Dynabead system was found to be the more efficient separation technique, and by using it we were able to make the following observations. Inactivated Mp, membranes and culture supernatant stimulated B cells, whereas T cells were only slightly stimulated by inactivated Mp and membranes. There was an increase in proliferation when T cells were incubated with adherent cells from peripheral blood. Finally, we showed that spleen cells from infected animals produce more IL-4 and less IFN-gamma than cells from non-infected animals when stimulated with membranes, inactivated Mp, culture supernatant or phytohemagglutinin. Altogether, these results show that lymphocytes from Mycoplasma-infected animals are directly affected and this effect is probably due to superantigen-like molecules from M. pulmonis.
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PMID:Immunomodulatory properties of Mycoplasma pulmonis. III. Lymphocyte stimulation and cytokine production by Mycoplasma pulmonis products. 1156 62

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 prevalence of rheumatoid arthritis (RA) is relatively constant in many populations, at 0.5-1.0%. However, a high prevalence of RA has been reported in the Pima Indians (5.3%) and in the Chippewa Indians (6.8%). In contrast, low occurrences have been reported in populations from China and Japan. These data support a genetic role in disease risk. Studies have so far shown that the familial recurrence risk in RA is small compared with other autoimmune diseases. The main genetic risk factor of RA is the HLA DRB1 alleles, and this has consistently been shown in many populations throughout the world. The strongest susceptibility factor so far has been the HLA DRB1*0404 allele. Tumour necrosis factor alleles have also been linked with RA. However, it is estimated that these genes can explain only 50% of the genetic effect. A number of other non-MHC genes have thus been investigated and linked with RA (e.g. corticotrophin releasing hormone, oestrogen synthase, IFN-gamma and other cytokines). Environmental factors have also been studied in relation to RA. Female sex hormones may play a protective role in RA; for example, the use of the oral contraceptive pill and pregnancy are both associated with a decreased risk. However, the postpartum period has been highlighted as a risk period for the development of RA. Furthermore, breastfeeding after a first pregnancy poses the greatest risk. Exposure to infection may act as a trigger for RA, and a number of agents have been implicated (e.g. Epstein-Barr virus, parvovirus and some bacteria such as Proteus and Mycoplasma). However, the epidemiological data so far are inconclusive. There has recently been renewed interest in the link between cigarette smoking and RA, and the data presented so far are consistent with and suggestive of an increased risk.
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PMID:Epidemiology and genetics of rheumatoid arthritis. 1211 Jan 46

The aim of this study was to evaluate cytokine secretion in children with acute Mycoplasma pneumoniae infection and wheeze. We studied 25 patients aged 2-14 years with an acute episode of wheezing (15 with acute M. pneumoniae infection) and 16 healthy controls of similar gender and age (8 with laboratory evidence of asymptomatic acute M. pneumoniae infection). Serum interleukin (IL)-2, interferon (IFN)-gamma, IL-4, and IL-5 concentrations were measured in samples obtained at enrollment, using enzyme-linked immunosorbent assay kits. In the presence of wheezing, IL-5 concentrations were significantly higher in subjects with acute M. pneumoniae infection (33.415 +/- 22.138 pg/mL) than in those without such infection (2.320 +/- 1.846 pg/mL, P < 0.0001). The children with acute M. pneumoniae infection and wheeze had higher IL-5 concentrations (33.415+/-22.138 pg/mL) than those with asymptomatic acute infection and without wheeze (1.740 +/- 2.299 pg/mL, P < 0.0001). No significant between-group differences were observed in terms of IL-2, IFN-gamma, or IL-4 levels, or the prevalence of atopy. Our results show that children with wheezing and acute M. pneumoniae infection have a specific cytokine profile characterized by a significant increase in serum levels of IL-5. This immune response may be important for understanding the pathophysiological mechanisms by which this pathogen contributes to the development of wheeze-related symptoms, and for identifying new treatment strategies.
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PMID:Cytokine secretion in children with acute Mycoplasma pneumoniae infection and wheeze. 1211 78

