Asthma is a common respiratory disease worldwide. Cytokines play a crucial role in the immune system and the inflammatory response to asthma. Abnormal cytokine expression may lead to the development of asthma, which may contribute to pathologies of this disease. As cytokines exhibit pleiotropy and redundancy characteristics, we summarized them according to their biologic activity in asthma development. We classified cytokines in three stages as follows: Group 1 cytokines for the epithelial environment stage, Group 2 cytokines for the Th2 polarization stage, and Group 3 cytokines for the tissue damage stage. The recent cytokine-targeting therapy for clinical use (anti-cytokine antibody/anti-cytokine receptor antibody) and traditional medicinal herbs (pure compounds, single herb, or natural formula) have been discussed in this review. Studies of the Group 2 anti-cytokine/anti-cytokine receptor therapies are more prominent than the studies of the other two groups. Anti-cytokine antibodies/anti-cytokine receptor antibodies for clinical use can be applied for patients who did not respond to standard treatments. For traditional medicinal herbs, anti-asthmatic bioactive compounds derived from medicinal herbs can be divided into five classes: alkaloids, flavonoids, glycosides, polyphenols, and terpenoids. However, the exact pathways targeted by these natural compounds need to be clarified. Using relevant knowledge to develop more comprehensive strategies may provide appropriate treatment for patients with asthma in the future.

Congenital tuberculosis (TB) is difficult to detect because the disease presents few or no symptoms in the fetus during pregnancy and nonspecific symptoms in neonates. We reviewed 20 cases of congenital TB reported between 2011 and 2017 and report a case of a mother and her 8 days old neonate with congenital TB. In these 21 cases (including our case), the most common clinical presentations were respiratory distress, fever, and hepatosplenomegaly. The most common chest imaging findings were pneumonia, multiple pulmonary nodules, and miliary pattern. The mortality rate of infants with TB was increased ~2.2-fold if their mothers had no symptoms. The case reported herein concerns an 8 days old neonate with the rare presentation of a 2 days history of fever, followed by abdominal distension without respiratory symptoms. Computed tomography (CT) imaging exhibited a large amount of right pleural effusion. Multiple antimicrobial therapies were administered to the neonate; however, his symptoms persisted. Repeat CT was used to identify a progressed disease with multiple nodules over the lung, spleen, and hepatic hilar region. Standard anti-TB medications were prescribed, and the patient recovered gradually. Both gastric lavage and pleural effusion cultures confirmed the diagnosis of TB. The neonate's mother denied any TB contact history and the diagnosis of any medical disease during pregnancy, but she experienced a fulminant course of miliary TB and was admitted to the intensive care unit 24 days postpartum. She died despite receiving anti-TB treatment. In TB-endemic areas, congenital TB should be taken into consideration when neonates develop fever, respond poorly to antimicrobial treatment, and when their mothers deny any TB contact history.

Asthma is a chronic inflammatory disease affecting the airway, and it is characterized by a wheezing breathing sound, variable airflow obstruction and the presence of inflammatory cells in the submucosa of the bronchi. Viral infection, pollutants and sensitivity to aeroallergens damage the epithelium from childhood, which causes asthma. The pathogenesis of asthma includes pathways of innate stimulation by environmental microbes and irritant pathogens. Damaged epithelial cells produce thymic stromal lymphopoietin (TSLP) and stimulate myeloid dendritic cell maturation through the thymic stromal lymphopoietin receptor (TSLPR) heterocomplex. TSLP-activated myeloid dendritic cells promote naive CD4⁺ T cells to differentiate into T helper type 2 (Th2) phenotype CD4⁺ T cells. Re-exposure to allergens or environmental stimuli causes an adaptive immune response. TSLP-activated dendritic cells expressing the OX40 ligand (OX40L; CD252) trigger naive CD4⁺ T cells to differentiate into inflammatory Th2 effector cells secreting the cytokines interleukin-4, 5, 9, and 13 (IL-4, IL-5, IL-9 and IL-13), and the dendritic cells (DCs) promote the proliferation of allergen-specific Th2 memory cells. Allergen presentation by Th2 cells through its interaction with their receptors in the presence of major histocompatibility complex (MHC) class II on B cells and through costimulation involving CD40 and CD40L interactions results in immunoglobulin class switching from IgM to IgE. DCs and other blood cell subsets express the TSLPR heterocomplex. The regulatory mechanism of the TSLPR heterocomplex on these different cell subsets remains unclear. The TSLPR heterocomplex is composed of the IL-7Rα chain and TSLPR chain. Moreover, two isoforms of TSLP, short isoform TSLP (sfTSLP) and long isoform TSLP (lfTSLP), have roles in atopic and allergic development. Identifying and clarifying the regulation of TSLPR and IL-7Rα in pediatric asthma are still difficult, because the type of blood cell and the expression for each blood cell in different stages of atopic diseases are poorly understood. We believe that further integrated assessments of the regulation mechanism of the TSLP–TSLPR heterocomplex axis in vitro and in vivo can provide a faster and earlier diagnosis of pediatric asthma and promote the development of more effective preventive strategies at the onset of allergies.

