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1.
Ann Allergy Asthma Immunol ; 119(2): 146-152.e2, 2017 08.
Artigo em Inglês | MEDLINE | ID: mdl-28634021

RESUMO

BACKGROUND: Acute infections with Mycoplasma pneumoniae (Mp) have been associated with worsening asthma in children. Mp can be present in the respiratory tract for extended periods; it is unknown whether the long-term persistence of Mp in the respiratory tract affects long-term asthma control. OBJECTIVE: To determine the effect of Mp on asthma control. METHODS: We enrolled 31 pediatric subjects 3 to 10 years of age with persistent asthma who completed up to 8 visits over a 24-month period. We detected Mp by antigen capture and polymerase chain reaction. Primary outcome measurements included symptom scores, quality of life, medication scores, oral corticosteroid use, health care usage, school absences, and exhaled breath condensate pH. RESULTS: Low levels of Mp community-acquired respiratory distress syndrome toxin were detected in 20 subjects (64.5%) at enrollment. Subjects with Mp positivity at a given visit had a .579 probability of remaining Mp positive at the subsequent visit, whereas those with Mp negativity had a .348 probability of becoming Mp positive at the following visit. The incidence of Mp overall was higher in the spring and summer months. Overall, we found no significant relation between the detection of Mp and worse outcome measurements at the same visit or at subsequent visits. CONCLUSION: The long-term persistence of Mp in the respiratory tract is common in children with asthma. However, the detection of Mp was not associated significantly with worse asthma symptoms, quality of life, health care usage, school absences, or exhaled breath condensate pH in this pediatric asthma cohort.


Assuntos
Asma/imunologia , Asma/microbiologia , Nível de Saúde , Mycoplasma pneumoniae/isolamento & purificação , Qualidade de Vida , Sistema Respiratório/microbiologia , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Mycoplasma pneumoniae/imunologia , Pneumonia por Mycoplasma/imunologia , Pneumonia por Mycoplasma/microbiologia , Estudos Prospectivos , Estações do Ano
2.
Infect Immun ; 80(1): 289-97, 2012 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22083707

RESUMO

Yersinia enterocolitica is a food-borne pathogen that preferentially infects the Peyer's patches and mesenteric lymph nodes, causing an acute inflammatory reaction. Even though Y. enterocolitica induces a robust inflammatory response during infection, the bacterium has evolved a number of virulence factors to limit the extent of this response. We previously demonstrated that interleukin-1α (IL-1α) was critical for the induction of gut inflammation characteristic of Y. enterocolitica infection. More recently, the known actions of IL-1α are becoming more complex because IL-1α can function both as a proinflammatory cytokine and as a nuclear factor. In this study, we tested the ability of Y. enterocolitica to modulate intracellular IL-1α-dependent IL-8 production in epithelial cells. Nuclear translocation of pre-IL-1α protein and IL-1α-dependent secretion of IL-8 into the culture supernatant were increased during infection with a strain lacking the 70-kDa virulence plasmid compared to the case during infection with the wild type, suggesting that Yersinia outer proteins (Yops) might be involved in modulating intracellular IL-1α signaling. Infection of HeLa cells with a strain lacking the yopP gene resulted in increased nuclear translocation of pre-IL-1α and IL-1α-dependent secretion of IL-8 similar to what is observed with bacteria lacking the virulence plasmid. YopP is a protein acetylase that inhibits mitogen-activated protein kinase (MAP kinase)- and NF-κB-dependent signal transduction pathways. Nuclear translocation of pre-IL-1α and IL-1α-dependent secretion of IL-8 in response to Yersinia enterocolitica infection were dependent on extracellular signal-regulated kinase (ERK) and p38 MAP kinase signaling but independent of NF-κB. These data suggest that Y. enterocolitica inhibits intracellular pre-IL-1α signaling and subsequent proinflammatory responses through inhibition of MAP kinase pathways.


Assuntos
Proteínas de Bactérias/metabolismo , Células Epiteliais/microbiologia , Interleucina-1alfa/antagonistas & inibidores , Interleucina-8/biossíntese , Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores , Transdução de Sinais , Yersinia enterocolitica/patogenicidade , Transporte Ativo do Núcleo Celular , Proteínas de Bactérias/imunologia , Núcleo Celular/química , Citoplasma/química , Regulação para Baixo , Células Epiteliais/imunologia , Células HeLa , Humanos , Interleucina-8/antagonistas & inibidores , Fatores de Virulência/imunologia , Fatores de Virulência/metabolismo , Yersinia enterocolitica/imunologia
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