Traditionally, adjuvants have been administered with antigens to enhance immunity. We studied the effect of several adjuvants such as Freund's complete adjuvant (FCA), Freund's incomplete adjuvant (FIA), lipopolysaccharide (LPS), homopolymers of polyinosinic-polycytidylic acid (poly I:C) and polyadenylic-polyuridylic acid (poly A:U), lithium chloride (LiCl), saponin Quil A and calcium phosphate gel (CaHPO(4)) on the immune response of mice to formalin-inactivated Mycoplasma agalactiae. The specific antibody or cytokine producing splenocytes were detected by ELISAspot and immunocytochemistry, respectively. Depending on the adjuvant given, the number of M. agalactiae-specific antibody producing cells was increased 2.5-6-fold. IgG was the major class of M. agalactiae-specific antibodies followed by IgM, IgA and IgE. Among IgG isotypes, FCA, FIA, Quil A and CaHPO(4) induced an IgG1 response with substantial increase of the IgG2a, IgG2b and IgG3 isotypes while poly I:C shifted the response toward an IgG2a/IgG3 production. Finally, poly A:U induced an IgG2b response while LPS and LiCl augmented the IgG3/IgG1/IgG2a secretion. FCA augmented IL-4, IL-5 and IL-10 production suggesting a strong Th2 response, while IFN-gamma and IL-12 remained low; poly I:C enhanced IFN-gamma, IL-12 and TNF-alpha eliciting a Th1 response; poly A:U resulted in a IL-10, IL-5, IL-6 and IL-12 secretion; and LPS enhanced the IL-10, IL-6 and TNF-alpha production. Our data show that adjuvants augment M. agalactiae-specific antibody production and lead to B cell isotype-switching via the appropriate cytokine milieu. Certain adjuvants, such as poly I:C, therefore, appear as promising immune enhancers for vaccination against M. agalactiae infections.
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PMID:Adjuvant regulation of cytokine profile and antibody isotype of immune responses to Mycoplasma agalactiae in mice. 1222 Aug 8

Airway mycoplasma infection may be associated with asthma pathophysiology. However, the direct effects of mycoplasma infection on asthma remain unknown. Using a murine allergic-asthma model, we evaluated the effects of different timing of airway Mycoplasma pneumoniae infection on bronchial hyperresponsiveness (BHR), lung inflammation, and the protein levels of Th1 (gamma interferon [IFN-gamma]) and Th2 (interleukin 4 [IL-4]) cytokines in bronchoalveolar lavage fluid. When mycoplasma infection occurred 3 days before allergen (ovalbumin) sensitization and challenge, the infection reduced the BHR and inflammatory-cell influx into the lung. This was accompanied by a significant induction of Th1 responses (increased IFN-gamma and decreased IL-4 production). Conversely, when mycoplasma infection occurred 2 days after allergen sensitization and challenge, the infection initially caused a temporary reduction of BHR and then increased BHR, lung inflammation, and IL-4 levels. Our data suggest that mycoplasma infection could modulate both physiological and immunological responses in the murine asthma model. Our animal models may also provide a new means to understand the role of infection in asthma pathogenesis and give evidence for the asthma hygiene hypothesis.
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PMID:Effects of respiratory Mycoplasma pneumoniae infection on allergen-induced bronchial hyperresponsiveness and lung inflammation in mice. 1259 71

Dendritic cells (DC) modulate immune responses depending on the nature of the antigens. Receptors capable of discriminating these antigens on the basis of the pathogen-associated molecular patterns (PAMP) belong to the Toll-like receptor (TLR) family. The macrophage-activating lipopeptide 2 kDa (MALP-2), a synthetic lipopeptide derived from Mycoplasma fermentans, signals through TLR-2 and TLR-6. The aim of this study was to examine whether MALP-2 can modulate the functional properties of human monocyte-derived DC. The effects of this treatment were compared to those of the TLR-4 agonist lipopolysaccharide (LPS). To ensure clinical applicability, DC were generated under serum-free conditions. MALP-2 and LPS stimulation induced the expression of CD83 and increased the expressions of CD80, CD86, HLA-ABC and CD40. Furthermore, both substances decreased the endocytotic capacity of DC and induced the release of bioactive TNF-alpha and IL-10, whereas LPS additionally increased IL-12 release. Pretreatment with both substances boosted the allostimulatory capacity of DC. In a coculture with autologous lymphocytes, either MALP-2 or LPS pretreated DC induced a marked proliferation of lymphocytes, but only DC prestimulated with MALP-2 activated lymphocytes to produce the cytokines IL-4, IL-5 and IFN-gamma. No polarisation of lymphocytes into T-helper (Th)1 or Th2 was detected. These data indicate that MALP-2 is a potential candidate to modulate DC for clinical applications.
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PMID:Synthetic mycoplasma-derived lipopeptide MALP-2 induces maturation and function of dendritic cells. 1277 64

To better understand the interaction between Mycoplasma bovis and its bovine host, we have characterized the immune response generated during an experimental lung infection with M. bovis. Proliferation ([3H]-thymidine blastogenesis) and Th1/Th2 cytokine production were used to monitor peripheral cellular immune responses. Flow cytometry analysis was used to determine T-cell subset activity by CD25 expression. Humoral immune response was monitored by the identification of antigen-specific IgG1 and IgG2 isotypes over time. Herein, we show that M. bovis antigen stimulates activation of CD4+ and CD8+ cells in vitro in a manner consistent with memory, and that gammadelta-T cells are activated by antigen in a manner consistent with innate immunity. In addition, the percentage of cells producing IFN-gamma during recall response is equal to that of IL-4 producing cells. Serological analysis shows M. bovis stimulates increased production of antigen-specific IgG1 while very little IgG2 is produced. We therefore submit that experimental lung infection of cattle with M. bovis results in a Th2-skewed immune response.
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PMID:Characterization of the immune response to Mycoplasma bovis lung infection. 1284 9


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