Delayed Hypersensitivity in Mycoplasma Pneumoniæ Infections

Mizutani, Hiromichi; Kitayama, T; Hayakawa, A.; Nagayama, E.; Kato, Joichi; Nakamura, Kazuo; Tamura, Eiichiro; Izuchi, Toshiro

doi:10.1016/s0140-6736(71)91956-8

Cited by 33 publications

(20 citation statements)

References 8 publications

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“…These cytokines are also important in the phenotypic development of lymphoid responses, as IFN-␥ promotes a cell-mediated response, while IL-4 promotes a humoral response (26). Lymphoid responses are critical in mycoplasma lower respiratory tract disease, as they play both protective and pathological roles; however, immune responses of the upper respiratory tract are unknown (11)(12)(13)(14)(15). Studies in the upper respiratory tract do suggest that the nasal passages have a separate and distinct immune response from the lower respiratory tract (1,19,21,40).…”

Section: Discussionmentioning

confidence: 99%

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The Upper and Lower Respiratory Tracts Differ in Their Requirement of IFN-γ and IL-4 in Controlling Respiratory Mycoplasma Infection and Disease

Woolard

Hodge

Jones

et al. 2004

The Journal of Immunology

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The purpose of this study is to evaluate the significance of IFN-γ and IL-4 production in controlling mycoplasma infection and the pathogenesis of disease in the upper and lower respiratory tract. By using IFN-γ knockout and IL-4 knockout BALB/c mice, we were able to study the contribution of these cytokines in the development of pathogenesis and/or protection in response to mycoplasma respiratory infection, in both the upper and lower respiratory tracts. The loss of either IFN-γ or IL-4 does not affect disease pathogenesis or mycoplasma organism numbers in the upper respiratory tract. However, in the absence of IL-4, the nasal passages developed a compensatory immune response, characterized by higher numbers of macrophages and CD8+ T cells, which may be masking detrimental effects due to IL-4 deficiency. This is in contrast to the lower respiratory tract, where the loss of IFN-γ, but not IL-4, leads to higher mycoplasma numbers and increased disease severity. The loss of IFN-γ impacted the innate immune system’s ability to effectively clear mycoplasma, as the number of organisms was higher by day 3 postinfection. This higher organism burden most likely impacted disease pathogenesis; however, the development of Th2 cell-mediated adaptive immune response most likely contributed to lesion severity at later time points during infection. Our studies demonstrate that the upper and lower respiratory tracts are separate and distinct in their cytokine requirements for generating immunity against mycoplasma infection.

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Section: Discussionmentioning

confidence: 99%

“…This suggests that the activation and recruitment of macrophages and lymphocytes are important in the development of both acute and chronic states of the disease. In support, several studies demonstrate that a component of mycoplasma respiratory disease is immunopathologic (11)(12)(13)(14)(15).…”

mentioning

confidence: 87%

The Upper and Lower Respiratory Tracts Differ in Their Requirement of IFN-γ and IL-4 in Controlling Respiratory Mycoplasma Infection and Disease

Woolard

Hodge

Jones

et al. 2004

The Journal of Immunology

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“…Nevertheless, other observations suggest that delayed hypersensitivity develops during M. pneumoniae infection. Thus, guinea-pigs and man develop skin hypersensitivity (Fernald, 1971 ;Mizutani et al, 1971). Furthermore, lymphocytes from previously infected human subjects and guinea-pigs can be stimulated in vitro by M. pneumoniae antigens to undergo blast transformation (Leventhal et al, 1969;Fernald, 1971; Biberfeld, 1972;Fernald, 1972), and the migration of macrophages can be inhibited by M. pneumoniae antigen (Arai et al, 1971).…”

Section: Plate Xi1mentioning

confidence: 99%

Reduction in the Severity of Mycoplasma Pneumoniae-Induced Pneumonia in Hamsters by Immunosuppressive Treatment with Anti-Thymocyte Sera

