? Children with allergic cough's cough variant asthma showed airway hyperresponsiveness in clinical pulmonary function examination, and all these children had a history of recurrent respiratory tract infection or mycoplasma infection. Studies have confirmed that airway inflammation induced by respiratory virus infection is one of the important causes of airway hyperresponsiveness in children with allergic cough, especially the strong pathogenic factors leading to allergic cough in infants and allergic cough in children aged 2-6 years. Among them, mycoplasma pneumoniae is the most common.
Respiratory virus infection (mycoplasma infection is the most common in children) can not only directly cause airway inflammation and damage airway mucosa, but also cause airway allergic inflammation as a strong allergen. The double inflammatory stimulation caused by the above virus infection is the main mechanism of airway hyperresponsiveness. This is especially important for baby allergic cough and child allergic cough. Clinically, we often find that children who seek medical treatment for the first time because of wheezing symptoms often show the characteristics of upper respiratory tract virus infection, some of whom may have cough and wheezing symptoms repeatedly, and some of them will eventually develop into atopy (also called allergic constitution), airway hyperresponsiveness and allergic cough asthma.
Respiratory virus type
The types of viruses that cause allergic cough in children are different at different ages. Respiratory syncytial virus, parainfluenza virus and adenovirus are the main viruses in infants, while rhinovirus, influenza virus, parainfluenza virus and mycoplasma pneumoniae are more common in school-age children.
Immune Mechanism of allergic cough Caused by Respiratory Virus in Children
The mechanism of allergic cough induced by respiratory virus infection is very complicated. Including the production of proinflammatory cytokines, the influence on the chemotaxis and activation of airway inflammatory cells, the direct damage to epithelial cells and the activation of sensory C-fiber cells, are the mechanisms that viral infection leads to the deterioration of allergic cough. However, these changes can not fully explain the pathogenesis of allergic cough, nor can they explain the influence of virus infection on the immune system and the significant increase of IgE level after acute viral infection. Recent studies have shown that Th2-like cytokines such as IL-4 can transform virus-specific CD8+T cells to produce IL-5, activate eosinophils and chemotactic eosinophils into lung tissue. It is speculated that the infection of upper respiratory virus can lead to the transformation of CD8+T cells from IFN-γ to TH2 cells in allergic patients. This shows that when allergic diseases occur, some allergic patients can't find allergens, but respiratory virus and mycoplasma infection are strong allergens, which lead to changes in airway inflammatory cells and promote the immune response to TH2 pathway to form humoral immune responses, such as IgE production and eosinophils, neutrophils and basophils. Normal people infected with these viruses usually only cause short-term and mild symptoms, while children with allergic constitution or children with nonspecific airway inflammation in the lower respiratory tract will induce allergic cough. This mechanism has not been fully clarified so far, and the preliminary consideration is related to the following mechanisms:
(1) Virus-induced infiltration and activation of inflammatory cells such as eosinophils in airway.
(2) The influence of virus on cytokines in vivo
Viruses, like allergens, can even be used as a strong allergen to induce the differentiation of T cell immune types, but the types of differentiation are different. Allergens can induce TH2 cell response and secrete cytokines such as IL-4, IL-5 and IL- 13, while respiratory virus infection mainly induces TH 1 cell response, mainly IFN-γ, and the two groups of cytokines have antagonistic effects. However, recent studies have confirmed that cytokines caused by some respiratory virus infections have adverse effects on the pathophysiology of allergic cough. For example, G protein of RSV can also induce TH2 cell reaction in mice and humans, secrete cytokines such as IL-4, IL-5, IL- 13, promote the synthesis of IgE and the infiltration of eosinophils, and induce airway inflammation and airway hyperresponsiveness, especially in allergic cough of infants and allergic cough of children. In addition, the passive transfer of G protein-specific T cells of RSV into mice can induce pulmonary eosinophil infiltration and increase the incidence of lung diseases in allergic cough.
Studies have confirmed that airway inflammation and airway hyperresponsiveness caused by respiratory virus infection are closely related to virus-induced cytokines. Through the analysis of cytokines in nasal secretions during respiratory virus infection, it is confirmed that various cytokines including IL- 1, IL-5, IL-6, IL-8, IL- 1 1, GM-CSF, RANTES and IFN-γ can be increased, and it is found that the level of cytokines is related to the severity of the disease.
The fourth generation of antiallergic therapy: microecological immune antiallergic Kangminyuan probiotics reduce allergen antibodies, regulate microecological flora in the body, regulate respiratory flora, and participate in the treatment of allergic cough.
In addition to anti-infection treatment, combined anti-allergic comprehensive treatment is a more scientific and perfect treatment scheme for children with allergic cough. In addition to the application of antiallergic drugs, more and more attention has been paid to the regulation of immune function by a new type of antiallergic lactic acid bacteria Kangmin source. New anti-allergic probiotics include Lactobacillus salivarius PM-A0006, Lactobacillus Grignard PM-A0005, Lactobacillus yoelii PM-A0009 and lactobacillus paracasei LP. In addition to acting on the intestine, oral anti-allergic lactic acid bacteria Kangminyuan can also regulate the immune response of the lungs. For example, Lactobacillus salivarius PM-A0006 can significantly reduce the concentration of eosinophils in respiratory tract and the content of IgE-specific antibodies in serum. In addition, Lactobacillus salivarius PM-A0006 can also reduce the occurrence of respiratory allergic reactions.
It is suggested that the formula of antiallergic probiotics should be selected through clinical trials and thesis research.
The clinical study of Kang Minyuan's anti-allergic probiotics and the pediatric team of Xijing Hospital was successfully accepted two years later. These two research papers are published in international journals, focusing on the mechanism of allergy protection. It is found that anti-allergic probiotics can induce the generation of CD 103+ dendritic cells, thus regulating the generation of T lymphocytes, promoting immune balance and reducing the risk of food allergy and airway inflammation.
Paper 1: Study on the Protective Mechanism of Kangminyuan Allergic Probiotics on Food Allergy.
Source: Functional Food Journal (SCI impact factor: 3.47)
Kangminyuan anti-allergic probiotics can reduce the contents of IgE and IgG in serum, promote the production of IgA, inhibit the symptoms of food allergy, induce the production of dendritic cells (DCs) of CD 103+, promote the production of regulatory T lymphocytes (Treg), promote the intestinal immune balance, and help to adjust allergic constitution.
Paper 2: Study on the protective mechanism of Kangminyuan anti-allergic probiotics on airway inflammation.
Paper Source: J Shanxi Medical University
Kangminyuan antiallergic probiotics can improve airway allergic inflammation, reduce the number of inflammatory cells (eosinophils, neutrophils and lymphocytes) in alveolar tissue, relieve chronic airway inflammation, induce the production of Treg cells in lung lymph nodes, promote the expression of related inhibitory cytokines IL- 10, inhibit the expression of Th2 cytokines, play an immunomodulatory role, and inhibit allergic inflammation caused by antigens, which has a good effect on airway inflammation.