The effect of Mycoplasma arthritidis infection on the kinetics of colloidal carbon clearance in mice

Abstract The activity of phagocytes from A/J mice was estimated by the carbon clearance test following injection of Mycoplasma arthritidis . Phagocytic activity was significantly depressed 12 h post-infection ( P =0.001) and returned to normal values at 24 h. For animals examined 2 and 7 days post-infection, the overall phagocytic activity increased significantly ( P <10⁻⁴). Phagocytic activity gradually decreased and returned to that of the control group by the end of the fourth week. The relative weights of liver and spleen were significantly increased from the 2nd day post infection ( P =0.0028 and P =0.0014 respectively) and remained increased until the end of the experiment. The early depressive effect on phagocytic activity may be related to superantigen activity with the production of mediators such as macrophage deactivating factor. The later expansion of the macrophage population might bring about the stimulation of autoreactive clones of T and B cells and be responsible for the chronic arthritis that developed in the mycoplasma treated mice.     

The effect of Mycoplasma arthritidis infection on the phagocytic activity of macrophages in rats and mice

The phagocytic activity of mononuclear phagocytes of A/J mice and Wistar rats was estimated by the carbon clearance test following injection of Mycoplasma arthritidis. In mice, the overall phagocytic activity was significantly increased at the end of the first week (P less than 0.0001), but the increase was marginal by the third and fourth weeks after injection. A significant increase in the relative weight of liver and spleen was observed even when phagocytic activity had returned to levels similar to those of controls (P less than 0.001). In rats, the overall phagocytic activity was significantly increased until the fourth week (P less than 0.00001). There was not, however, an increase in the relative weight of liver and spleen as observed for the mice. The results are discussed in the context of factors contributing to the pathogenic mechanisms responsible for differences in the patterns of arthritis due to mycoplasma observed in mice and rats.     

Identification of an isoschizomer of the HhaI DNA methyltransferase in Mycoplasma arthritidis

The genome of Mycoplasma arthritidis strain 158 has modified cytosine residues at AGCT sequences that render the DNA resistant to digestion with the AluI restriction endonuclease. The DNA methyltransferase responsible for the base modification has previously been designated MarI. From the complete genome sequence of M. arthritidis , we identify Marth_orf138 as a candidate marI gene. Marth_orf138 was cloned in Escherichia coli and its TGA codons converted to TGG. DNA isolated from E. coli cells expressing the modified Marth_orf138 gene was degraded by the AluI nuclease, indicating that Marth_orf138 does not code for MarI. However, the DNA from E. coli was found to have acquired resistance to the restriction endonuclease HhaI. Genomic DNA from M. arthritidis was also found to be resistant to HhaI (recognizes GCGC). The M. arthritidis isoschizomer of the HhaI DNA methyltransferase, coded by Marth_orf138, is designated MarII. Transformation of M. arthritidis was not significantly affected by modification of plasmid at HhaI sites, indicating that the mycoplasma lacks a restriction endonuclease that recognizes GCGC sites.     

Investigation into the origin of the antigens of Mycoplasma arthritidis cross-reacting with host tissue antigens

Abstract The electrophoretical separations of Mycoplasma arthritidis and the serum used in the cultivation medium show a high number of protein bands with identical molecular weights. Proteins with molecular weights of 84, 72 and 52 kDa also appeared to be identical with proteins of Mycoplasma arthritidis in their antigenic properties as demonstrated by Western blotting with rat-anti- Mycoplasma arthritidis serum. The autoradiography of electrophoretically separated Mycoplasma arthritidis cells metabolically labeled with ³⁵S-methionine and ³⁵S-cysteine revealed that the proteins of Mycoplasma arthiritidis identical in molecular weight and antigenic structure with serum proteins are synthesized by Mycoplasma arthritidis , and represent true translation products.     

The effect of Mycoplasma arthritidis superantigen on immunogenesis in transplacental infection

The immune responsiveness of the progeny of BALB/c mice, responsive to M. arthritidis superantigen (MAS), and C57BL/6 mice, nonresponsive to MAS, infected with M. arthritidis during the second half of pregnancy was studied. The investigation revealed that in responsive animals the proliferative response of spleen cells to MAS was suppressed with the level of response to concanavalin A remaining unchanged. The spleen cells of the test mice reacted to syngenic intact cells as to xenogenic ones and suppressed reaction to MAS and the production of interleukin 1 in the culture of spleen cells taken from the intact syngenic animals. The data obtained in this study suggest that after the infection of pregnant BALB/c mice with M. arthritidis immune tolerance to MAS developed in their progeny, which was accompanied by the induction of suppressor cells inhibiting the production of interleukin 1.     