Taylor¹,

Taylor‐Robinson²,

Fernald³

1974

Journal of Medical Microbiology

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PLATE XI1THE pathogenesis of pneumonia in man caused by Mycoplasma pnewnoniae is poorly understood. However, the M. pneumoniae-infected Syrian hamster is a useful model, not only because this is one of the few small animals that can be successfully infected, but also because the histological characteristics of the pneumonia and the temporal development of antibody are similar to these features in man (Dajani, Clyde and Denny, 1965;Fernald, 1969).Pneumonia in hamsters infected with M. pneumoniae consists of peribronchial and perivascular cuffing by lymphocytes, and this suggests that it is the result of a delayed hypersensitivity response in the lung. However, immunoglobulin is associated with many of the cells (Fernald, Clyde and Bienenstock, 1972), indicating that the response may not be a pure delayed hypersensitivity reaction. Nevertheless, other observations suggest that delayed hypersensitivity develops during M. pneumoniae infection. Thus, guinea-pigs and man develop skin hypersensitivity (Fernald, 1971 ;Mizutani et al., 1971). Furthermore, lymphocytes from previously infected human subjects and guinea-pigs can be stimulated in vitro by M. pneumoniae antigens to undergo blast transformation (Leventhal et al., 1969;Fernald, 1971; Biberfeld, 1972;Fernald, 1972), and the migration of macrophages can be inhibited by M. pneumoniae antigen (Arai et al., 1971). Nevertheless, these in-vitro demonstrations of delayed hypersensitivity may not be relevant in vivo. However, with regard to the latter situation, Denny, Taylor-Robinson and Allison (1972) demonstrated that mice, immunosuppressed by thymectomy and X-irradiation and infected intranasally with M. pulmonis, developed lung lesions that were much less severe than those observed in infected but immunologically normal mice. Although the lung lesions in these mice and in M. pneumoniae-infected hamsters appear similar, this does not necessarily mean that thymusdependent mechanisms are also important in the development of hamster lung lesions.Because we are particularly interested in the hamster as a model for the human disease, the effect of thymus-dependent lymphocyte depletion on the development of M. pneumoniae-induced lung lesions in hamsters was investigated. Immunosuppression was effected by the use of anti-thymocyte serum. The present report records findings obtained with this model in two laboratories. MATERIALS AND METHODSMycoplasma pneumoniae strains. Virulent M. pneumoniae strains P1-104166, B8-Ml29 and P5-427AY known to produce pneumonia in hamsters were used. The mycoplasmas

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“…Although the glycophospholipid of M. pneumoniae is the serologically active component responsible for the reaction with complementfixing and metabolism-inhibition antibodies [2,4,7,11,[15][16][17], comparatively little is known about the cell component responsible for cell-mediated immunity in M. pneumoniae infection. Mizutani et al have recently reported that an acetone-insoluble fraction of M. pneumoniae cells elicits antigen(s) to the skin reaction in guinea pigs sensitized with whole cells [13]. In this report, we describe the isolation of water-soluble antigen fractions in nature which elicit activities for delayed hypersensitivity as measured by skin reactions in sensitized guinea pigs and macrophage migration inhibition by sensitized spleen cells, but not for complementfixing antibodies.…”

mentioning

confidence: 73%

“…The cell-mediated immune reaction to Mycobacterium pneumoniae in natural and experimental infections has recently been demonstrated by the use of lymphocyte transformation, macrophage migration inhibition and skin tests [1, 3,13]. Although the glycophospholipid of M. pneumoniae is the serologically active component responsible for the reaction with complementfixing and metabolism-inhibition antibodies [2,4,7,11,[15][16][17], comparatively little is known about the cell component responsible for cell-mediated immunity in M. pneumoniae infection.…”

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confidence: 99%

Studies on Delayed Hypersensitivity of Antigens Isolated from Mycoplasma pneumoniae Cells

Suzuki

Hayashi

Arai

et al. 1976

Japanese Journal of Microbiology

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Cells of Mycoplasma pneumoniae Mac strain were fractionated into acetone-soluble and insoluble fractions.Acetone-insoluble fractions were digested with pronase and further purified by chromatography on Sephadex G-75, yielding three water-soluble fractions which were free from lipid and consisted mainly of polysaccharide-protein complex.All these water-soluble fractions possessed eliciting antigenicity to delayed hypersensitivity for M. pneumoniae as measured by skin reactions and macrophage migration inhibition tests, but not to complement-fixing antibodies.In contrast, the acetone-soluble fraction was reactive with the complement-fixing antibodies but not for the delayed hypersensitivity. M. pneumoniae and their cultivation. The Mac strain of M. pneumoniae was used. The organisms were grown in 10-liter Roux bottles in a broth medium consisting of seven parts PPLO broth (Difco), two parts horse serum and one part 25% yeast extract [4]. The medium was supplemented with 1.0% glucose, 0.05% thallium acetate and 0.002% phenol red, and adjusted to pH 7.8. The bottles were incubated in a stationary position for 5 days at 37 C under aerobic conditions. The organisms were then sedimented from the medium by centrifugation. The sediment was washed three times in 0.15 M phosphatebuffered saline pH 7.2 (PBS) by further centrifugation in a Spinco model L centrifuge at 14 000 rpm.Carbohydrate analysis. Quantitative determination of carbohydrates was performed according to the methods described by Winzler [20]. Carbohydrate components Requests for reprints should be addressed to Dr.

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Delayed Hypersensitivity in Mycoplasma Pneumoniæ Infections

Cited by 33 publications

References 8 publications

The Upper and Lower Respiratory Tracts Differ in Their Requirement of IFN-γ and IL-4 in Controlling Respiratory Mycoplasma Infection and Disease

The Upper and Lower Respiratory Tracts Differ in Their Requirement of IFN-γ and IL-4 in Controlling Respiratory Mycoplasma Infection and Disease

Reduction in the Severity of Mycoplasma Pneumoniae-Induced Pneumonia in Hamsters by Immunosuppressive Treatment with Anti-Thymocyte Sera

Studies on Delayed Hypersensitivity of Antigens Isolated from Mycoplasma pneumoniae Cells

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