Kawasaki disease (KD), also called mucocutaneous lymph node syndrome, is a febrile multisystem vasculitis mainly affecting children younger than 5 years. KD typically manifests as skin lesions and in the lymph nodes and oral and conjunctival mucosa. It may induce coronary artery abnormalities, such as aneurysms, but gastrointestinal and hepatobiliary involvement are not common. We reviewed 32 cases of patients with a diagnosis of KD with hepatobiliary involvement between 2000 and 2021 and present the case of a 4-year-old girl who received a diagnosis of KD with combined cholestatic hepatitis and Mycoplasma pneumoniae infection. In the 33 cases reviewed, in addition to the classical clinical findings of KD, the most common clinical presentations were jaundice and abdominal pain. Moreover, abnormal laboratory results indicating hyperbilirubinemia, cholestasis, and hepatitis, among other conditions, were noted. Abdominal ultrasonography revealed abnormal findings in more than half children with KD with hepatobiliary involvement. Furthermore, cardiac involvement was noted in a high proportion of the patients. In particular, we noted the case of a 4-year-old girl with a rare presentation of 3-day fever combined with abdominal pain and jaundice. Her levels of aspartate aminotransferase, alanine aminotransferase, total bilirubin, direct bilirubin, alkaline phosphatase, and γ-glutamyl transpeptidase were 489 (15–50) U/L, 253 (5–45) U/L, 4.3 (<1.5) mg/dl, 2.4 (<0.2) mg/dl, 337 (134–315) U/L, and 145 (5–32) U/L, respectively. These results were indicative of cholestatic hepatitis. Furthermore, her serological test results for mycoplasma infection were positive. KD was diagnosed because the patient had high fever for more than 5 days and presented with lymphadenopathy on the left side of neck, a polymorphic skin rash, redness of oral mucosa with strawberry tongue, and nonpurulent conjunctival congestion. After intravenous immunoglobulin injection (IVIG) and acetylsalicylic acid administration, the fever subsided rapidly and clinical manifestations, such as jaundice and abdominal pain, were mitigated. The laboratory parameters gradually returned to within normal ranges. Echocardiography revealed no aneurysm. In conclusion, KD with cholestatic hepatitis should be considered when pediatric patients present with fever combined with abdominal pain and jaundice. Early treatment with IVIG and aspirin is recommended and can effectively relieve cholestatic hepatitis.

Human noroviruses (HuNoV) are major causes of acute gastroenteritis around the world. The high mutation rate and recombination potential of noroviruses are significant challenges in studying the genetic diversity and evolution pattern of novel strains. In this review, we describe recent advances in the development of technologies for not only the detection but also the analysis of complete genome sequences of noroviruses and the future prospects of detection methods for tracing the evolution and genetic diversity of human noroviruses. The mechanisms of HuNoV infection and the development of antiviral drugs have been hampered by failure to develop the infectious virus in a cell model. However, recent studies have demonstrated the potential of reverse genetics for the recovery and generation of infectious viral particles, suggesting the utility of this genetics-based system as an alternative for studying the mechanisms of viral infection, such as cell entry and replication.