Humoral and Cellular Immunity in Children withMycoplasma pneumoniaeInfection: a 1-Year Prospective Study

التفاصيل البيبلوغرافية
العنوان: Humoral and Cellular Immunity in Children withMycoplasma pneumoniaeInfection: a 1-Year Prospective Study
المؤلفون: Marta Popławska, Włodzimierz Stelmach, Tomasz Grzelewski, Paweł Majak, Małgorzata Podsiadłowicz-Borzęcka, Iwona Stelmach, Joanna Jerzyńska, Jarosław Dziadek
المصدر: Clinical and Vaccine Immunology. 12:1246-1250
بيانات النشر: American Society for Microbiology, 2005.
سنة النشر: 2005
مصطلحات موضوعية: Male, Microbiology (medical), Immunoglobulin A, Cellular immunity, Mycoplasma pneumoniae, Time Factors, Clinical Biochemistry, Immunology, Antibodies and Mediators of Immunity, Immunoglobulin E, medicine.disease_cause, Immunoglobulin G, Immunophenotyping, Immune system, Pneumonia, Mycoplasma, medicine, Humans, Immunology and Allergy, Lymphocytes, Prospective Studies, Immunity, Cellular, biology, respiratory tract diseases, Immunoglobulin Isotypes, Child, Preschool, Immune System, Antibody Formation, Humoral immunity, biology.protein, Female, Antibody
الوصف: To determine whether children have persistent abnormalities in cellular and humoral immunity development after acute Mycoplasma pneumoniae infection, serum immunoglobulin G (IgG), IgA, IgM, and IgE levels and lymphocyte phenotypes were determined. There were no changes in the levels of IgG, IgM, IgA, or CD4 or CD19 lymphocytes that were measured in M. pneumoniae-positive patients after 3 months or after 12 months, but there were increases in these in M. pneumoniae-negative patients. Serum IgE increased in M. pneumoniae-positive patients. We have shown alterations in immunity development after M. pneumoniae infection. Mycoplasma pneumoniae is a common pathogen of children’s respiratory tracts (8), and its abilities to act as a polyclonal activator of lymphocytes and autoantibodies to various tissues and immune complexes are well known (2, 16). CD4 T cells, B cells, and plasma cells infiltrate the lungs, which is followed by further amplification of the immune response, namely, proliferation of lymphocytes, production of immunoglobulins, and release of proinflammatory cytokines (3, 14). It has been previously described that the levels of total immunoglobulins, immunoglobulin A (IgA), IgM, and IgG, in serum increase during the convalescent phase of the disease (19) and that there is production of IgE specific to M. pneumoniae during infection (18). The bronchoalveolar lavage cytokine data suggest a predominant Th2-like cytokine response in M. pneumoniae infections, thus representing a favorable condition for IgE production (7), although other results suggest a Th1 cytokine response predominance (5, 21). Previous studies are confined to the acute phase of M. pneumoniae infection and do not answer questions about the possible duration of the humoral and cellular imbalance after M. pneumoniae infection in children. In this study, we hypothesized that children may have persistent abnormalities in cellular and humoral immunity development after acute M. pneumoniae infection. The study participants included 110 patients (52 male and 58 female) aged 1 to 5 years, all suffering from recurrent respiratory tract infections, defined according to Ribeiro (15). The diagnosis of M. pneumoniae infection was based on clinical symptoms (12, 20) and the presence of IgM, determined by enzyme-linked immunosorbent assay (ELISA) and confirmed by PCR. Children diagnosed with M. pneumoniae infection were treated with clarithromycin (4). None of the patients had previously suffered from allergic disease or immunodeficiency syndrome. The characteristics of the patients are presented in Table 1. There were five study visits. At the first visit, patients were informed about the purpose of the study and were told that the second visit would occur after 3 months or earlier (in the case of respiratory tract infection). The patient’s medical history was recorded, a physical examination was done, and blood samples for IgG, IgA, IgM, and IgE serum levels and lymphocyte phenotypes were taken at each visit. During the second visit, a blood sample was taken to determine the presence of M. pneumoniae-specific IgM by ELISA. For patients who had M. pneumoniae IgM, the third visit occurred 1 week after the second, for determination of M. pneumoniae DNA by PCR. For patients without M. pneumoniae IgM, the third visit occurred 3 weeks after the second, when a blood sample was collected for the second determination of M. pneumoniaespecific IgM by ELISA. The fourth visit was 3 months after the second, and the fifth visit was 12 months after the second. Blood samples (5 ml) were collected, serum specimens were stored frozen, and the acute- and convalescent-phase serum specimens from each patient were tested for IgM antibodies in the same run. Upon their receipt, serum samples were serologically investigated for M. pneumoniae-specific IgM antibodies, using a commercial ELISA kit (Viro-Immun Labor-Diagnostica, Germany). We used capillary PCR to diagnose M. pneumoniae infection (6). Two whole-blood samples (3 ml) were obtained from each patient and were collected into sterile sodium heparinized tubes. The presence of Mycoplasma DNA in the clinical samples collected was tested using a nested-PCR assay with primers MPP-11, MPP-12, and MPSW-1 (TGCCATCAACCCGCG
تدمد: 1556-679X
1556-6811
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a16d52abfb6d824c075a07fec2aaa59fTest
https://doi.org/10.1128/cdli.12.10.1246-1250.2005Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....a16d52abfb6d824c075a07fec2aaa59f
قاعدة البيانات: OpenAIRE