Nitric oxide in both bronchoalveolar lavage fluid and serum is associated with pathogenesis and severity of antigen-induced pulmonary inflammation in rats.
BACKGROUND
Nitric oxide (NO) is considered as a hallmark for allergic airway inflammation in asthmatics and animal models. But the correlation between NO and antigen-induced pulmonary inflammation (AIPI), a rat model for asthma, in varying genetic background population has not been completely understood.


OBJECTIVE
The objective in this study is to observe the different responsiveness to AIPI in two commonly used inbred rat strains and verify the correlation between NO from different sources and pathological parameters of AIPI by using Dark Agouti (DA), E3, F1 (E3 x DA), and F2 rat populations.


METHODS
AIPI was induced by systemically immunizing and intranasally challenging E3, DA, F1 (DA x E3), and F2 rats with ovalbumin (OVA). Pathological changes and mucus secretion in lungs were observed after hematoxylin and eosin (HE) and periodic acid Schiff (PAS) staining, whereas eosinophils in bronchoalveolar lavage fluid (BALF) were counted after Giemsa staining. Delayed-type hyperresponsiveness was determined by subcutaneous injection of OVA in ear. Total immunoglobulin E (IgE) and OVA-specific IgG1 were detected with enzyme-linked immunosorbent assay (ELISA). NO concentration was measured by the Griess method.


RESULTS
DA rats were unresponsive to OVA treatment, whereas E3 rats were susceptible to AIPI. F1 rats manifested the same responsiveness to OVA treatment as DA rats, and individual F2 rats showed the variable severity of AIPI. NO concentration in BALF and serum was significantly elevated in E3 rats but not in DA and F1 rats after OVA treatment. In F2 rats, NO concentration in serum was positively correlated with eosinophils in BALF, total IgE, and pathological scores, whereas NO concentration in BALF correlated only with eosinophils in BALF and total IgE.


CONCLUSIONS
DA and F1 rats are resistant, whereas E3 rats are sensitive, to AIPI. NO in serum can represent the severity of allergic inflammation and pathological changes in lungs in F2 population.
Yang
Xudong
X
Department of Genetics and Molecular Biology, Xi'an Jiaotong University School of Medicine, Xir'an, Shaanxi 710061, PR China.
Sun
Qingzhu
Q
Asim
M B Raza
MB
Jiang
Xiaogang
X
Zhong
Bo
B
Shahzad
Muhammad
M
Zhang
Fujun
F
Han
Yan
Y
Lu
Shemin
S
D000818:Animals; D000941:Antigens / Q000276:immunology*; D001249:Asthma / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers / Q000032:analysis / Q000097:blood / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry*; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000473:pathology; D005260:Female; D006824:Hybridization, Genetic; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D009569:Nitric Oxide / Q000032:analysis / Q000097:blood* / Q000378:metabolism*; D010047:Ovalbumin / Q000276:immunology; D051381:Rats; D011919:Rats, Inbred Strains; D012727:Sex Characteristics; D014611:Vaccination
D000941:Antigens; D015415:Biomarkers; D007074:Immunoglobulin G; D009569:Nitric Oxide; D007073:Immunoglobulin E; D010047:Ovalbumin