Adherence of Mycoplasma pneumoniae to human alveolar macrophages

Abstract The human pathogen Mycoplasma pneumoniae causes primary atypical-cold agglutinin-positive pneumonia. Since alveolar macrophages internalize mycoplasma as part of their immune defense, we studied characteristics of the human macrophage receptor for opsonized and nonopsonized M. pneumoniae . The glass-adhering subpopulation of M. pneumoniae attached more than the non-adherent subpopulation. The attachment was dose-dependent and enhanced by opsonization in the presence of human serum. It is inhibited by sulfated compounds such as dextran-sulfate and polyanetholsulfonic acid, but not by dextran or several monosaccharides, suggesting that sulfated glycolipids on the macrophage surface may act as receptors for M. pneumoniae binding. In addition, sialylated compounds, such as fetuin and α 1-acid glycoprotein, were found to be potent inhibitors of the attachment, also indicating the role of sialic acid residue in recognition and attachment of M. pneumoniae to human alveolar macrophages.     

Splenic marginal-zone macrophages and marginal metallophils in rats and mice

Summary The splenic macrophages of rats and mice were studied by light and fluorescence microscopy to determine their phagocytotic uptake of carbon and neutral polysaccharide (Fic-F), and their lysosomal enzyme activities. In rats, the large macrophages of the marginal zone (MZ) showed a moderate to strong acid phosphatase activity, and took up most of the Fic-F, even though they showed a weak phagocytotic activity to carbon particles. Red-pulp macrophages, however, ingested a large quantity of carbon particles, and are considered to be the major scavengers in the rat spleen. In contrast, the MZ macrophages in the mouse spleen were the major scavengers and showed a vigorous uptake of both carbon and Fic-F. In rats, the marginal metallophils (MM), located at the outer border of the periarterial lymphatic sheath and boundary between the MZ bridging channel and surrounding tissue, ingested Fic-F, whereas those located around the follicular area did not. In mice, on the other hand, the MM never ingested Fic-F. Lightly carbon-ladened small cells were constantly seen in the MZ of both rats and mice. They showed little acid phosphatase activity and did not ingest Fic-F. They were also present in the blood circulation.     

Influence of the genotype of mice on the effect of interferon on phagocytic activity of macrophages

The influence of genotype on interferon effect on phagocytic activity of unstimulated mouse peritoneal macrophages (MPM) was studied in in vitro experiments. Treatment of MPM from BALB/c and ICR mice with mouse fibroblast interferon (MuIFN-beta) enhanced the ingestion of non-opsonized Escherichia coli. This effect was dose-dependent and neutralized by anti-interferon globulin. MPM from C57B1/6 mice were not stimulated by the same treatment. Treatment of MPM with pH 2-sensitive immune interferon (MuIFN-gamma) depressed the ingestion independently on the genotype of mice.     

Mycoplasma arthritidis superantigen (MAM)-induced macrophage nitric oxide release is MHC class II restricted,interferongamma dependent,and toll-like receptor 4 independent

Mycoplasma arthritidis causes arthritis in rodents that resembles human rheumatoid arthritis. It produces a superantigen (MAM) that stimulates production of cytokines by making a bridge between lymphocyte T-cell receptor with the appropriate Vbeta chain, and H-2 1-Ealpha MHC class II molecules. Here we studied MAM-induced nitric oxide (NO) production in mouse peritoneal macrophages and found that it was: (1) time and concentration dependent, (2) possibly derived from inducible NOS synthase since it was reduced significantly by amino guanidine pretreatment, (3) restricted to H-2(K) (C3H/HePas and C3H/HeJ) and H-2(d) strains (BALB/c), (4) independent of TLR4 signaling since the coisogenic strains C3H/HePas and C3H/HeJ (TLR4 deficient) produced similar levels of NO following MAM stimulation, (5) potentiated by lipopolysaccharide, and (6) dependent on the presence of nonadherent peritoneal cells. Neutralization of interferon-gamma (IFNgamma in the peritoneal cell cultures with monoclonal antibodies abolished MAM-induced NO production. Addition of rIFNgamma to the adherent cells substituted the nonadherent cells for MAM-induced NO production. A macrophage cell line, J774A.1 (H-2(d)), also produced NO upon MAM stimulation but only when BALB/c spleen lymphocytes were added. Thus, in murine macrophages, MAM induces NO production that is dependent on signaling through MHC class II molecules and IFNgamma but independent of TLR4 expression.     

