| Pneumonia is one of the most common diseases in children and bacteria, virus, mycoplasma, chlamydia are the major pathogens of children's pneumonia. A series of proper prevention and treatment are of great benefit to patients with pneumonia. Many cases of the pneumonia were induced by more than one pathogen and increasing drug resistance and lack of effective antiviral drugs make the treatment of children's pneumonia much more difficult than before. It is urgent to develop new and proper treatment. It is widely accepted that pathogens destroy lung tissue not only by their proliferation but also by inducing immune reaction which results in the unbalance between inflammatory and anti-inflammatory response. Generally, high dose of gamma globulin and systematically used glucocorticoid are used to regulate the inflammatory response. Although gamma globulin is effective, it is expensive and has uncertain side effects, such as occasional allergic reaction, hematuria and so on. Systemic glucocorticoid also has many side effects all. So both of them can not serve as routine therapeutic method. It has been widely accepted that ICS inhibit the inflammatory response of airway in asthma and BUD is the only ICS that can be applicated by aerosol inhalation. It has been reported that BUD is effective on pneumonia and acute bronchitis but seldom reports have ever mentioned about the mechanisms involved. How does BUD work? How does BUD regulate the inflammatory response in pneumonia? To elucidate the possible mechanisms mentioned above, we determined serum levels of Tumor necrosis factor-alpha (TNF-α), Gamma Interferon(IFN-γ), and Interleukin-4(IL-4) in patients with pneumonia before and after treatment.40 cases of pneumonia were selected, and all of the cases were diagnosed according to the diagnostic criteria of Practical Paediatrics compiled by Zhu Futang. Patients were randomly divided into 2 groups. Patients of group 1 were treated with conventional methods while Patients of group 2 were treated with both of conventional treatment and BUD aerosol inhalation at the same time. Meanwhile, 14 healthy children(of the same age) without inflammation were randomly selected as control.Serum levels of TNF-α,IFN-γand IL-4 were determined with sandwich ELISA before and after 1 week of treatment in experimental and control gropus, respectively. The data were then statistically analyzed with SPSS software.The result showed: Compared with control group, serum levels of TNF-α, IFN-γand IL-4 of routine treatment group were higher than those of control group(P<0.01); The expression of TNF-αand IL-4 decreased(P<0.001) after routine treatment and BUD administration resulted in the significant decrease comparing with routine treatment group as well as control group(P<0.05). The expression of IFN-γwas not changed after routine treatment(P>0.05), while it was down-regulated by adding BUD(P<0.05). All of the evidence we got demonstrated that inflammatory response and activating of anti-inflammatory response occurred during the pathophysiological process of paediatric pneumonia and several cytokines(such as TNF-α, IFN-γand IL-4) were potentially involved in this process; Compared with routine treatment group, the expression of TNF-αand IL-4 in serum was down-regulated significantly in patients who accepted BUD aerosol inhalation implying that BUD aerosol inhalation may worked by inhibiting the synthesis of TNF-αand IL-4.Similar to other infections, the balance of anti-inflammatory factors and inflammatory factors directs the prognosis of penumonia. Tumor necrosis factor-alpha(TNF-α) is the most fundamental factor in SIRS, which plays an important role in the development of pneumonia. It has been regarded as a criteria to evaluate the severity and recovery of pneumonia. The balance of T helper cell 1(Th1) and T helper 2 cell (Th2) is critical in regulating cell immune function; the expression of IFN-γand interleukin-4 IL-4 can reflect the immune state of Th1 and Th2 respectively.This study demonstrated that the expression of TNF-α, IL-4, IFN-γwas up-regulated in children with pneumonia, implying that pulmonary infection may simultaneously activates inflammatory response and anti-inflammatory reaction, mediates tissue necrosis and leads to the immune damage of lung; The elevation of IL-4 may result in chronicity of the infection. Routine treatment plus BUD aerosol inhalation may inhibit the effect of over-expressed TNF-αand IL-4 and this inhibition maybe one of the interpretations for therapeutic effect of BUD on pneumonia. On the other hand, the decreased expression of IFN-γinduced by BUD administration may delay the elimination of the pathogen. However, since inflammation reaction is a complicated process and a network composed of multiple cytokines has involved in its regulatory, further investigation is required to elucidate the exact therapeutic mechanism of BUD aerosol inhalation in pneumonia.
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