Asthma ; immunology ; virology ; Bronchiolitis, Viral ; complications ; immunology ; virology ; Child ; Humans ; Respiratory Syncytial Virus Infections ; complications ; genetics ; immunology ; Risk Factors ; Severity of Illness Index

AIMTo study the relation between Respiratory Syncytial Virus infection and asthma development by measuring airway responsiveness (AR) and M2R function.

METHODSGuinea pigs (n = 34) were randomly divided into 4 groups: Hep-2/NS group (group A, n = 9), RSV/NS group (group B, n =9), Hep-2/OVA group (group C, n = 8) and RSV/OVA group(group D, n = 8). On day 21 after infection we tested AR and M2R. Then counted eosinophils in BALF and observed pathological change.

RESULTSIntraairway pressure(IP mmH20) of group B had no significant difference with group A(P > 0.01), and the extent of IP decrease also had no difference between groups A and B (P > 0. 05), but IP of C group were much higher than group A (P<0.05), with extent of IP decrease lower than group A (P < 0.05). And IP of group D were higher than group C (P < 0.01), with the extent of IP decrease much lower than group C (P < 0.05).

CONCLUSIONRSV infection could enhance OVA-induced M2R dysfunction, then develop AHR.

Animals ; Asthma ; immunology ; physiopathology ; virology ; Bronchial Hyperreactivity ; immunology ; physiopathology ; virology ; Female ; Guinea Pigs ; Male ; Ovalbumin ; immunology ; Random Allocation ; Receptor, Muscarinic M2 ; physiology ; Respiratory Syncytial Virus Infections ; immunology ; Respiratory Syncytial Viruses ; immunology

OBJECTIVETo determine the role of serum leptin in infants with wheezing after respiratory syncytial virus infected.

METHODS43 infants infected with RSV were given blood samples to detect leptin concentration with radioimmunoassays (RIA) within 24 hours after admission into hospital, discharged and 12 weeks later. Then, they were followed up for 2 years. 10 healthy children of the same age served as controls.

RESULTS41.9% infants developed asthma after infected with RSV. Compared to control group, the serum level of leptin in the asthma group and non-asthma group were significantly higher before treatment (t = 3.41 and 2.64 respectively, P < 0.05). When they were discharged, the serum level of leptin in the asthma group was significantly higher than that in non-asthma group and control group (t = 5.74 and 6.23, respectively, P < 0.05). 12 weeks later, the serum level of leptin in the asthma group was still significantly higher than that in non-asthma group and control group (t = 6.32 and 6.11, respectively, P < 0.05), but there were no difference between non-asthma group and control group (t = 0.81, P > 0.05).

CONCLUSIONThe serum level of leptin in infants with asthma after RSV infected was higher than that in healthy and non-asthma children. Persistent higher level of leptin may play an important role in infants with asthma after RSV infected.

Asthma ; blood ; immunology ; virology ; Case-Control Studies ; Child, Preschool ; Female ; Follow-Up Studies ; Humans ; Infant ; Leptin ; blood ; immunology ; Male ; Respiratory Sounds ; immunology ; Respiratory Syncytial Virus Infections ; blood ; immunology ; virology ; Respiratory Syncytial Viruses ; immunology ; physiology

Asthma is characterized by airway inflammation induced by immune dysfunction to inhaled antigens. Although respiratory viral infections are the most common cause of asthma exacerbation, immunologic mechanisms underlying virus-associated asthma exacerbation are controversial. Clinical evidence indicates that nitric oxide (NO) levels in exhaled air are increased in exacerbated asthma patients compared to stable patients. Here, we evaluated the immunologic mechanisms and the role of NO synthases (NOSs) in the development of virus-associated asthma exacerbation. A murine model of virus-associated asthma exacerbation was established using intranasal challenge with ovalbumin (OVA) plus dsRNA for 4 weeks in mice sensitized with OVA plus dsRNA. Lung infiltration of inflammatory cells, especially neutrophils, was increased by repeated challenge with OVA plus dsRNA, as compared to OVA alone. The neutrophilic inflammation enhanced by dsRNA was partly abolished in the absence of IFN-gamma or IL-17 gene expression, whereas unaffected in the absence of IL-13. In terms of the roles of NOSs, dsRNA-enhanced neutrophilic inflammation was significantly decreased in inducible NOS (iNOS)-deficient mice compared to wild type controls; in addition, this phenotype was inhibited by treatment with a non-specific NOS inhibitor (L-NAME) or an specific inhibitor (1400 W), but not with a specific endothelial NOS inhibitor (AP-CAV peptide). Taken together, these findings suggest that iNOS pathway is important in the development of virus-associated exacerbation of neutrophilic inflammation, which is dependent on both Th1 and Th17 cell responses.
Animals ; Asthma/*immunology/virology ; Imines/pharmacology ; Mice ; Mice, Inbred BALB C ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase Type II/antagonists & inhibitors/*metabolism ; RNA, Double-Stranded/metabolism ; Th1 Cells/*immunology ; Th17 Cells/*immunology

Acute Disease ; Adolescent ; Asthma ; immunology ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; RNA, Viral ; genetics ; Respiratory Syncytial Viruses ; genetics ; Respiratory Tract Infections ; immunology ; virology ; Reverse Transcriptase Polymerase Chain Reaction