Effect of Mycoplasma arthritidis on mouse and rat lymphoid cells in experimental Mycoplasma infection]

Early stages of mycoplasma infection of mice and rats were accompanied by suppression of the populations of rosette- and plaque-forming cells. Later the character and dynamics of the immune response to M. arthritidis differed in mice and rats. In mice mycoplasma infection was accompanied by stimulation of rosette-forming cells with some suppression of the plaque-forming cells from the 7th to the 36th day of infection. In rats by the 7th day the number of plaque- and rosette-forming cells decreased in comparison with control, and the immune response was restored by the 15h day; at later periods the immune response of the infected rats exceeded the normal level considerably. The cellular and humoral immune reactions proved to depend on the mycoplasma dose.     

Contrasting effects of Mycoplasma fermentans and M. felis on the viability and chemiluminescence response of human polymorphonuclear leukocytes

Abstract Trypan blue exclusion was used to estimate the viability of human polymorphonuclear leukocytes (PMNL) in the presence of Mycoplasma felis and two strains of M. fermentans (PG18 and incognitus). The competence of PMNL to mount a respiratory burst when challenged with the mycoplasmas was also monitored by luminol-dependent chemiluminescence (CL). Both un-opsonised and non-immune human serum opsonised M. felis cells had little effect on PMNL viability. In contrast, PMNL viability was reduced markedly by un-opsonised cells of M. fermentans strain incognitus and, to a lesser extent, strain PG18, and opsonisation of these mycoplasmas further enhanced killing. Death of PMNL in the presence of M. fermentans was not associated with the autonomous production of active oxygen species during the respiratory burst as M. felis induced a high CL response from PMNL, whereas that induced by M. fermentans strain incognitus was significantly lower. M. fermentans may invade mammalian cells and it is suggested that the mechanism of PMNL death could be related to the ability of M. fermentans to penetrate host cell membranes.     

Effect of low-frequency ultrasound on the chemotactic and phagocytic activity of peritoneal macrophages in rats

The influence of low-frequency ultrasound on the chemotactic, ingestive and digestive activity of peritoneal macrophages in rats was studied. The intraoperative treatment of the peritoneum with ultrasound enhanced chemotactic activity 3.3-fold in comparison with that in the control animals. The digestive function of peritoneal macrophages considerably increased, the stimulation of their ingestive capacity also occurred. The activation of the phagocytic function of macrophages was observed within 7 days after a single sonar treatment. The authors believe that the stimulation of the macrophage system is probably one of the mechanisms of the sanative action of ultrasound which is used at present in purulent surgery.     

The effect of bilirubin on the fc receptor expression and phagocytic activity of mouse peritoneal macrophages

The effect of bilirubin on the phagocytic activity of mouse peritoneal macrophages and on the expression of Fc receptors and receptors for SRBC was studied. Intraperitoneally administered bilirubin influenced the expression of Fc receptors for IgM, IgG2B, IgA and IgE, whereas the expression of other receptors as well as the phagocytic activity of peritoneal macrophages remained unchanged. The possible mechanism of the effect of bilirubin on Fc receptors is discussed.     

The effect of humoral factors on phagocytic activity of central macrophages in the erythroblast islet culture

A 24-hour cultivation of erythroblast islets (El) in presence of erythropoietin (EP) and macrophage colony stimulating factor (MCSF) led to a concentration-dependent enhancement of phagocytic activity (PA) of the El's "central" macrophages. The latter phenomenon was revealed in "mature" El classes only. The PA of "central" macrophages in "proliferating" El appeared to be affected neither by EP, nor by MCSF.     

Persistence of Mycoplasma arthritidis in the body of mice of different strains

Mice belonging to 3 strains were shown to differ greatly in their sensitivity to M. arthritidis. This organism persisted for a year in (C57BL/6 X A/Sn)F1 mice, for 6 weeks in BALB/c mice and for 1-3 weeks in C57BL/6 mice. The sensitivity of mice to M. arthritidis infection and the persistence of the infective agent in the organs of the animals were found to depend on the state of their cell-mediated immunity.     

儿科呼吸道疾病中肺炎支原体感染的结果分析

目的探讨儿科肺炎支原体（MP）感染特点,辅助临床医师早期诊断,合理用药。方法测定我院一年来2013例儿科呼吸道疾病患儿的肺炎支原体抗体（IgM）。结果2013例呼吸道感染患儿,检出肺炎支原体抗体（IgM）阳性者769例,占38.2%,769例阳性分别表现为肺炎369例（48%）,支气管炎238例（31%）,咽炎92例（12%）,哮喘70例（9%）。其中,肺炎组与各组相比较,具有统计学意义。MP IgM感染的检出率明显高于其他各组（P〈0.01）。结论MP感染是患儿不可忽视的病原体,检测患儿血清MP抗体能够及早诊断,指导治疗。